AJR 2001; 176:387-391
© American Roentgen Ray Society
Osteomyelitis Originating In and Around Bone Infarcts
Giant Sequestrum Phenomena
Marcia F. Blacksin1,
Kathleen C. Finzel2 and
Joseph Benevenia3
1
Department of Radiology, University of Medicine and Dentistry of New Jersey,
University Hospital, Rm. C320, 150 Bergen St., Newark, NJ 07103-2426.
2
Department of Radiology, SUNY Stony Brook, L-4 Health Sciences Center, Stony
Brook, NY 11794-2906.
3
Department of Orthopedic Surgery, University of Medicine and Dentistry of New
Jersey, Newark, NJ 07103-2426.
Received March 29, 2000;
accepted after revision July 17, 2000.
Address correspondence to M. F. Blacksin.
Abstract
OBJECTIVE. We describe four cases of osteomyelitis that occurred in
and around foci of preexisting osteonecrosis in the medullary cavity. Although
sequestration is a well-known complication of osteomyelitis, there is little
information known about infection occurring in proximity to large regions of
already necrotic bone.
CONCLUSION. Osteomyelitis and bone infarction can be seen in the
same patient population. Medullary infarcts may function as sequestra,
predisposing patients to osteomyelitis and soft-tissue infection.
Introduction
MR imaging has emerged as a formidable diagnostic tool in musculoskeletal
radiology, enabling easy diagnosis of entities once considered difficult to
assess. Bone infarction and avascular necrosis (AVN) are two such entities.
Bone and soft-tissue infections are more complex problems, and MR imaging is
evolving in its usefulness and specificity for these two processes
[1,
2]. Marrow infarction and
osteomyelitis should be seen in association with one another, because these
two entities occur in the same patient population. Individuals with sickle
cell anemia, systemic lupus erythematosus, and human immunodeficiency disease
as well as patients who have undergone renal transplantation are all
predisposed to develop these osseous complications either by way of their
primary disease or its treatment
[3,4,5].
We report the CT and MR imaging characteristics of four patients who had
osteomyelitis found in the medullary cavities of long bones adjacent to or in
foci of marrow infarction. To our knowledge, only three other reports of
osteomyelitis in necrotic bone are known
[6,7,8],
and only one describes MR imaging of this phenomenon
[8].
Subjects and Methods
From June 1998 through June 1999, all patients with a CT or MR imaging
diagnosis of abscess or osteomyelitis were prospectively reviewed for evidence
of bone infarction or AVN. The hypothesis for this study anticipated an
association between osteomyelitis and bone infarction and that these entities
should be found together. Any patient with the imaging criteria for
osteomyelitis and bone infarction or AVN, as outlined in this section, could
be entered into the study. An infecting organism had to be identified in all
cases. Four patients were identified using the imaging criteria, and their
clinical records were reviewed to identify predisposing factors for
development of bone infarcts. The patients (three males and one female) were
7-54 years old (mean age, 38.5 years).
MR imaging was performed on a Signa 1.5-T scanner (General Electric Medical
Systems, Milwaukee, WI) or a 1.0-T Vista scanner (Picker, Cleveland, OH).
Lesions in the distal femur and tibia were imaged with a transmit-receive
extremity coil. The proximal femoral lesion was imaged with a torso array
coil. Because the studies were performed at different sites, the imaging
protocols varied. All imaging protocols included axial and coronal T1-weighted
spin-echo sequences (TR range/TE range, 551-750/10-16) and axial, coronal, or
sagittal fat-saturated fast spin-echo sequences (2640-5000/92-96). One study
used a fast spin-echo inversion recovery sequence (TR/TE, 5166/36; inversion
time, 150 msec). Slice thickness ranged from 3 to 7 mm, each done at 1-mm
intervals. The number of excitations varied between 2 and 4, with image matrix
from 256 x 160 to 256 x 256. The fields of view varied with the
body part imaged. No gadolinium was injected.
CT was performed on either an Instaview helical scanner (Picker) or a
Twinflash scanner (Elscint, Haifa, Israel). Slice thickness ranged from 2.5 to
3 mm. IV contrast material was administered during one of the
examinations.
An MR diagnosis of osteomyelitis was based on several imaging findings.
Diagnosis was made when a region of bone marrow edema (low signal intensity on
T1-weighted images that brightened on T2-weighted fat-saturated or inversion
recovery images) was noted in the medullary cavity. Proximity to a fluid
collection in the soft tissues (abscess), cortical destruction, regions of
cortical thickening, and periostitis were other imaging characteristics
identified [2]. Because
osteomyelitis can reveal imaging findings seen with other marrow infiltrative
processes, the diagnosis was made tentatively until bacteriologic confirmation
of infection was established.
An MR diagnosis of AVN or marrow infarction was based on imaging
characteristics outlined by Mitchell et al.
[9]. A focus of AVN was
identified by a peripheral band of low signal intensity on all sequences. On
T2-weighted images, a band of high signal intensity paralleling the peripheral
band of low signal, the "double-line sign," was believed to be
pathognomonic of AVN [9]. CT
diagnosis of bone infarct consisted of a region outlined by a serpiginous band
of sclerosis in the medullary cavity
[10].
Results
Four patients were identified with both osteomyelitis and bone infarcts in
and around the infected regions. Bacterial cultures of two patients, a
54-year-old woman and a 43-year-old man, grew Staphlococcus aureus
from abscess or bone cultures and that from a 50-year-old man grew
Mycobacterium tuberculosis. A culture from a 7-year-old boy grew
methicillin-resistant S. aureus. On the basis of the belief that the
infarcts were acting as sequestra, all the patients were diagnosed as having
chronic or subacute osteomyelitis. All patients had a clinical history of
pain, tenderness, or fevers for time periods ranging from 1 to 3 months.
Predisposing factors for AVN were identified in three patients. The woman
had a long history of asthma and chronic, intermittent steroid use. The
43-year-old man had human immunodeficiency virus
[5] and a history of steroid
use for dermatitis. The boy had sickle cell anemia.
Frontal radiography of the 54-year-old woman showed a well-defined lytic
lesion (Fig. 1A). Cortical
thickening was seen on both radiography and CT (Figs.
1B and
1C), and the lytic lesion was
seen within the sclerotic border of an infarct. Multiple preexisting infarcts
were seen in other bones (Fig.
1C).
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Fig. 1A. —54-year-old woman with Staphylococcus aureus
osteomyelitis. Frontal radiograph of left knee shows cortical thickening
(open arrows), lytic lesion (arrowheads), and bone infarct
(solid arrows).
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Fig. 1B. —54-year-old woman with Staphylococcus aureus
osteomyelitis. CT scan of distal femoral shafts shows cortical thickening
(arrows) and sclerotic borders (arrowheads) of bilateral
bone infarcts.
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Fig. 1C. —54-year-old woman with Staphylococcus aureus
osteomyelitis. CT scan of supracondylar region of left knee shows cortical
destruction (large arrowhead) and osteolysis within borders
(small arrowheads) of infarct.
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MR imaging of the 43-year-old man showed multiple infarcts and an abscess
(Figs. 2A and
2B). Bone marrow edema was
visualized in the femoral infarct, which was believed to be infected (Fig.
2C). Its marrow signal
characteristics differed from that of the tibial infarct. The femoral infarct
was seen opening into an abscess cavity (Fig.
2B), and a double-line sign was
noted at its periphery (Fig.
2C).
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Fig. 2A. —43-year-old man with Staphylococcus aureus
infection. IV contrast-enhanced CT scan of left distal femur shows
rim-enhancing abscesses (small arrowheads) in soft tissues and
enhancement of synovium (large arrowheads) lining the surapatellar
bursa. Increased attenuation (open arrow) is also noted in medullary
cavity consistent with site of infection. Medullary cavity on right side is
normal.
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Fig. 2B. —43-year-old man with Staphylococcus aureus
infection. Sagittal T1-weighted MR image (TR/TE, 551/16) shows bone infarct
(arrowheads) in proximal tibia and inferior border of distal femoral
infarct (open arrow). Cortical destruction (curved arrow) is
seen opening into abscess. Distal femoral infarct is low signal centrally
(straight arrows) compared with tibial infarct.
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Fig. 2C. —43-year-old man with Staphylococcus aureus
infection. Coronal fat-suppressed fast spin-echo MR image (2640/92) shows
"double-line" sign at border of infarct (black
arrowheads) with increased signal intensity (arrows) inside
infarct. Note infarct (white arrowheads) in proximal tibia.
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The 50-year-old man had a well-defined lytic lesion in the proximal femur
(Fig. 3A). Bone marrow edema
was visualized completely surrounding a bone infarct within the shaft. The
edema was believed to represent osteomyelitis, and a soft-tissue abscess was
also noted (Figs. 3B and
3C).
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Fig. 3B. —50-year-old man with Mycobacterium tuberculosis
osteomyelitis. Coronal fast spin-echo MR image (TR/TE, 5000/90) shows bone
infarct (arrow) in marrow cavity of left femur surrounded by
low-signal-intensity process in marrow (arrowheads).
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Fig. 3C. —50-year-old man with Mycobacterium tuberculosis
osteomyelitis. Coronal fast spin-echo inversion-recovery MR image (5166/36;
inversion time, 150 msec) shows no change in appearance of infarct (solid
arrow) and increased signal intensity in surrounding marrow
(arrowheads). Note abscess (open arrow) adjacent to greater
trochanter.
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The 7-year-old boy showed infarcts in the distal tibia and subperiosteal
abscesses (Figs. 4A and
4B) of the tibia and fibula.
One tibial infarct showed central bone marrow edema and this was interpreted
as an infected infarct. The fibular shaft may have been infected by local
extension.
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Fig. 4A. —7-year-old boy with methicillin-resistant Staphlococcus
aureus osteomyelitis. Axial T1-weighted image MR image (TR/TE, 500/14) in
distal tibia shows infarct (arrowheads) with central low signal
intensity.
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Fig. 4B. —7-year-old boy with methicillin-resistant Staphlococcus
aureus osteomyelitis. Axial fat-suppressed fast spin-echo MR image
(5000/90) shows increased signal inside infarct (open arrow). Note
subperiosteal abscesses (arrowheads) around tibia and fibula and
edema (white arrows) in flexor and extensor muscles.
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Discussion
There are few reports in the medical literature describing osteomyelitis in
conjunction with osteonecrosis. Cooper et al.
[7] described a case of
Candida albicans in the femoral head of a patient with
steroid-induced AVN. Kahn and Bade
[6] reported S. aureus
osteomyelitis in the lunate of a patient with
Kienböck's disease. Epps et al.
[3] reported that tissue
infarction predisposes patients with sickle cell disease to osteomyelitis, but
there is a paucity of literature showing infarction with osteomyelitis on MR
imaging or CT in this population.
We believe that there is an association between preexisting AVN and
osteomyelitis. However, epidemiologic data tying the presence of preexisting
infarction to the development of osteomyelitis does not exist. The patient
population that develops AVN is also one that frequently presents with
osteomyelitis. Patients with lupus are immunocompromised from steroids and at
an increased risk of thrombosis as a result of the steroids and elevated
anticardiolipin antibodies [4].
The patient with human immunodeficiency virus is not only immunocompromised by
the nature of the disease, but may also have been treated with steroids for
pneumonia [5] and developed
infarcts. Patients with sickle cell disease develop AVN from vasoocclusive
crises and are susceptible to infection as a result of defective white cell
phagocytosis, splenic hypofunction, and the presence of dead tissue
[3]. Additional patients at
risk for both osteomyelitis and osteonecrosis include patients who have
undergone renal transplantation and those with lymphoproliferative disorders
because of steroid and immuno-suppressive therapy, but these patients were not
seen in this study.
Before the advent of MR imaging, differentiating between osteomyelitis and
infarction could be quite difficult. Fever, bone pain, and erythema are
characteristics of both processes. In the early phases of both diseases,
radiographs show soft-tissue swelling, focal osteopenia, or a permeative
pattern [3]. MR imaging
characteristics of both processes can also overlap. Both diseases, at some
point in their evolution, show a pattern of bone marrow edema. Erdman et al.
[11] has reported a "rim
sign," believed to represent fibrous tissue, as an MR finding of chronic
osteomyelitis. Tang et al.
[12] described a similar
finding in subacute osteomyelitis. The hallmark of AVN is a
low-signal-intensity peripheral band seen on all sequences, which may appear
similar to the rim sign. However, as with our 43-year-old male patient,
identification of the double-line sign on T2-weighted images
[9] is believed to be
pathognomonic for osteonecrosis.
Umans et al. [8] studied the
usefulness of MR imaging in differentiating between acute osteomyelitis and
acute bone infarction. That study identified three patients with both
processes in patients with sickle cell disease or lupus and found that IV
gadolinium can be used to differentiate between infarction and osteomyelitis.
Those with osteomyelitis showed a thick, irregular peripheral enhancement
around a nonenhancing center. Medullary infarction showed thin, linear rim
enhancement or a long segment of serpiginous central medullary
enhancement.
There are also significant differences between the two diseases. Tang et
al. [12] used MR imaging to
identify abscesses in cases of subacute osteomyelitis; they found sinus
tracts, sequestra, and involucra present in their patients with chronic
osteomyelitis. These findings are not seen with medullary infarction.
Sequestra are fragments of dead bone, usually cortical, that harbor the
infectious organisms [12]. To
develop infection, there must be vascular stasis and an environment that will
support bacterial growth. Regions of marrow infarction may supply this
medullary culture medium. All three adult patients in our study developed
osteomyelitis in a diametaphyseal location, not the typical subchondral
location [13]. We hypothesize
that the infarcts acted as "giant sequestra" in these patients,
and base these conclusions on the signal characteristics of the infarcts and
their position in the infected bone. These conclusions are speculative and are
based on imaging features seen in these cases.
The female patient and the 43-year-old man showed infarcts in several
bones, and there were unique imaging findings consistent with infection of one
infarct in each patient. Imaging of the 54-year-old woman showed osteomyelitis
within the outline of a bone infarct (Fig.
1A,1B,1C).
The 43-year-old man showed marrow edema within the peripheral borders of an
infarct on MR imaging (Figs. 2B
and 2C). Although it is
possible that this may have been a class C infarct as described by Mitchell et
al. [9] (low signal intensity
on short TR/TE sequences and high signal on long TR/TE sequences), the man
also showed cortical destruction at the edge of the infarct opening into an
abscess (Figs. 2A and
2B). The boy had subperiosteal
abscesses visualized on the same MR image depicting an infarct with a central
edema pattern (Fig. 4B). It
would seem more logical to attribute edema within these infarcts to infection,
rather than to call it a stage in infarct evolution.
The 50-year-old man showed radiographic features typical for M.
tuberculosis with a lytic lesion and little periostitis
[14] (Fig.
3A). Kahn and Pritzker
[13] stated that it is rare to
see extensive disruption of the vascular supply and sequestration of the bone
with a tuberculous exudate. This would make infarction as a complication of
this infection unlikely. Given the position of the infarct centrally within
the infection (Figs. 3B and
3C), we believe the infarct may
have acted as a sequestrum. There are some difficulties in proving the
association between preexisting osteonecrosis and osteomyelitis. First, there
are no prior radiographs available to prove that infarction was present before
infection occurred. However, 75% of the patients had conditions that would
have predisposed them to develop multiple infarcts. Two of the patients had
infarcts in other bones. Second, we are postulating that the visualized
infarcts are infected on the basis of the imaging findings, a fact that cannot
be proven histologically in this study. This report seeks to point out the
unique imaging features of these two processes when they are seen together,
and the strong likelihood that they should be seen together. The role of the
infarct as a sequestrum will need to be proven through larger studies.
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Abstract
Introduction
