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Case
Report -
A 43-year-old man with migrating arthralgias
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Jeff
Allen,
MD
He
is a 43-year-old white male with a history of hepatitis
C (treated with interferon and ribavirin for eight months)
who presented with migrating arthralgias for approximately
two months. Pain was initially noted in his right hip which
then migrated to his left knee followed by his left ankle
and was currently affecting his right ankle and foot. Around
the same time that he found the pain settling into his right
ankle, he noticed a painless lump developing over the head
of his clavicle. The lump had grown slowly in size, and
other than being unsightly, had caused no distress to the
patient. On review, he denied any recurrent fevers or chills
or any intravenous drug abuse, but did admit to having frequent
night sweats, fatigue, and some mild weight loss (five pounds
over two months). He was initially admitted to the oncology
service for a workup of his new clavicular mass. Imaging
of the mass revealed some bony destruction at the head of
the clavicle and an incidental loculated right pleural effusion.
Fluid aspirated from the loculated pleural effusion and
blood cultures head both grew out S. aureus and a
diagnosis of subacute hematogenous osteomyelitis was made.
He was treated with intravenous antibiotics in the hospital
for one week and discharged to home for continuation of
intravenous antibiotic therapy for a total of six weeks.
DISCUSSION
Osteomyelitis
is an infection of the bone which frequently leads to progressive
destruction of the bone, necrosis, and new bone formation.
It is often divided into three subgroups relating to the
pathogenesis of the disease: those cases arising from hematogenous
spread, those arising from contiguous spread, and those
associated with vascular insufficiency (i.e., the “diabetic
foot”). The time course of the infection is also used in
classifying infections as either acute (less than one week
of symptoms), subacute (one week to two months), or chronic
(more than two months). In normal bone, there is a high
degree of intrinsic resistance to infection. As such, there
are several factors that mitigate the development of osteomyelitis
including the underlying immune competence of the host,
the virulence of the organism, and the type and location
of the bone involved.
Certain
organisms, Staphylococcus aureus among them, have
virulence factors that make them particularly well adapted
to infecting bone. In vitro studies have suggested that
S. aureus can live intracellularly within osteoclasts.
In addition, S. aureus has the ability to up regulate
the production of certain adhesion molecules, which facilitate
its attachment to cartilage, especially in the early stages
of infection. The production of local cytokines can impair
the immune response of the host, making osteomyelitis a
difficult infection to treat.
Making
the diagnosis of osteomyelitis can be difficult. No one
diagnostic test can definitively rule in or sufficiently
rule out osteomyelitis. Acute osteomyelitis from hematogenous
spread has a biphasic occurrence pattern, peaking in those
patients under the age of seventeen and over the age of
fifty. In childhood it is believed that the architecture
of bone (with an increase in capillary density) accounts
for the increased incidence of hematogenous spread whereas
adults accumulate their increased risk as a result of exogenous
introduction (central venous catheters, dialysis ports,
urethral catheterization, intravenous drug abuse, etc).
In adults, the vertebrae, sternoclavicular, and sacroiliac
bones are the most common sites of infection, while the
long bones are the most common sites in children. Contiguous
spread of infection from a site of previous trauma (particularly
penetrating trauma) or surgery and direct extension from
adjacent soft tissue infections accounts for the greatest
number of cases, and is most commonly seen in adults. Spread
from a contiguous focus is notorious for being diagnosed
in the chronic time period as the signs and symptoms are
often misdiagnosed as being related to the underlying focus,
be it a prior surgery or an overlying cellulitis.
Signs
and symptoms of osteomyelitis vary depending on the duration
of infection. In acute osteomyelitis, symptoms often gradually
develop over the course of several days to one week with
patients experiencing bone pain, tenderness, warmth, and
swelling over the infected bone. Importantly, pain is usually
noted even without movement. The presence of fevers and
rigors are often present, but not in all patients. Certain
bony sites, particularly the hip, vertebrae, and the pelvis
are often without notable symptoms to the patient. Subacute
disease usually presents with a longer duration of symptoms
while chronic osteomyelitis is most frequently recognized
when a patient with a known infection presents with recurrent
symptoms, sometimes in the presence of a draining sinus
tract.
Laboratory
tests that can be useful in the diagnosis include an elevated
white blood cell count and an elevated erythrocyte sedimentation
rate (particularly to levels over 100 mm/hr). Blood cultures
are positive in roughly 50% of cases of acute osteomyelitis,
and the presence of radiographic evidence coupled with positive
blood cultures eliminates the need for tissue diagnosis.
Plain films can display classic findings such as soft tissue
swelling, bone destruction, and peri-osteal reaction, but
these findings typically take at least ten days to become
apparent. The presence of all three of these findings is
probably sufficient to warrant a course of empiric therapy,
but often the diagnosis is not clinched by plain films.
Computed tomography scans (CT) can be used to further substantiate
findings, being particularly useful in demonstrating cortical
destruction, intraosseous gas, peri-osteal reaction, and
soft tissue extension. Magnetic resonance scans (MRI) make
for an alternative to CT scans and can be especially useful
in cases involving the vertebrae and the foot. Nuclear
medicine scans such as labeled leukocyte scans and bone
marrow scans can be used alternatively if other studies
fail to definitively clinch the diagnosis.
Once
the diagnosis is made, organism information must be obtained
to guide therapy, either from positive blood cultures or
from tissue biopsy. In adults, the most common cause of
osteomyelitis is S. aureus. Pseudomonas aeruginosa
is the most common Gram negative rod and Peptostreptococcus
spp. are the most common anaerobic organisms. Hematogenous
osteomyelitis is most commonly monomicrobial. Treatment
of osteomyelitis requires the use of long term antibiotics,
typically for four to six weeks of therapy. Most experts
recommend initiating therapy empirically while awaiting
the results of tissue biopsy which can be used to tailor
therapy. Therapy is typically started parenterally, though
recent studies have suggested that enteral after two weeks
of intravenous therapy may be equivalent to long duration
intravenous therapy. Adults with contiguous foci or chronic
osteomyelitis frequently require surgical debridement.
Even in cases of acute hematogenous osteomyelitis, indications
for surgical intervention include patients who fail to respond
to antibiotics within 48 hours, those who have evidence
of persistent soft tissue abscess, and those who have either
documented or suspected concomitant joint infections.
With
appropriate therapy, only about 5% of hematogenous cases
will progress to chronic osteomyelitis. Prompt therapy
can avoid the dreaded complication of necrosis of the involved
bone. Surviving bone adjacent to and involving the prior
site of osteomyelitis is frequently osteoporotic as a result
of the infection. In most patients, the return to normal
activity after resolution of the infection will enable the
bone to regain its initial density. Supplemental therapies
with calcium, bisphosphonates, vitamin D, and/or testosterone
can help patients to regain bone density in the correct
clinical situation. In time, adequately treated osteomyelitis
can be indistinguishable from adjacent, normal, bone.
REFERENCES
- Mader
JT, Shirtliff ME, Bergquist S, Calhoun JH.
Principles of the Management and Treatment of Osteomyelitis,
UpToDate Online, Version 10.2.
- Mader
JT, Du Y, Simmons D, Calhoun J. Pathogenesis
of Osteomyelitis, UpToDate Online, Version
10.2.
- Mader
JT, Du Y, Simmons D, Calhoun J. Clinical
Features and Microbiology of Osteomyelitis, UpToDate
Online, Version 10.2.
- Ghiorzi
T, Mackowiak P. Diagnosis of Osteomyelitis,
UpToDate Online, Version 10.2
- Harrison’s Principles of Internal
Medicine, 15th Edition, Braunwald, Fauci, Kasper,
Hauser, Longo, and Jameson editors, 2001, pp. 825-829.
- The Washington Manual of Medical
Therapeutics, 30th Edition, Ahya,
Flood, and Paranjothi editors, 2001, pp. 309-310.
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