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Osteomyelitis
Ifeanyi I. Momodu; Vipul Savaliya.

Author Information and Affiliations

Last Update: May 31, 2023.

Continuing Education Activity

Osteomyelitis is a serious infection of the bone that can be either acute or chronic. It is an
inflammatory process involving the bone and its structures caused by pyogenic organisms that
spread through the bloodstream, fractures, or surgery. This activity outlines the evaluation and
management of osteomyelitis and explains the role of the interprofessional team in improving
care for patients with this condition.

Objectives:

Summarize the Cierny and Madar scheme in the histopathological classification of

osteomyelitis.

Describe the presentation of a patient with osteomyelitis.

Identify the essential role of radiographic imaging in the evaluation of patients with
osteomyelitis.

Outline the importance of collaboration and communication among the interprofessional

team to educate the patient on prolonged therapy and the need for compliance which will
improve outcomes for those with osteomyelitis.

Access free multiple choice questions on this topic.

Introduction
Bone infection is called osteomyelitis. It is an acute or chronic inflammatory process involving
the bone and its structures secondary to infection with pyogenic organisms, including bacteria,
fungi, and mycobacteria. Interestingly, archeological finds showed animal fossils with evidence
of bone infection, making this a relatively old disease.[1] Various terms were used to describe
infected bone over the years until Nelaton came up with the term osteomyelitis in 1844.
[1] Before the introduction of penicillin in the 1940s, management of osteomyelitis was mainly
surgically consisting of extensive debridement, saucerization, and wound packing following
which the affected area is left to heal by secondary intention[1] resulting in high mortality from
sepsis. Since the availability of antibiotics, mortality rates from osteomyelitis, including
staphylococcal osteomyelitis, has improved significantly.

Etiology
Healthy intact bone is resistant to infection. The bone becomes susceptible to disease with the
introduction of a large inoculum of bacteria, from trauma, ischemia, or the presence of foreign
bodies because bone sites to which microorganisms can bind are exposed.[2] Certain bacteria
such as Staphylococcus aureus adhere to the bone by expressing receptors, called adhesins, for
some components of the bone matrix, including laminin, collagen, fibronectin, and bone
sialoglycoprotein. S. aureus expresses a collagen-binding adhesin, which permits its attachment
to bone cartilage while the fibronectin-binding adhesin's role in attachment of bacteria to
surgically implanted devices in bone was recently discovered.[2] Also interesting to note is that
S. aureus can survive intracellularly after being internalized by cultured osteoblasts. Some
bacteria create a protective biofilm coating around themselves and underlying surfaces. This
characteristic of some bacteria to adhere to the bone and surgically implanted devices following
which they express phenotypic resistance to antibiotic therapy and their ability to survive
intracellularly may explain the persistence of bone infections and high failure rates of shorter
courses of antimicrobial treatment.[2]

Epidemiology
The overall incidence of osteomyelitis in the United States is mostly unknown, but reports show
it to be as high as 1 in 675 US hospital admissions each year or about 50,000 cases annually.
[3] Other studies show an overall incidence of osteomyelitis of 21.8 cases per 100,000 person-
years.[4] The incidence was higher in men for unknown reasons but increases with age, mainly
due to an increase in the prevalence of comorbid factors such as diabetes mellitus and peripheral
vascular disease.[4] Also, an increase in the availability of sensitive imaging tests, such as
magnetic resonance imaging (MRI) and bone scintigraphy has improved diagnostic accuracy and
the ability to characterize the infection.[5]

Pathophysiology
Bone can get infected via the hematogenous route of infection through bacteremic seeding of
bone from a distant source of infection, contiguous spread from surrounding tissue and joints, or
direct inoculation of bone from trauma or surgery.[1][2] Hematogenous osteomyelitis occurs
more frequently in children compared to adults, and long bones are usually affected.[5] In adults,
hematogenous osteomyelitis affects the vertebrae most commonly. Contiguous osteomyelitis in
young adults usually occurs in the setting of trauma and related surgery, while in older adults,
infection is typically related to decubitus ulcers and infected joint arthroplasties.
[1] Osteomyelitis associated with vascular insufficiency frequently occurs in the presence of
underlying diabetes mellitus.

In patients with diabetes, osteomyelitis usually results from compromised blood supply to the
lower extremities, which contributes to impaired local immunity and skin healing, promoting the
spread of infection. Sensory neuropathy in the setting of diabetes mellitus predisposes to the
formation of skin ulceration at pressure and trauma points, complicating matters even worse.[1]
[2][5]

Contiguous osteomyelitis frequently develops in debilitated patients who are wheelchair or

bedbound and are predisposed to pressure-related skin ulcerations, especially in the sacrum,
buttock, hips, and heel. These ulcers are typically colonized by polymicrobial flora from the skin
and gastrointestinal tract such that soft tissue infection can quickly spread to the underlying bone.
[1] Other sources of contiguous osteomyelitis are trauma leading to infected, exposed skin, and
soft tissue. Osteomyelitis with direct inoculation of bacteria may occur in the setting of open
fractures, bone reconstructive surgery, or with placing orthopedic hardware.[1][2]

Histopathology
The well-perfused metaphyses, which have scarce functioning phagocytes, are the most common
site of infection in hematogenous osteomyelitis affecting the long bones. The blood supply to the
long bones penetrates the bone at the mid-shaft then splits into two traveling to both metaphyseal
endplates. Slowing of blood flow in vascular loops at the metaphysis encourages the deposition
of microbes and the establishment of infection. To contain the disease, phagocytes release
enzymes that lyse bone, creating an inflammatory response. This inflammatory response forms
pus (a protein-rich exudate containing dead phagocytes, tissue debris, and microorganisms) and
causes increased intramedullary pressure. The inflammatory exudate can rupture through the
cortex to the periosteum if left unchecked. Disruption of the periosteum impairs the periosteal
blood supply leading to bone ischemia then necrosis.[1][2] Separated pieces of necrotic bone are
called sequestra, which occasionally contain pus. New bone formation over the injured
periosteum is called involucrum, and it may partially surround a sequestrum. Discharge from a
sequestrum can lead to sinus tract formation.

The main histopathological finding in acute osteomyelitis are microorganisms, congested or

thrombosed blood vessels, and infiltrates of neutrophils. On the other hand, the hallmark
histopathological finding in chronic osteomyelitis is necrotic bone. Other features of chronic
osteomyelitis include a predominance of mononuclear cells, replacement of osteoclast resorbed
bone by granulation, and fibrous tissue leading to bone loss and the formation of sinus tracts,
which is pathognomic.

Native vertebral osteomyelitis (NVO) is usually a hematogenous infection affecting two adjacent
vertebral endplates.[6] This presentation is explained by the blood supply of the vertebrae as
segmental arteries typically bifurcate to supply two adjacent endplates of contiguous vertebrae.
[1] Venous drainage from Batson's plexus may explain spondylodiscitis metastasizing from a
urinary tract focus, especially in senior men.

The categorization of osteomyelitis as acute or chronic is based on the histopathological findings

rather than the duration of illness.[5] Acute osteomyelitis refers to infection occurring before the
development of sequestra and usually takes place within two weeks of disease onset. However,
the development of sequestra may be slow in some settings, such as vertebral osteomyelitis, and
rapid in others as when associated with prosthetic devices or open fractures. Following the
development of necrotic bone and the formation of sequestra, the infection is considered
chronic.

There are two major classification schemes for osteomyelitis. The first is by Lew and Waldvogel,
while the other is by Cierny and Mader. Lew and Waldvogel classified osteomyelitis based on the
duration of illness as acute or chronic and by the mechanism of infection (either hematogenous
or contiguous infection). Contiguous infection is further classified based on the presence or
absence of associated vascular insufficiency.

The Cierny and Mader scheme provides guidance in patient management. In this scheme, the
classification of osteomyelitis is by anatomic stage and the host health status.

The categories and corresponding anatomic types are:

Stage 1: Disease confined to the medullary of the bone

Stage 2: Superficial disease

Stage 3: Localized spread

 Stage 4: Diffuse disease

The local and systemic factors which define host health status are:

A: Normal host

Bs: Host with systemic compromising factors

Bl: Host with local compromising factors

Bsl: Host with both local and systemic compromising factors

C: Host for whom treatment of the osteomyelitis is worse than the disease itself.

Causes of systemic host compromise are malnutrition, renal and hepatic failure, diabetes
mellitus, chronic hypoxia, neoplasm, and immunodeficiency disease. Local compromising
factors of the host health status are chronic lymphedema, venous stasis, major and small vessel
disease, arteritis, peripheral neuropathy, and tobacco use.

History and Physical

The clinical presentation of osteomyelitis depends on the etiology. Sometimes diagnosis in adults
can be tricky, and it requires a high index of suspicion. A good history and physical is always the
right place to start and are essential parts of the initial evaluation. Some patients are at high risk
for osteomyelitis, and these include those with bacteremia, endocarditis, intravenous drug use,
trauma, and open fractures. Also, patients with chronic poorly healing wounds in the setting of
diabetes mellitus, peripheral vascular disease, peripheral neuropathy, or orthopedic hardware are
at increased risk.[1] Acute osteomyelitis may present gradually with onset over a few days but
usually manifests within two weeks. Patients may have local symptoms such as erythema,
swelling, and warmth at the site of infection. There may be a dull pain with or without motion
and sometimes constitutional symptoms such as fever or chills. In subacute presentations, some
patients may have generalized malaise, mild pain over several weeks with minimal fever, or
other constitutional symptoms. Acute osteomyelitis may also present as septic arthritis, especially
if the metaphyses of the bone is within the infected joint capsule. Septic arthritis of the elbow,
shoulder and hip joints may complicate osteomyelitis of the proximal radius, humerus, and
femur, respectively. New or worsening neck or back pain in a patient with fever, elevated
inflammatory markers (CRP, erythrocyte sedimentation rate [ESR]),[6] bacteremia, or
endocarditis should raise the suspicion for native vertebral osteomyelitis (NVO).[7]

In chronic osteomyelitis, symptoms may occur over a longer duration of time, usually more than
two weeks. As with acute osteomyelitis, patients may also present with swelling, pain, and
erythema at the site of infection, but constitutional symptoms like fever are less common.
Patients who have deep or extensive ulcers that do not heal after several weeks of
appropriate therapy, especially in people with diabetes or debilitated patients, should raise the
suspicion for osteomyelitis. Physical examination should focus primarily on finding a
possible nidus of infection, assessing sensory function, and peripheral vasculature. Tenderness to
palpation over vertebral bone may be a significant finding in vertebral osteomyelitis. The ability
to probe an ulcer to the bone with a blunt sterile instrument is highly suggestive of osteomyelitis.
[2] The probe to bone test is a screening tool in conjunction with the patient's pretest probability
for osteomyelitis to determine whether additional diagnostic tests such as radiographic imaging
or bone biopsy are required for therapeutic decisions.[8]
Evaluation
Laboratory data can be useful in the assessment of osteomyelitis but are usually nonspecific for
osteomyelitis. There may or may not be leukocytosis, the elevation of ESR, and C-reactive
protein (CRP). The CRP level correlates with clinical response to therapy and may be used to
monitor treatment. Blood cultures may be positive, especially in hematogenous osteomyelitis
involving the vertebrae, clavicle, or pubis.

Radiographic imaging is an essential component of the evaluation of a patient with suspected

osteomyelitis. Clinically, the most useful studies are plain radiographs, magnetic resonance
imaging (MRI), and technetium-99 bone scintigraphy.[5] A plain radiograph is usually the initial
imaging of choice but may have a delay of about 14 days before the appearance of findings
suggestive of osteomyelitis.[1][5] They are, however, used to rule out other potential causes of
symptoms such as metastasis or osteoporotic fractures. Typically seen are soft tissue swelling,
osteopenia, osteolysis, bony destruction, and nonspecific periosteal reaction. Lytic lesions are
detectable on plain radiographs after approximately 50% to 75% of the bone matrix has been
lost, making this modality inadequate for the detection of early bone disease.[5] Rarely, Brodie's
abscess, which is a well-circumscribed lytic lesion, may be seen in a child who has been in pain
for months without fever.

Of all the imaging modalities currently in use, MRI has the highest combined sensitivity and
specificity (78% to 90% and 60 % to 90% respectively) for detecting osteomyelitis. It can detect
early bone infection within 3 to 5 days of disease onset [5][6], but its use is limited in the setting
of surgical hardware. MRI has a high negative predictive value, so a negative result is sufficient
for the exclusion of disease if symptoms have been present for at least one week. The use of
intravenous contrast does not improve the detection of disease but helps provide the distinction
between a phlegmon, necrotic tissue, and abscess. Nuclear imaging has a high sensitivity for
detecting early evidence of bone disease but has very poor specificity. It is especially useful if
metal hardware prevents the use of MRI. Three-phase technetium-99 bone scan and tagged white
blood cell scans are the modalities commonly used.

Other imaging modalities less commonly used are positron emission tomography (PET), which is
expensive and not routinely available, leukocyte scintigraphy, gallium scan, and computed
tomography (CT scan). A CT scan is more sensitive than a plain radiograph for assessing cortical
and trabecular integrity, periosteal reaction, intraosseous and soft tissue gas, the extent of a sinus
tract, and is superior to MRI in detecting necrotic bone fragments. However, though the CT scan
is readily available compared to the MRI, it is more expensive than plain radiograph and has a
limited role in the diagnosis of osteomyelitis. It should be used mainly to determine the extent of
bony destruction (especially in the spine) to guide biopsies or in patients with contraindications
to MRI.

Bone biopsy (either open or percutaneously) is essential to establish the histopathological

diagnosis in osteomyelitis, identify the causative pathogen, and provide susceptibility data that
helps direct antibiotic therapy. Superficial wound cultures or material from needle puncture or
sinus tracts should not be used in diagnosis as these specimens do not correlate well with bone
biopsy results.[1] In patients with positive blood cultures and radiographic evidence of
osteomyelitis, a bone biopsy may not be very useful[7]. An open bone biopsy is preferred over
percutaneous biopsy, if possible. Cessation of antibiotics 48 to 72 hours before open bone biopsy
may increase microbiological yield but is not routinely necessary as bone cultures are often
positive regardless of prior antibiotic therapy because these infections occur in areas of infection-
induced infarction or necrosis. Percutaneous biopsy should be done through intact skin to prevent
sampling errors, and fluoroscopic or CT guidance is preferable. Percutaneous biopsy should be
done ideally before initiation of antibiotic therapy, if possible, to increase the microbiological
yield. Usually recommended is the collection of 2 samples, one for histopathology and the other
for culture and gram stain.

Treatment / Management
Hematogenous osteomyelitis is primarily monomicrobial, while osteomyelitis due to contiguous
spread or direct inoculation is usually polymicrobial or monomicrobial.[1] The most common
pathogens in osteomyelitis depend on the patient's age. Staphylococcus aureus is the most
common cause of acute and chronic hematogenous osteomyelitis in adults and children.[1]
[5] Increasingly isolated from patients with osteomyelitis is methicillin-resistant Staphylococcus
aureus (MRSA). In some studies, MRSA accounted for over one-third of all staphylococcal
isolates.[5] Other common pathogens are coagulase-negative staphylococcus, beta-hemolytic
streptococcus, enterococci, aerobic gram-negative bacilli (including Pseudomonas species,
Enterobacter species, Escherichia coli), and anaerobic gram-negative bacilli (such as
Peptostreptococcus, Clostridium species, Bacteroides).

It is crucial to consider less common pathogens in the appropriate epidemiological setting and
immunocompromised patients. These include Mycobacterium tuberculosis, which may spread to
the spine from the lungs; nontuberculous mycobacteria (Mycobacterium avium intracellulare,
Bacille Calmette-Guerin, which may complicate intravesical therapy for bladder cancer);
Candida species; fungi such as Blastomyces, Coccidiodes, Cryptococcus, and Aspergillus.
Infection with Actinomyces and Sporothrix usually follow traumatic inoculation. Salmonella and
S. aureus are implicated in hematogenous osteomyelitis in sickle cell disease, while Brucella and
Salmonella occur in spinal infections.[1][2] Bartonella henselae may be associated with HIV-
related osteomyelitis and Pasteurella multocida or Eikenella corrodens seen in human or animal
bites.

Effective treatment of osteomyelitis involves a collaborative effort among various medical and
surgical specialties. The two main aspects of therapy are surgical containment of the infection
and prolonged antibiotics. Surgical debridement of all diseased bone is often required as
antibiotics penetrate poorly into infected fluid collections such as abscesses and injured or
necrotic bone.[1] Thus, the removal of necrotic tissue and bone is usually indicated where
feasible.[2][1] Preoperative use of imaging modalities such as MRI allows for delineation of the
extent of the infection, but intraoperatively it is still difficult for the surgeon to determine if all
necrotic bone and tissue have been successfully removed. Examination of the pathology report
helps determine if repeat debridement is necessary. In osteomyelitis associated with prosthetic
joints, removal of the hardware is indicated.[2] However, if the infected prosthesis is in a stable
joint such as the hip and is infected with a very susceptible organism such as streptococci,
therapy with an extended antibiotic course for several months without removing the device has
been successful.[2] When the prosthesis has to be removed, a two-stage exchange arthroplasty is
more commonly used as this carries less risk of recurrent infection compared to the 1-stage
arthroplasty, especially if more virulent bacteria such as S. aureus is involved.[2] If surgical
debridement is not feasible based on the location of the infection, e.g., some cases of pelvic
osteomyelitis, then extended antibiotic therapy for months may be used. NVO rarely requires
surgical debridement except if there are associated neurological complications necessitating
relief of spinal cord compression, failure of medical treatment, or need to drain epidural or
paravertebral abscesses.[2] Debridement, however, is needed in cases of osteomyelitis associated
with spinal implants.[6]

Also important is the need for revascularization of the affected limb before surgical intervention
if there is evidence of significant peripheral vascular disease, control diabetes mellitus and
address other host factors that may impede wound healing, including tobacco use, malnutrition,
chronic hypoxia, immunodeficiency states, chronic lymphedema and peripheral neuropathy[2].

Prolonged antibiotic therapy is the cornerstone of treatment for osteomyelitis. Results of culture
and sensitivity should guide antibiotic treatment if possible, but in the absence of this data, it is
reasonable to start empiric antibiotics. A commonly used broad-spectrum empiric antibiotic
regimen against both gram-positive and negative organisms, including MRSA, is vancomycin
(15 mg/kg intravenously [IV] every 12 hours) plus a third a generation cephalosporin (e.g.,
ceftriaxone 2 gm IV daily) or a beta-lactam/beta-lactamase inhibitor combination (e.g.,
piperacillin/tazobactam 3.375 IV every 8 hours).[1] Once sensitivity data becomes available,
then the antibiotic therapy should be narrowed for targeted coverage of the susceptible
organisms.

Pathogen-Specific Antibiotic Therapy for Osteomyelitis in Adults [1] [5] [2] [6]

Staphylococcus aureus penicillin-sensitive

Treatment of choice is penicillin G 4 million units every 6 hours

Alternative regimens are a first-generation cephalosporin, e.g., cefazolin 2 g IV every 8 hours,

clindamycin 900 mg IV every 8 hours, vancomycin 15 mg/kg IV every 12 hours, oxacillin or
nafcillin 2 g IV every 4 hours

Staphylococcus aureus penicillin-resistant

Treatment of choice is nafcillin 2 gm IV every 4 hours

Alternative therapies are cefazolin, clindamycin, or vancomycin (doses as above)

Staphylococcus aureus methicillin-resistant

Treatment of choice is vancomycin IV

An alternative regimen is linezolid 600 mg IV every 12 hours.

Streptococci (group A, B, Beta hemolytic, Streptococcus pneumoniae)

Treatment of choice is penicillin G 4 million units every 6 hours

Alternative regimens include ceftriaxone 2 gm IV daily, clindamycin IV, vancomycin IV,

cefazolin IV (doses as above)

Enterobacteriaceae quinolone sensitive

Treatment of choice is ciprofloxacin 400 mg IV twice per day (bid) or 750 mg orally (PO) bid,
levofloxacin 500 to 750 mg PO or IV daily

Alternative regimens include ceftriaxone 2g IV daily, cefepime 2 gm IV every 12 hours,

ceftazidime 2 gm IV every 8 hours

Enterobacteriaceae, quinolone-resistant (Escherichia coli)

Treatment of choice is piperacillin/tazobactam 3.375 g IV every 8 hours, Ticarcillin/clavulanate
3.1 gm IV every 4 hours

An alternative regimen is ceftriaxone 2 g IV daily

Pseudomonas aeruginosa

Treatment of choice is cefepime 2 gm IV every 12 hours, ceftazidime 2 gm IV every 8 hours

Alternative regimens include meropenem 1 gm IV every 8 hours, Imipenem 500 mg IV every

6 hours, ciprofloxacin 400 mg IV every 12 hours, or 750 mg PO daily

Enterococci

Treatment of choice is penicillin G 4 million units every 6 hours

Alternatively, vancomycin 15 mg/kg every 12 hours, daptomycin 6 mg/kg IV daily, linezolid 600
mg IV or PO every 12 hours

Anaerobes

Treatment of choice is clindamycin 900 mg IV every 8 hours, ticarcillin/clavulanate 3.1 gm IV

every 4 hours

Alternatively, metronidazole 500 mg IV every 8 hours (for gram-negative anaerobes)[1][2][5]

The recommended duration of treatment for osteomyelitis in adults is 4 to 6 weeks of parenteral

antibiotic therapy to achieve acceptable cure rates with a decreased risk of recurrence.[7][6][2] In
cases where the infected bone is wholly debrided or amputated with clean disease-free margins
documented, a shorter duration of antibiotic therapy is acceptable. A 2-week course of antibiotics
postoperatively is sufficient to allow for the treatment of any residual tissue infection and wound
healing of the surgical site.[1]

Vacuum-assisted wound closure devices are used in the right clinical setting, especially where
large or deep wounds are left after extensive debridement. These devices have been shown to
promote healing by both direct and indirect effects on the wound.[9] Hyperbaric oxygen therapy
is not routinely recommended in the treatment of osteomyelitis.

Differential Diagnosis
The differential diagnosis for osteomyelitis is broad, and it is essential to keep these in mind
during the evaluation of a patient with a suspected bone infection. These differentials include:

Charcot arthropathy especially in people with diabetes

SAPHO syndrome (synovitis, acne, pustulosis, hyperostosis, and osteitis)

Arthritis including rheumatoid arthritis

Metastatic bone disease

Fracture, including pathological and stress fractures.

Gout

Avascular necrosis of the bone

Bursitis
 Sickle cell vaso-occlusive pain crises

Prognosis
With aggressive early treatment, the prognosis of acute osteomyelitis is good. However, there is a
possibility that the infection could recur years after successful treatment if there is new trauma to
the same area or if host immunity is compromised.[10] In adults, the recurrence rate of chronic
osteomyelitis is about 30% at 12 months, but in cases involving P. aeruginosa, the recurrence rate
may be as high as 50%.[5] Cases involving prosthetic devices are more difficult to treat, causing
increased morbidity due to the need for more surgical procedures and extended antibiotic courses
required for treatment. Various measures used to prevent postoperative infections include good
preoperative preparation where possible and the use of surgical rooms with laminar airflow.
Recommended also is the use of prophylactic preoperative antibiotic treatment administered
parenterally 30 minutes before skin incision with first-generation (cefazolin) or second-
generation cephalosporins (cefuroxime). All these measures have been shown to decrease the rate
of postoperative infections from 0.5% to 2%, thereby improving patient outcomes.[2]

Complications
Early treatment, including antibiotic therapy, is necessary to prevent the development of
complications. Some complications which may arise with untreated or inadequately treated
osteomyelitis are:

Septic arthritis

Pathological fractures

Squamous cell carcinoma

Sinus tract formation

Amyloidosis (rare)

Abscess

Bone deformity

Systemic infection

Contiguous soft tissue infection

Deterrence and Patient Education

Patient education about the prolonged nature of therapy and the need for compliance with
treatment recommendations to ensure adequate wound healing thereby reducing the risk for
recurrence is an essential part of the care in these patients.

Enhancing Healthcare Team Outcomes

Osteomyelitis is a complicated infection to treat. In most cases, management involves a
multifaceted, interprofessional approach, including the primary care provider, radiologist,
surgeons (orthopedic, vascular), a podiatrist, an infectious disease specialist, pharmacist, nurse
wound care team, and sometimes a plastic surgeon, a pain specialist or interventional radiologist.
The primary care provider often plays a vital role in the initial diagnosis and coordination of care
across these medical and surgical specialties.

The therapeutic approach to management is guided sometimes by the site of infection and the
presence of vascular insufficiency. Minimally invasive CT or fluoroscopically guided aspiration
of the disc space (usually by interventional radiology) for microbiological and histopathological
testing is recommended for the diagnosis of suspected NVO if clinical, imaging and other
laboratory data suggest osteomyelitis in the absence of positive blood cultures with an organism
known to cause osteomyelitis (S. aureus, Staphylococcus lugdunensis, Brucella).[7] However, in
patients with suspected subacute NVO and strongly positive Brucella serology or those with
suspected NVO based on available clinical, radiological, laboratory data and positive blood
cultures involving an organism known to cause osteomyelitis, image-guided aspiration biopsy is
not recommended. A 6-week course of parenteral antibiotics is reserved for cases with
neurological complications or failure of medical therapy.[7]

Once again, a strong collaboration between the surgical and vascular teams is essential for the
effective management of osteomyelitis due to vascular insufficiency, especially if associated with
diabetes mellitus. Revascularization of the affected limb is critical for proper wound healing.
Procedures to restore adequate blood flow, including therapeutic angiogram by either
interventional radiology or vascular surgery and even femoral to popliteal by-pass, are used
before amputation depending on the severity of vascular insufficiency. Surgical revascularization
procedures that use local pedicle muscle flaps and myocutaneous flaps maintain vascular supply
to the surgical site, fill the space left by surgical debridement, and also fight infection.[2]

Following surgical debridement, the need for close follow-up with prolonged antibiotics and
meticulous wound care cannot be overemphasized. Infectious disease specialists involved in the
patient's care often monitor response to therapy and adjust antibiotics regimens where needed.
Many patients can continue with parental antibiotics outpatient via peripherally inserted
intravenous access to complete their antibiotic course while others can transition to highly
bioavailable oral antibiotic therapy such as quinolones when feasible based on microbiological
results. Qualified home-bound patients benefit from home health wound nurse visits several
times a week, while those who are ambulatory are encouraged to use wound care clinics if
available. Family members and caregivers are also an integral part of the care team, providing
support and care between healthcare provider visits. Only through such an approach can the
morbidity of osteomyelitis be decreased.[11] [Level 5]

Review Questions

Access free multiple choice questions on this topic.

Comment on this article.

Figure

MRI T1-Weighted Postcontrast Knee Osteomyelitis

Contributed by Scott Dulebohn, MD

Figure
 Digital Amputation. Surgical amputation of the right hallux
secondary to osteomyelitis; not the exposed first metatarsal
head within the wound. Contributed by MA Dreyer, DPM,
FACFAS

Figure

Osteomyelitis CT Scan of Chronic osteomyelitis of the leg

demonstrating classic cloaca, sequestrum and involucrum
Contributed by Mark A. Dreyer, DPM, FACFAS

Figure

Osteomyelitis CT Scan of chronic osteomyelitis of the leg

demonstrating classic cloaca, sequestrum, and involucrum
Contributed by Mark A. Dreyer, DPM, FACFAS

Figure

T2-weighted MRI image of a patient's right foot. Patient had

history of uncontrolled diabetes, peripheral neuropathy and a
long-standing ulceration under the 5th metatarsal head
resulting in osteomyelitis of the 5th metatarsal head and shaft.
Patient (more...)

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Disclosure: Ifeanyi Momodu declares no relevant financial relationships with ineligible companies.

Disclosure: Vipul Savaliya declares no relevant financial relationships with ineligible companies.

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