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Khoirunnisa Humairoh


An arteriole theory was proposed, in which bacteria

become entrapped in the end arteriole system near the
vertebral end plate. In Batsons venous theory, bacteria
gain entry into the perivertebral venous system via
retrograde flow from the pelvic venous plexus.

Hematogenous VO is a serious infection that is associated with

a mortality rate of up to 15%. In developed countries,
Staphylococcus aureus accounts for approximately 50% of
cases of VO; however, gram-negative and other gram-positive
bacteria, mycobacteria, and fungi also should be considered.
Although patients with VO often will have an identifiable source
of infection or an immunocompromised state, healthy patients
without any risk factor may also present with spontaneous VO.
Clinical Presentation

Pain in the affected region, which occurs in 90% of patients

with VO, is the most common complaint and is associated
with paraspinal muscle spasm.

1. The pain may be described as dull or sharp, constant or


2. Constitutional signs and symptoms including fever and

malaise occur in about half of affected patients.

3. Range of motion may become limited by pain, and focal

tenderness can be present
4. The physician must be alert to meningeal symptoms and
signs. In patients with psoas involvement, resisted hip
flexion or passive hip extension may exacerbate pain. Upper
cervical involvement may result in torticollis.

Plain radiography is helpful in the evaluation of

infection and if possible should be performed with the patient
standing to detect structural changes under physiologic

A thorough assessment must be made of the prevertebral

soft-tissue shadows in the cervical spine and mediastinal
width, and soft-tissue gas must be ruled out in cases of
anaerobic infection.
CT with coronal and sagittal reconstructions is very
useful in delineating psoas abscess and the pattern and extent of
structural degradation, and should be a part of any workup in
patients with advanced VO
MRI with gadolinium is a standard imaging technique
and has a sensitivity of 96% and a specificity of 93% in
diagnosing VO. T1-weighted images demonstrate hypointense
signal intensity in the disk space and adjacent vertebral bodies.
Conversely, the same regions appear hyperintense on T2-
weighted images. Contrasted images are helpful in identifying
abscess formation and in delineating neoplasm.
Laboratory Assessment

All patients should have a complete white blood cell

(WBC) count with differential, Westergren erythrocyte
sedimentation rate (ESR), and C-reactive protein (CRP) level.
It is important to note that WBC count is often normal in
patients with VO, particularly with indolent organisms.
Blood cultures should be obtained in all patients with
suspected VO and will yield a positive culture in 85% of
patients. If blood cultures do not identify an organism, then a
CT-guided biopsy is indicated and will be successful in
organism identification in 50% to 75% of patients


Multiple organisms including Mycobacterium species,

Nocardia, Brucella, Actinomyces and fungi induce a
granulomatous immune response and can result in nonpyogenic
VO. Tuberculosis, caused by M tuberculosis, is the most
common cause of granulomatous spinal VO (Potts disease).
Systemic tuberculosis results in spine involvement in
approximately 50% of patients, and it is thought that
hematogenous seeding from the lungs or genitourinary tract
is the primary route.

M tuberculosis is an acid-fast bacteria that causes a unique

pattern of infection. The disk space is resistant to infection,
and thus is typically spared. Hence the radiographic hallmark
is osseous destruction with preservation of the disk space.
Tuberculosis of the spine is an indolent infection that is often
diagnosed late, and this underscores why many patients
present with large kyphotic deformities
Three types of body involvement have been defined: anterior,
peridiskal, and central. Anterior involvement refers to
progression of the infection along the dorsal side of the
anterior longitudinal ligament resulting in scalloping of the
ventral vertebral bodies. Peridiskal involvement involves the
metaphyseal portion of the vertebral bodies and can result in
substantial collapse and deformity. The infection may be
confined to the central body (central pattern) and is often
confused with malignancy.
Clinical Presentation and Laboratory Diagnosis

The clinical presentations of pyogenic and nonpyogenic VO

share similarities. Both result in pain due to loss of structural
integrity, which occurs later in nonpyogenic VO and is a result
of the indolent pathogenesis. Fever may or may not be
Patients with nonpyogenic VO often have a history and
appearance of chronic illness and malnourishment (characterized
by weight loss, fatigue, night sweats, temporal wasting, and
depletion of nutritional markers). In patients with advanced
stages of tuberculosis, a kyphotic or gibbus deformity is often

The MRI characteristics of nonpyogenic VO are similar to

those of pyogenic VO, but there are features such as
tuberculosis that are unique to nonpyogenic VO. Tuberculosis
is often accompanied by abscess formation, a heterogenous
signal, preservation of disk spaces, multiple affected vertebral
bodies, and a predisposition for the thoracic spine.
Radionuclide studies can be helpful.
Like pyogenic disease, ESR and CRP levels in nonpyogenic
VO will be elevated, and the WBC count is often normal. A
tuberculin skin test should be performed, but a false-negative
test can occur in anergic patients who have advanced
immunoincompetency. In patients with tuberculosis, a biopsy
specimen positive for acid-fast bacillus is ideal; however, this
identification method has a sensitivity of only about 50%.
1. Medical Management
Parenteral antibiotics tailored to the identified organism are
administered for 2 to 6 weeks, and then oral therapy is administered.
The length of each treatment arm will be predicated, in part, on the
type of organism, host factors such as immune and nutritional status,
and risk factors and whether the patient has retained
instrumentation. The nutritional status must be optimized.


Epidural abscess is a rare but serious disease that is

associated with the risk of neurologic demise and even fatality.
Epidural abscesses are more common dorsally, and are more
common in the thoracolumbar spine.
Clinical Presentation

The pathogenesis of neurologic demise may stem from direct

compression and/or septic thrombophlebitis with resultant
venous spinal cord infarction. The precise mechanism is not
known. The clinical presentation varies and will be predicated
on the degree and type of neurologic compression and region
of the spine involved.
1. Common findings include pain (three fourths of patients) in
the affected region.

2. Radicular pain from root compression, or neurologic deficit

(one third of patients) correlative to the compressed level of
the spinal cord, cauda equina, or nerve root.

3. Fever is present in about 50% of patients.

Laboratory and Diagnostic Imaging

Both MRI with gadolinium and CT myelography have a

sensitivity greater than 90% for detection of an abscess, but
the former is less invasive and the modality of choice to make
the diagnosis.
MRI with gadolinium will demonstrate the size and degree of
neurologic compression. A ring-enhancing lesion is
pathognomonic for abscess and distinguishes it from
neoplasm. In patients who have associated diskitis or VO,
then plain radiography and CT are essential to define the
extent of osseous destruction.
Most retrospective studies have demonstrated that the
mainstay of treatment is direct surgical decompression followed
by antibiotic administration tailored to the organism isolated
during surgery. The type of surgery performed is predicated on
the site of the abscess and degree of bony involvement. Indirect
decompression (laminectomy for a ventral cervical or thoracic
abscess) is typically not the procedure of choice. Antibiotic
therapy alone is controversial, and results are limited to few
retrospective series.

Infections are a relatively common acute postoperative
complication.10 The likelihood of infection varies with several
factors: predisposing factors of the patient, complexity of the
case, and prophylactic antibiotics.
Clinical Presentation

This pain usually will begin several days after the surgery and
typically is progressive. Constitutional symptoms and signs
such as fever, fatigue, and malaise are also common.
Examination findings include drainage, which can range from
serosanguinous to frankly purulent, and peri-incisional
erythema, induration, warmth, and tenderness.
Laboratory and Diagnostic Imaging

Laboratory studies should include ESR, CRP level, and

complete blood cell count with differential. ESR will often
remain elevated for up to 6 weeks after surgery, and this
makes ESR a less useful study in the immediate postoperative
period. CRP level remains elevated for up to 2 weeks
postoperatively. Cultures or swabs of incision drainage often
will confound the diagnosis because of skin colonization. The
most reliable cultures are obtained at surgery.
Plain radiographs typically contribute much information, as
the time frame between surgery and early infection is narrow.
CT may show fluid collections. MRI with gadolinium should
be obtained, but the results must be interpreted carefully. The
normal postoperative changes can look very similar to the
infection. Enhancing fluid collections are pathognomonic for
Postoperative wound infections generally respond
poorly to antibiotic therapy alone, and surgical irrigation and
dbridement is indicated in most patients.