Sabtu, 25 Oktober 2008

Spinal Infection

Spinal Infections

Dr Harry Sunaryo SpOT

Before the introduction of modern
antibiotic therapy, mortality in
patients with vertebral osteomyelitis
was as high as 25%.1 Antibiotic
therapy combined with surgical
débridement and stabilization has
decreased mortality to less than 5%
to 15%.2-4 Early diagnosis also has
improved outcomes by facilitating
rapid initiation of antibiotic treatment
and preventing abscess formation,
structural instability, and neurologic
Spinal infections are evaluated
according to their location, the pathogen
or pathogens involved, route of
the infection, age of the patient, and
immune status of the host. The location
of the infection may involve the
osseous vertebra, the intervertebral
disk, the epidural space, or the surrounding
soft tissues. The pathogens
are usually either bacterial or fungal;
however, the widespread use of
broad-spectrum antibiotics and the
increasing number of immunocompromised
patients have led to infections
with unusual organisms.
A systematic approach must be
taken in the diagnosis and treatment
of each type of spinal infection.
The presentation and efficacy
of the various elements of the initial
evaluation differ markedly for acute
hematogenous infection, granulomatous
spinal infection, pediatric
hematogenous diskitis, epidural
abscess, and postoperative spinal
Pathophysiology of Spinal
Pyogenic vertebral osteomyelitis is a
bacterial infection that can arise
from a number of sources—direct
inoculation, contiguous spread from
an adjacent infection, or hematogenous
seeding. Direct inoculation
can result from penetrating injuries
or from percutaneous or open spinal
procedures (eg, chemonucleolysis,
diskography, diskectomy) done on
the intervertebral disk. Local spread
of bacteria or fungi can occur following
intra-abdominal and retroperitoneal
abscesses. Although
local spread from direct inoculation
of bacteria into the spinal canal is
likely to become more prevalent as
the number of spinal procedures
increases, hematogenous seeding of
infection is still by far the most common
mechanism of spinal infection.
Potential sources of pathogenic
organisms include skin and softtissue
infections, infected vascular
access sites, and the urinary tract.
The two major theories for hematogenous
dissemination are the
venous theory and the arteriolar
theory. Batson5 developed the
venous theory using both live animal
and human cadaveric models.
He demonstrated retrograde flow
from the pelvic venous plexus to the
perivertebral venous plexus via
valveless meningorrhachidian veins.
In the arteriolar theory, Wiley and
Trueta6 proposed that bacteria can
become lodged in the end-arteriolar

Spinal infections can occur in a variety of clinical situations. Their presenta-
tion ranges from the infant with diskitis who is unwilling to crawl or walk to
the adult who develops an infection after a spinal procedure. The most common
types of spinal infections are hematogenous bacterial or fungal infections, pedi-
atric diskitis, epidural abscess, and postoperative infections. Prompt and accu-
rate diagnosis of spinal infections, the cornerstone of treatment, requires a high
index of suspicion in at-risk patients and the appropriate evaluation to identify
the organism and determine the extent of infection. Neurologic function and
spinal stability also should be carefully evaluated. The goals of therapy should
include eradicating the infection, relieving pain, preserving or restoring neuro-
logic function, improving nutrition, and maintaining spinal stability.

Both mechanisms are likely
significant in the establishment of
an infectious focus in the spinal column.
In the cervical spine, an extensive
prevertebral pharyngeal
venous plexus also may act as a
conduit for the spread of bacteria.7
Local spread of infection can
occur in a number of ways. Once
the infection is established adjacent
to the end plate of one vertebral
body, it can rupture through that
structure into the adjoining disk and
infect the next vertebral body. The
disk material is relatively avascular
and is rapidly destroyed by the bacterial
enzymes . In the cervical
spine, if the infection penetrates
the prevertebral fascia, it can extend
into the mediastinum or into the
supraclavicular fossa, markedly
increasing the extent and severity of
the process. From the lumbar spine,
abscess formation may track along
the psoas muscle and into the buttock
(piriformis fossa), the perianal
region, the groin, or even the popliteal
fossa. The extension of infection
from the vertebral body or disk
into the spinal canal may result in an
epidural abscess or even bacterial
meningitis. Destruction of the vertebral
body and intervertebral disk
can potentially lead to instability
and collapse. In addition, with collapse
of the vertebral body, infected
bone or granulation tissue may be
retropulsed into the spinal canal,
causing neural compression or vascular
occlusion. With pyogenic
osteomyelitis, the lumbar spine is
more commonly affected than the
thoracic or cervical spine.8
The pathogenesis of spinal infection
differs markedly between children
and adults because of anatomic
differences in the vascular anatomy
of the vertebrae. In children, vascular
channels cross the cartilaginous
growth plate and end within the
nucleus pulposus. These channels
provide pathways for direct inoculation
of organisms into the avascular
nucleus pulposus. Since these
vascular channels are not present in
adults, the direct seeding of the disk
does not occur, but rather spreading
occurs by direct extension with rupture
of the infective focus through
the end plate into the disk.
Neurologic deterioration can be a
devastating consequence of spinal
infection. A number of different
factors can cause neural deficit.
Direct spread of infected material
into the spinal canal can produce an
epidural abscess that may compress
the neural elements or cause thrombosis
or infarction of the regional
vascular supply to the spinal cord.
Direct hematogenous spread rarely
results in epidural abscess without
the presence of associated diskitis or
osteomyelitis. Pathologic fracture
can occur, with associated extrusion
of either infected material or bony
elements into the spinal canal.
Kyphosis and/or spinal instability
resulting from destruction of the
disk, vertebral bone, and posterior
stabilizing structures can cause
neural impingement. Eismont et al4
reported several additional risk factors
that predispose to neurologic
deterioration: diabetes, rheumatoid
arthritis, steroid use, advanced age,
a more cephalad level of infection
(ie, high thoracic or cervical), and
infection with Staphylococcus species.
The pathophysiology of granulomatous
spinal infection differs from
that of pyogenic infections. The
most common form of granulomatous
disease of the spine is caused
by Mycobacterium tuberculosis (Pott’s
disease). Although endemic in
many developing countries, tuberculosis
(TB) was nearly eradicated in
56-year-old man presented with severe back pain following a urologic procedure.
He had an elevated ESR but no leukocytosis. A, T1-weighted sagittal MR image of
the lumbar spine shows severe edema of the L3-4 disk and adjacent soft tissues. B, T2-
weighted sagittal MR image shows high signal intensity in the L3-4 disk and adjacent vertebral
bodies, consistent with pyogenic diskitis and osteomyelitis. Cultures obtained from
a CT-guided biopsy of the disk space grew Staphylococcus aureus.
Spinal Infections; however, there
has been a recent resurgence of TB
with resistant strains and in patients
with human immunodeficiency
virus (HIV). Although less than 10%
of patients with TB have skeletal
involvement, 50% of the skeletal involvement
occurs in the spine.
Depending on the series, between
10% and 61% of patients present
with or develop a neurologic
With TB, the primary route of
infection to the spine is hematogenous
from a pulmonary or genitourinary
source, although direct
spread from adjacent structures can
occur. Three major patterns of spinal
vertebral body involvement
have been documented: peridiscal,
central, and anterior.10 The most
common form, peridiscal, occurs
adjacent to the vertebral end plate
and spreads around a single intervertebral
disk. Extension to the adjacent
vertebra occurs as the granulomatous
abscess material tracks
beneath the anterior longitudinal
ligament. Unlike the situation in
pyogenic infections, the intervertebral
disk is usually spared. Central
involvement occurs in the middle
of the vertebral body and can be
mistaken for a tumor. Destruction
of the vertebral body will then lead
to spinal deformity. Anterior
involvement begins beneath the
anterior longitudinal ligament,
causing scalloping of the vertebral
body . In contrast with
peridiscal involvement, which
affects a single motion segment,
anterior involvement can produce
a spinal abscess that extends over
multiple levels. Primary involvement
of the posterior structures is
uncommon. Regionally, the thoracic
spine is most often involved,
followed by the lumbar spine and
cervical spine. Paraspinal extension
with abscess formation is common
and can occur at any level.
Spinal infections can be classified
as acute, subacute, or chronic depending
on the duration of symptoms.
Symptoms that have persisted
for <3 weeks are acute; those lasting
from 3 weeks to 3 months are subacute.
Chronic infections last >3
months and either are caused by
indolent organisms, are granulomatous
in nature, or are incompletely
treated (eg, infections with resistant
organisms, or the presence of foreign
material in the area of infection).
Clinical Evaluation
Pyogenic Vertebral
Pyogenic vertebral osteomyelitis
is more common in males than in
females and also more common in
elderly populations.2,11 However,
the incidence of infection is increasing
in younger age groups in populations
with intravenous drug abuse
or immunocompromise after organ
transplantation or chemotherapy.
Accordingly, spinal infection should
be considered in the differential
diagnosis of acute-onset spinal pain
in patients older than 50 years or
with diabetes, rheumatoid arthritis,
immunocompromise (from medical
illness or pharmacologic immunosuppression),
or a history of intravenous
drug abuse.
The clinical presentation of vertebral
osteomyelitis depends on the
location of the infection, the virulence
of the organism, and the immune
status of the host. Back or
neck pain is the most consistent
symptom of pyogenic infection.
Observed in >90% of patients, the
pain is often quite severe and is
associated with notable paraspinal
muscle spasm. The pain may occur
Figure 2 A 33-year-old woman presented with back pain of several months’ duration. A, Anteroposterior radiograph shows collapse of
the vertebral body and paraspinal soft-tissue shadow (arrowheads). B, Lateral radiograph also shows collapse and interior scalloping
(arrow). C, Sagittal T1-weighted MR image shows a large anterior abscess, extensive vertebral body involvement, and relative sparing of
disk spaces. D, The patient underwent CT-guided biopsy and aspiration with placement of a pigtail catheter for 1 week to drain this
abscess. She underwent anti-TB treatment for 1 year, with resolution of pain and no development of deformity.
at night and is usually present regardless
of activity level. Radicular
leg or arm pain is less common but
may be present with neurologic
involvement, which occurs in less
then 10% of patients. Fevers are
documented in approximately
50% of the affected population.12
Weight loss is common but may
not be easily recognized by patients
because it may occur slowly over a
period of weeks to months before
the infection is diagnosed and
The presence of other signs or
symptoms depends on the extent of
the infectious process. A patient
with a psoas abscess may have pain
with hip extension. Cervical abscess
formation may lead to torticollis or
dysphagia. Radiculopathy, myelopathy,
or even complete paralysis can
occur with neural compression as a
result of abscess, instability, or
spinal deformity. Direct spread of
the infection into the epidural space
can cause meningitis.
Gram-positive organisms are responsible
for the majority of vertebral
column infections in both adults
and children, with Staphylococcus
aureus accounting for >50%. Infection
with gram-negative organisms
such as Escherichia coli, Pseudomonas,
and Proteus may occur following
genitourinary infections or procedures.
Intravenous drug abusers are
also prone to Pseudomonas infections.
Anaerobic infections may be encountered
in patients with diabetes
or following penetrating trauma.
Low-virulence organisms such as
coagulase-negative staphylococci
and Streptococcus viridans may cause
indolent infections. These organisms
may not be detected unless
blood cultures are held for more
than 10 days and should not be disregarded
as contaminants in the
presence of clinical infection. Salmo-
nella, presumably from an intestinal
source, can cause vertebral osteomyelitis
in children with sickle cell
Laboratory Studies
Laboratory studies may be useful
but are usually nonspecific. The
white blood cell count will be elevated
in approximately half the
cases of acute pyogenic osteomyelitis
but typically is normal in the
presence of subacute or chronic
infection. The erythrocyte sedimentation
rate (ESR) is a more sensitive
test and is elevated in >90% of patients.
The C-reactive protein (CRP)
level, an acute-phase reactant with a
much quicker normalization time,
may be more helpful in following
the course of treatment than the
ESR. A rapid decrease in the CRP
level indicates an adequate response
to treatment and can help determine
when to switch from intravenous to
oral antibiotics. Blood cultures may
be negative in up to 75% of patients,
particularly if the infection involves
a low-virulence organism. It is
extremely important to delay antibiotic
therapy until appropriate cultures
have been obtained unless the
patient is septic and critically ill.
Even then, blood and urine cultures
should be obtained before the administration
of antibiotics.
Evaluation of laboratory measurements
for malnutrition is as important
as the diagnostic tests that detect
the presence of infection. Weight
loss >30% of ideal body weight during
the course of the infection indicates
severe malnutrition. Other
laboratory measurements that are
associated with severe malnutrition
include a serum albumin level of <3
g/dL, serum transferrin measurement
of <150 μg/dL, and an absolute
lymphocyte count of <800/mL. Although
it is a measurement less commonly
used in orthopaedics, a 24-
hour urinary creatinine excretion of
<10.5 mg in men or <5.8 mg in
women indicates a negative nitrogen
balance associated with malnutrition.
The definitive diagnosis of spinal
pyogenic osteomyelitis requires
identification of the organism
through a positive blood culture or
from a biopsy and culture of the
infected site. Blood cultures may be
diagnostic in as few as 25% to 33%
of cases.2 Cultures taken during
fever spikes may provide better
diagnostic results. Biopsy of the
infected area is often necessary to
initiate the appropriate antibiotic
regimen. Other sources of obvious
infection, such as the urine, must
also be cultured. Spinal biopsies
may be done percutaneously, using
computed tomography (CT) or fluoroscopy
to localize the focus of infection.
The accuracy of closed biopsy
techniques varies and has been
reported to be about 70%.13 Key factors
may be insufficient tissue
retrieval or administration of antibiotics
prior to biopsy. A core sample
obtained from a Craig biopsy needle
for bone or a TruCut (Baxter Travenol,
Deerfield, IL) or similar needle
for soft tissue is preferable to fineneedle
aspiration except when an
abscess cavity is present. Antibiotics
must not be started until the biopsy
is done and sufficient tissue is obtained
for culture, gram stain, and
histology. If a diagnosis is not confirmed
on the first attempt, a second
closed biopsy should be considered
before open biopsy is done.
An open biopsy is indicated
when needle biopsy fails to identify
an organism, when the infection is
inaccessible by standard closed
techniques, or when there is marked
structural damage with neurologic
compromise. Open biopsies are
diagnostic in >80% of cases.14 Minimally
invasive techniques, such as a
laparoscopic or thoracoscopic approach,
may be considered when that
approach is appropriate to decrease
the morbidity of the procedure.
Biopsies should be sent for gram
stain, acid-fast stain, and aerobic,
anaerobic, fungal, and TB cultures.
Bacterial cultures should be maintained
for 10 days to detect low-virulence
organisms. Histologic studSpinal

ies also should be done, if possible,
to detect metabolic or neoplastic
processes. If tissue is available,
pathologic examination should be
conducted to differentiate between
acute and chronic infection and to
help detect the presence of acid-fast
bacilli and fungal elements. The
development of polymerase chain
reaction as a diagnostic tool has facilitated
rapid detection of the infecting
agent, especially when indolent
and low-virulence organisms are
involved.15,16 However, technical
problems with cross-contamination
can lead to false-positive results.
The clinical presentation of a
patient with a tuberculous spinal
infection is highly variable. As with
pyogenic infections, back pain is the
most common symptom; however,
it is usually less severe than in a
pyogenic infection. Patients with
chronic infection also may experience
weight loss, malaise, fevers,
and night sweats. Kyphotic deformities,
neurologic deficits, or cutaneous
sinuses may occur after prolonged
or very severe infections.
Neurologic deficit can occur from
epidural extension of the tuberculous
infection, from destruction of
bone with retropulsion of infected
material into the spinal canal, or
from progressive kyphotic deformity.
Elderly patients appear to be
at higher risk for developing a neurologic
deficit. The differential diagnosis
of spinal infection includes
primary and metastatic tumors; infections
with atypical bacteria such
as Actinomyces, Nocardia, and Bru-
cella; infections with atypical mycobacteria;
and fungal infections such
as coccidioidomycosis, blastomycosis,
cryptomycosis, candidiasis, and
aspergillosis. Immunocompromised
patients are at risk for developing
infections with atypical mycobacteria.
Fungal infections also have
become more common with the
increasing use of broad-spectrum
antibiotics, especially in combination
with central venous catheters for
parenteral nutrition .
Suspicion of a mycobacterial
infection is the basis for establishing
the diagnosis. Patients from Southeast
Asia or South America, prison
populations, and frequenters of
homeless shelters are at high risk for
contracting TB. A patient with a
family member or household contact
with TB also should be considered
as at high risk. Laboratory tests
are usually nonspecific. A leukocytosis
may or may not be present.
The ESR may be normal in up to
25% of cases. Although the purified
protein derivative skin test can help
detect active infection or past exposure
to TB, the test is not fully reliable
because of false-negative results
that can occur in the malnourished
and the immunocompromised.
Polymerase chain reaction for detection
of tuberculous infection holds
great promise for a faster diagnosis.
Pediatric Diskitis
The highly variable clinical presentation
of a child with diskitis may
lead to delays in recognition and
diagnosis. Active children may
often associate the onset of pain with
some activity or minor trauma. In
the absence of systemic symptoms
of infection, further workup is necessary
if the pain does not resolve in
1 to 2 weeks. In general, however,
vertebral infection should be suspected
when the child has a lowgrade
fever and pain, refuses to bear
weight, or assumes a flexed position
of the spine. The patient also may
complain of abdominal pain. These
nonspecific findings are more common
in children over the age of 5
years.17-19 In contrast, infants are
more likely to be systemically ill.
Older children are more likely to be
able to identify the spine as the
source of pain. Although uncommon,
these same symptoms can be
observed with spinal tumors in children,
such as Ewing’s sarcoma.
The white blood cell count may
or may not be elevated, but the ESR
is usually mildly elevated and the
CRP level, markedly elevated.
Infants typically will demonstrate a
leukocytosis and elevated ESR.20
Blood cultures can be positive in
up to 50% of cases.19
Acute infections are more likely
to yield positive blood cultures.19
Certainly the child who appears ill
and febrile should have all possible
sources of infection cultured. If a
biopsy is needed, it can be done
under CT guidance; a 60% to 70%
yield rate for infectious lesions can
be expected.21 If a trial of antibiotics
was initiated prior to biopsy without
response, antibiotics should be
suspended for 3 to 4 days before the
procedure to ensure greater accuracy
from the cultures.
A 40-year-old woman with
rheumatoid arthritis and chronic steroid
use developed severe back pain and paraplegia
after treatment with broad-spectrum
antibiotics for necrotizing fasciitis. A,
Lateral radiograph of the lumbar spine
shows bony destruction of the end plates
of L2 and L3. B, T2-weighted sagittal MR
image of the lumbar spine demonstrates
diskitis and vertebral osteomyelitis at L2-3,
with severe canal stenosis from an epidural
collection (arrowhead). Cultures taken at
the time of anterior débridement were consistent
with a Candida infection. The patient
obtained pain relief and improvement
in motor function after aggressive anterior
débridement and reconstruction with an
autogenous tricortical iliac graft and 6
weeks’ administration of intravenous liposomal
amphotericin B.
Epidural Abscess
The presence of a spinal epidural
abscess is usually associated with
the occurrence of diskitis or vertebral
osteomyelitis. Rarely does an
epidural abscess occur hematogenously
without spinal involvement.
This condition is caused by direct
seeding of bacteria into the epidural
venous plexus, in contrast with the
more common route of local extension
from adjacent disk or bone. In
the absence of diskitis or vertebral
osteomyelitis, an epidural abscess
can be difficult to diagnose and can
progress rapidly, with devastating
consequences; prompt diagnosis
and early treatment are critical in
these rare cases. Risk factors for the
development of epidural abscess
include history of intravenous drug
use, diabetes, trauma, obesity, percutaneous
or open procedures (eg,
spinal surgery, nerve or epidural
block, or diskography), HIV, and
renal failure.22-26 Patients may present
with back pain, progressive
neurologic deficit, or fever. Although
leukocytosis may not be
present, the ESR is almost always
Radiographic Evaluation
Imaging studies are crucial to localize
the infection, assess the extent of
involvement, and determine the
response to treatment. Radiographs
may demonstrate progressive osteolysis
and end plate destruction,
often best seen on the anteroposterior
view (Fig. 2, A). As the disease progresses,
the disk space narrows and
eventually collapses (Fig. 3). Plain
radiographs, however, may not
demonstrate abnormal findings for
up to several weeks after the process
has begun. Soft-tissue extension
must be suspected in the presence
of an abnormal psoas shadow,
widening of the mediastinum , or enlargement of the retropharyngeal
soft-tissue shadow. The
presence of gas in the soft tissues
suggests an infection with an anaerobic
In contrast with pyogenic infections,
skeletal radiographs in a
tuberculous infection often demonstrate
vertebral destruction with
relative preservation of the disk
spaces. As the infection progresses,
the disk is also destroyed and a
kyphotic deformity may be present,
especially in the thoracic spine. A
chest radiograph always should be
obtained to assess for active pulmonary
In pediatric diskitis, radiographs
of the spine should be assessed for
disk space narrowing, end plate erosions,
bony destruction, and paravertebral
soft-tissue swelling. These
changes may not occur for several
days or weeks after onset of symptoms.
They usually persist, eventually
leading to disk space narrowing
or autofusion.18,27 Although late
kyphosis is rarely seen in pediatric
spinal infections, a notable exception
is infantile osteomyelitis, which generally
is associated with more initial
bony destruction and resembles congenital
kyphosis in late stages.20
Radionuclide studies can be
much more sensitive than radiographs
in detecting early infections.
Technetium 99m bone scintigraphy
is sensitive (~90%) but nonspecific,
especially in adults with degenerative
joint disease.28 Because the
study is dependent on local blood
flow, false-negative results have
occurred in areas of relative ischemia
in very young and elderly patients.
In pediatric vertebral osteomyelitis,
the technetium 99m bone
scan is positive in 74% to 100% of
cases,17,19 facilitating earlier diagnosis
of diskitis in children. Wenger et
al19 showed that use of bone scans
allowed diskitis to be diagnosed an
average of 8.3 days earlier than
When used in conjunction with
technetium 99m scans, gallium 67
citrate scans have high sensitivity
and specificity in detecting foci of
infection. The tracer, an analog of
ferritin, is secreted by leukocytes at
sites of infection. Gallium scans also
normalize during the recovery phase
and may be used to follow treatment
response. This test, however, may
not be effective in leukopenic patients
and may not detect low-virulence
organisms. Indium 111-labeled
scans have a poor sensitivity in vertebral
osteomyelitis (17%) and are
not recommended.29
CT is useful in delineating the
extent of bony destruction and softtissue
extension and is helpful in preoperative
planning. However, the
status of the neural elements cannot
be accurately assessed without the
use of myelographic dye, which is
contraindicated in suspected infection
because it places the patient at
risk for developing meningitis or
arachnoiditis. Although the CT scan
with intravenous contrast also can
demonstrate soft-tissue extension,
distinction between abscess and
granulation tissue may be difficult.
Magnetic resonance imaging
(MRI) is the modality of choice in
the diagnosis and evaluation of
spinal infections because it provides
excellent imaging of the soft tissue,
neural elements, and inflammatory
changes in the bone (Figs. 2, B and
3, C). MRI has an extremely high
sensitivity (96%) and specificity
(93%) in detecting infections of the
vertebral column.28 It is noninvasive,
allows detection of paravertebral
and epidural extension, and
clearly visualizes neurologic structures.
T1-weighted sequences
demonstrate decreased signal intensity
in both the vertebral body
and disk from edema. T2-weighted
images show increased signal intensity
in both the vertebral body and
disk with loss of the normal intranuclear
cleft .
The administration of gadolinium
in combination with MRI improves
resolution and allows an infectious
process to be distinguished from
Spinal Infections

degenerative changes of the end
plate and intervertebral disk .
The vascular-based enhancement
also allows differentiation of an
epidural granulation from an epidural
abscess. An epidural mass
may be isointense or hypointense
on T1-weighted images, shows high
signal on T2-weighted images, and
may show peripheral enhancement
visible with gadolinium.30 Short T1
inversion recovery sequences often
can help to differentiate an infection
from other pathologic entities. Even
with MRI, however, granulomatous
infections can be difficult to distinguish
from tumors of the spine.
Thus, a biopsy is often required to
make a definitive diagnosis.

Pyogenic Infections
The goals for treatment of spinal
infections should be to establish a
diagnosis and identify the pathogen,
eradicate the infection, prevent or
minimize neurologic involvement,
maintain spinal stability, and provide
an adequate nutritional state
to combat infection. Establishing
a diagnosis and identifying the
pathogen is of primary importance.
Once the organism has been identified,
intravenous antibiotic therapy
should be initiated according to the
culture results and sensitivities. A
course of 2 to 6 weeks of parenteral
antibiotics is usually recommended.
This is followed by a course of oral
antibiotics, depending on the virulence
of the organism, susceptibility
of the host, and other factors, such as
retained hardware. Conversion to
oral antibiotics should be made only
with clinical improvement, normalization
of the ESR and CRP level, or
resolution of the infection as demonstrated
in imaging studies.
In addition to antibiotic therapy,
immobilization, rest, and proper nutrition
are recommended. Molded
contact braces are effective in the
lumbar region, whereas a halo or a
rigid cervicothoracic orthosis may
be required for cervical osteomyelitis.
Immobilization of the affected
area aids in pain relief and helps
prevent deformity.
Surgery is indicated in five circumstances:
to obtain a tissue diagnosis
after a failed closed needle
biopsy or from a location inaccessible
by closed methods; for drainage
of an abscess that is causing sepsis
or neurologic deficit; to treat neurologic
deficit secondary to compression
either by the infection (abscess
or granulation) or structural destruction;
for structural instability or
deformity; or for failure of medical
management to reduce persistent
symptoms or elevated laboratory
The location of the infection and
the intended purpose of the surgery
often dictate the surgical approach.
Because the majority of these infections
involve the vertebral body and
the disk, an anterior approach is
most commonly used to maximize
access to the infected tissue. A posterolateral
approach to the thoracic
spine may be considered in certain
instances, or a costotransversectomy
if only culture, biopsy, or abscess
drainage is necessary. Because these
and endoscopic approaches avoid
thoracotomy, they may cause less
morbidity in the medically fragile
If an anterior approach is used
for débridement and decompression
of the spinal canal, reconstruction
should be done with an autogenous
structural graft, such as tricortical
iliac crest or middle third of the
fibula. Iliac crest is preferable because
of the abundant amount of
cancellous bone. Fresh-frozen allografts
in combination with autogenous
bone may be considered for
structural support, but structural
autogenous bone grafts are preferred.
Vascularized bone grafts
have gained popularity during the
last decade because of their intrinsic
blood supply and faster rate of incorporation.
In the thoracolumbar
junction, a vascularized rib graft
may be used, and in the lumbar
spine, vascularized rib or iliac
grafts.31-34 Recently, titanium surgical
mesh filled with autogenous
bone has been used as an alternative
to structural autogenous graft.
Depending on the degree of preoperative
kyphosis and length of the
reconstruction, a posterior fusion
A 38-year-old man with HIV and a CD4 cell count of 20 presented with back
pain of several weeks’ duration and no radiculopathy. A, T1-weighted sagittal MR image
shows edema at the L5-S1 disk space and adjacent end plates. The asterisk (*) indicates an
epidural collection consistent with an epidural abscess. B, T1-weighted gadoliniumenhanced
sagittal MR image shows uptake at the L5-S1 disk space and the epidural collection.
C, T2-weighted sagittal MR image shows no notable canal compromise by the anterior
collection. However, there is severe destruction of the adjacent bone of L5 and S1.
with instrumentation may be required
to adequately stabilize the
spine. This is usually undertaken 1
to 2 weeks after the initial surgical
débridement. The staging of the
procedures allows for an interval of
intravenous antibiotics and optimization
of medical and nutritional
parameters before placement of the
Hyperalimentation is an effective
way to maximize the patient’s nutritional
status before and after surgery
and between stages. The infection
places the patient in a catabolic state
because of metabolic losses that have
occurred before the diagnosis of infection
is made. The goal of nutritional
supplementation is to restore
the patient to the premorbid nutritional
status. Nutrition consultation
and monitoring of laboratory measurements
are helpful in reaching a
positive nitrogen balance. These
include achieving a serum albumin
level >3 g/dL, an absolute lymphocyte
count >800/mL, and a 24-hour
urine creatinine excretion >10.5 mg
in men and >5.8 mg in women.
Once the diagnosis of a tuberculous
infection is established, aggressive
treatment is necessary to
eradicate the infection. A four-drug
regimen of isoniazid, rifampin,
ethambutol, and pyrazinamide is
used as first-line therapy for 6
months. The response to treatment
is assessed by routine clinical examinations
and radiographs. The
emergence of multidrug-resistant
mycobacteria will provide further
challenges in the treatment of these
infections in the future.
Indications for surgery in tubercular
infections are the same as for
pyogenic infections. The most common
surgical technique, the Hong
Kong procedure, involves débridement
of infected bone, decompression
of the spinal canal, and correction
of the kyphotic deformity using
structural grafting35 . Additional
posterior fusion with instrumentation
also may be required.
The second procedure can be either
staged or done on the same day,
depending on the tolerance of the
patient. Autogenous iliac crest or
fibula is ideal for structural grafting.
Rib graft alone has been shown to
be inadequate unless a vascularized
rib is used to accelerate the rate of
incorporation. The Hong Kong procedure
is preferred over anterior
débridement alone because the
addition of an anterior strut corrects
and prevents progressive kyphotic
deformity. Laminectomy without
adjunctive stabilization is contraindicated
because damage to the
posterior structures in the presence
of weakened anterior structures will
lead to progressive kyphosis and
neurologic injury.
Failure of medical treatment or
development of neurologic deficit is
A 22-year-old woman presented with a long history of back pain.
Anteroposterior (A) and lateral (B) radiographs show erosion and partial collapse of the
T12 vertebral body (arrow). C, T1-weighted MR image demonstrates extensive anterior
and posterior column involvement. Because of atypical MR image findings, a posterior
biopsy was performed, which revealed TB. D, Postoperative lateral radiograph. Because
of partial collapse and extensive involvement, the patient underwent anterior reconstruction
using autogenous rib graft.

a clear indication for surgical
débridement, decompression, and
stabilization. Early decompression
will maximize the patient’s functional
recovery. A more chronic
neurologic deficit due to cord compression
over structural deformity
also may be treated with decompression
and stabilization. However,
the prognosis for neurologic
recovery in the face of chronic
deficits is not as optimistic.
Pediatric Diskitis
Whether diskitis in children is
infectious or inflammatory in origin
remains controversial. Although
the recommended treatment will
vary depending on the suspected
origin, immobilization with casting
or bracing is uniformly recommended.
The use of antibiotics has been
controversial, with satisfactory
results reported in several studies
regardless whether a patient
received antibiotics. Scoles and
Quinn18 reported that all patients
were asymptomatic at the time of
hospital discharge, whether or not
antibiotics were administered. In
addition, none of these patients had
a relapse. In contrast, Ring and
Wenger36 observed that patients
treated with intravenous antibiotics
for at least 6 days had a more rapid
resolution of symptoms and the
lowest likelihood of developing
recurrent symptoms. Oral antibiotics
or no treatment were more
likely to lead to prolonged or recurrent
symptoms. Based on their
experience, they felt that a short
course of parenteral antibiotics was
more likely to result in rapid relief
of symptoms and a lower incidence
of recurrent symptoms. Crawford et
al17 reserved antibiotics for patients
who failed to respond to immobilization,
bed rest, traction, or casting.
Epidural Abscess
Surgical drainage is almost universally
recommended for treatment
of an epidural abscess (Fig. 4). Conservative
management of epidural
abscesses, however, may be appropriate
if the patient has no neurologic
deficit, if the involvement is extensive,
if the patient is not expected to
survive surgery, or if paralysis has
been present for >48 hours so that
neurologic improvement would be
unlikely.26,30 For example, patients
with lumbar involvement, no neural
compromise, and diagnostic cultures
can be effectively treated with
intravenous antibiotics. As with
osteomyelitis, from 2 to 6 weeks of
intravenous antibiotics is usually
recommended. An extended period
of oral antibiotics may be necessary
depending on the immunocompetency
of the patient and the sensitivity
of the organism.
Patients with neurologic deterioration
are best managed with surgical
decompression and débridement
in addition to antibiotic therapy.
Anterior abscesses, particularly
with vertebral body involvement,
should have anterior débridement.
This can be done using either an
open or endoscopic approach. Posteriorly
located infections can be
adequately treated by a laminectomy.
Patients with extensive involvement
can be treated through
multilevel laminectomies. However,
care should be taken not to remove
more bone than is indicated for
decompression because of the risk of
postlaminectomy deformity. Prompt
and aggressive treatment of neurologic
compression appears to favorably
affect neurologic recovery.26
The most common types of vertebral
osteomyelitis are hematogenous
bacterial or fungal infections
(pyogenic or granulomatous), pediatric
diskitis, epidural abscess, and
postoperative infections. Successful
diagnosis and treatment depend on
an appropriate index of suspicion.
The optimal management of patients
with spinal infection requires
understanding the circumstances
that resulted in the infection, the
organism involved, and the degree
of bony and neurologic compromise.
Early detection and medical
treatment may obviate the need for
surgical intervention. When surgical
débridement is indicated, its
prompt initiation appears to result
in good clinical outcomes. In addition,
maximizing the patient’s nutritional
status with hyperalimentation
improves the outcomes of both medical
and surgical treatment.
1. Guri JP: Pyogenic osteomyelitis of the
spine: Differential diagnosis through
clinical and radiographic observations.
J Bone Joint Surg Am 1946;28:29-39.
2. Carragee EJ: Pyogenic vertebral osteomyelitis.
J Bone Joint Surg Am 1997;79:
3. Garcia A Jr, Grantham SA: Hematogenous
pyogenic vertebral osteomyelitis.
J Bone Joint Surg Am 1960;42:429-436.
4. Eismont FJ, Bohlman HH, Soni PL,
Goldberg VM, Freehafer AA: Pyogenic
and fungal vertebral osteomyelitis with
paralysis. J Bone Joint Surg Am 1983;
5. Batson OV: The vertebral system of
veins as a means for cancer dissemination.
Prog Clin Cancer 1967;3:1-18.
6. Wiley AM, Trueta J: The vascular anatomy
of the spine and its relationship to
pyogenic vertebral osteomyelitis. J Bone
Joint Surg Br 1959;41:796-809.
7. Parke WW, Rothman RH, Brown MD:
The pharyngovertebral veins: An
anatomical rationale for Grisel’s syndrome.
J Bone Joint Surg Am 1984;66:
8. Sapico FL, Montgomerie JZ: Vertebral
osteomyelitis. Infect Dis Clin North Am
Bobby K-B Tay, MD, et al
Vol 10, No 3, May/June 2002 197
9. Boachie-Adjei O, Squillante RG:
Tuberculosis of the spine. Orthop Clin
North Am 1996;27:95-103.
10. Doub HP, Badgley CE: The roentgen
signs of tuberculosis of the vertebral
body. AJR Am J Roentgenol 1932;27:
11. Krogsgaard MR, Wagn P, Bengtsson J:
Epidemiology of acute vertebral
osteomyelitis in Denmark: 137 cases in
Denmark 1978-1982, compared to
cases reported to the National Patient
Register 1991-1993. Acta Orthop Scand
12. Torda AJ, Gottlieb T, Bradbury R:
Pyogenic vertebral osteomyelitis:
Analysis of 20 cases and review. Clin
Infect Dis 1995;20:320-328.
13. Kornblum MB, Wesolowski DP,
Fischgrund JS, Herkowitz HN: Computed
tomography-guided biopsy of
the spine: A review of 103 patients.
Spine 1998;23:81-85.
14. Sapico FL, Montgomerie JZ: Pyogenic
vertebral osteomyelitis: Report of nine
cases and review of the literature. Rev
Infect Dis 1979;1:754-776.
15. Berk RH, Yazici M, Atabey N, Ozdamar
OS, Pabuccuoglu U, Alici E:
Detection of Mycobacterium tuberculosis
in formaldehyde solution-fixed, paraffin-
embedded tissue by polymerase
chain reaction in Pott’s disease. Spine
16. Meier A, Persing DH, Finken M,
Bottger EC: Elimination of contaminating
DNA within polymerase chain
reaction reagents: Implications for a
general approach to detection of
uncultured pathogens. J Clin Microbiol
17. Crawford AH, Kucharzyk DW, Ruda
R, Smitherman HC Jr: Diskitis in children.
Clin Orthop 1991;266:70-79.
18. Scoles PV, Quinn TP: Intervertebral
discitis in children and adolescents.
Clin Orthop 1982;162:31-36.
19. Wenger DR, Bobechko WP, Gilday DL:
The spectrum of intervertebral discspace
infection in children. J Bone Joint
Surg Am 1978;60:100-108.
20. Eismont FJ, Bohlman HH, Soni PL,
Goldberg VM, Freehafer AA: Vertebral
osteomyelitis in infants. J Bone
Joint Surg Br 1982;64:32-35.
21. Omarini LP, Garcia J: CT-guided percutaneous
puncture-biopsy of the
spine: Review of 104 cases [French].
Schweiz Med Wochenschr 1993;123:2191-
22. Junila J, Niinimaki T, Tervonen O:
Epidural abscess after lumbar discography:
A case report. Spine 1997;22:
23. Kindler CH, Seeberger MD, Staender
SE: Epidural abscess complicating
epidural anesthesia and analgesia.
Acta Anaesthesiol Scand 1998;42:
24. Knight JW, Cordingley JJ, Palazzo MG:
Epidural abscess following epidural
steroid and local anaesthetic injection.
Anaesthesia 1997;52:576-578.
25. Prendergast H, Jerrard D, O’Connell J:
Atypical presentations of epidural
abscess in intravenous drug abusers.
Am J Emerg Med 1997;15:158-160.
26. Sampath P, Rigamonti D: Spinal
epidural abscess: A review of epidemiology,
diagnosis, and treatment. J Spinal
Disord 1999;12:89-93.
27. Song KS, Ogden JA, Ganey T, Guidera
KJ: Contiguous discitis and osteomyelitis
in children. J Pediatr Orthop 1997;
28. Modic MT, Feiglin DH, Piraino DW, et
al: Vertebral osteomyelitis: Assessment
using MR. Radiology 1985;157:157-166.
29. Whalen JL, Brown ML, McLeod R,
Fitzgerald RH Jr: Limitations of indium
leukocyte imaging for the diagnosis
of spine infections. Spine 1991;16:
30. Lang IM, Hughes DG, Jenkins JP, St
Clair Forbes W, McKenna F: MR imaging
appearances of cervical epidural
abscess. Clin Radiol 1995;50:466-471.
31. Ikeda K, Yokoyama M, Okada K,
Tomita K, Yoshimura M: Long-term
follow-up of the vascularized iliac bone
graft. Microsurgery 1998;18:419-423.
32. Hayashi A, Maruyama Y, Okajima Y,
Motegi M: Vascularized iliac bone
graft based on a pedicle of upper lumbar
vessels for anterior fusion of the
thoraco-lumbar spine. Br J Plast Surg
33. Mosheiff R, Meyer S, Floman Y, Kaplan
L, Eid A, Cohen I: Anterior vascularized
rib strut graft in the treatment of
Pott’s disease in the young child. Bull
Hosp Jt Dis 1993;53:61-65.
34. Lascombes P, Grosdidier G, Olry R,
Thomas C: Anatomical basis of the anterior
vertebral graft using a pediculated
rib. Surg Radiol Anat 1991;13:259-263.
35. A controlled trial of anterior spinal
fusion and debridement in the surgical
management of tuberculosis of the
spine in patients on standard chemotherapy:
A study in Hong Kong. Br J
Surg 1974;61:853-866.
36. Ring D, Wenger DR: Pyogenic infectious
spondylitis in children: The evolution
to current thought. Am J Orthop
Posting Komentar

Harryks Search Engine

Custom Search