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218
15 Acute Traumatic Atlantoaxial Dislocation (AAD) in Adults
10. Fielding, J.W., Hawkins, R.J.: Atlanto-axial rotatory fixation. (Fixed rotatory subluxation of the atlanto-axial joint). J
Bone Joint Surg Am 59, 37–44 (1977)
11. Fox, J.L., Jerez, A.: An unusual atlanto-axial dislocation.
Case report. J Neurosurg 47, 115–118 (1977)
12. Freeman, B.J., Bisbinas, I., Nelson, I.W.: Traumatic atlantoaxial subluxation and missed cervical spine injuries. Hosp
Med 59, 330–331 (1998)
13. Fuentes, S., Bouillot, P., Palombi, O., et al.: Traumatic atlantoaxial rotatory dislocation with odontoid fracture: case
report and review. Spine (Phila Pa 1976) 26, 830–834
(2001)
14. Gonzalez, L.F., Klopfenstein, J.D., Crawford, N.R., et al.:
Use of dual transarticular screws to fixate simultaneous
occipitoatlantal and atlantoaxial dislocations. J Neurosurg
Spine 3, 318–323 (2005)
15. Hamai, S., Harimaya, K., Maeda, T., et al.: Traumatic
atlanto-occipital dislocation with atlantoaxial subluxation.
Spine (Phila Pa 1976) 31, E421–E424 (2006)
16. Haralson 3rd, R.H., Boyd, H.B.: Posterior dislocation of the
atlas on the axis without fracture. Report of a case. J Bone
Joint Surg Am 51, 561–566 (1969)
17. Hopf, S., Buchalla, R., Elhoft, H., et al.: Atypical dislocated
dens fracture type II with rotational atlantoaxial luxation
after a riding accident. Unfallchirurg 112, 517–520 (2009)
18. Jamshidi, S., Dennis, M.W., Azzam, C., et al.: Traumatic
posterior atlantoaxial dislocation without neurological deficit: case report. Neurosurgery 12, 211–213 (1983)
19. Jiang, L.S., Shen, L., Wang, W., et al.: Posterior atlantoaxial
dislocation without fracture and neurologic deficit: a case
report and the review of literature. Eur Spine J 28, 28 (2009)
20. Jones, R.N.: Rotatory dislocation of both atlanto-axial joints.
J Bone Joint Surg Br 66, 6–7 (1984)
21. Kim, Y.S., Lee, J.K., Moon, S.J., et al.: Post-traumatic atlantoaxial rotatory fixation in an adult: a case report. Spine
(Phila Pa 1976) 32, E682–E687 (2007)
22. Kleweno, C.P., Zampini, J.M., White, A.P., et al.: Survival
after concurrent traumatic dislocation of the atlanto-occipital
and atlanto-axial joints: a case report and review of the literature. Spine (Phila Pa 1976) 33, E659–E662 (2008)
23. Levine, A.M., Edwards, C.C.: Treatment of injuries in the
C1-C2 complex. Orthop Clin North Am 17, 31–44 (1986)
24. Miyamoto, H., Doita, M., Nishida, K., et al.: Traumatic anterior atlantoaxial subluxation occurring in a professional
rugby athlete: case report and review of literature related to
atlantoaxial injuries in sports activities. Spine (Phila Pa
1976) 29, E61–E64 (2004)
25. Monckeberg, J.E., Tome, C.V., Matias, A., et al.: CT scan
study of atlantoaxial rotatory mobility in asymptomatic adult
subjects: a basis for better understanding C1-C2 rotatory
fixation and subluxation. Spine (Phila Pa 1976) 34, 1292–
1295 (2009)
26. Moore, K.R., Frank, E.H.: Traumatic atlantoaxial rotatory
subluxation and dislocation. Spine (Phila Pa 1976) 20,
1928–1930 (20)
27. Ono, K., Yonenobu, K., Fuji, T., et al.: Atlantoaxial rotatory
fixation. Radiographic study of its mechanism. Spine (Phila
Pa 1976) 10, 602–608 (1985)
28. Patzakis, M.J., Knopf, A., Elfering, M., et al.: Posterior dislocation of the atlas on the axis: a case report. J Bone Joint
Surg Am 56, 1260–1262 (1974)
29. Payer, M., Wetzel, S., Kelekis, A., et al.: Traumatic vertical
atlantoaxial dislocation. J Clin Neurosci 12, 704–706
(2005)
30. Przybylski, G.J., Welch, W.C.: Longitudinal atlantoaxial
dislocation with type III odontoid fracture. Case report and
review of the literature. J Neurosurg 84, 666–670 (1996)
31. Roche, C.J., O’Malley, M., Dorgan, J.C., et al.: A pictorial
review of atlanto-axial rotatory fixation: key points for the
radiologist. Clin Radiol 56, 947–958 (2001)
32. Sassard, W.R., Heinig, C.F., Pitts, W.R.: Posterior atlantoaxial dislocation without fracture. Case report with successful conservative treatment. J Bone Joint Surg Am 56,
625–628 (1974)
33. Sinigaglia, R., Bundy, A., Monterumici, D.A.: Traumatic
atlantoaxial rotatory dislocation in adults. Chir Narzadow
Ruchu Ortop Pol 73, 149–154 (2008)
34. Spoor, A.B., Diekerhof, C.H., Bonnet, M., et al.: Traumatic
complex dislocation of the atlanto-axial joint with odontoid
and C2 superior articular facet fracture. Spine (Phila Pa
1976) 33, E708–E711 (2008)
35. Weiner, B.K., Brower, R.S.: Traumatic vertical atlantoaxial
instability in a case of atlanto-occipital coalition. Spine
(Phila Pa 1976) 22, 1033–1035 (1997)
36. Wong, D.A., Mack, R.P., Craigmile, T.K.: Traumatic atlantoaxial dislocation without fracture of the odontoid. Spine
(Phila Pa 1976) 16, 587–589 (1991)
37. Yoon, D.H., Yang, K.H., Kim, K.N., et al.: Posterior atlantoaxial dislocation without fracture. Case report. J Neurosurg
98, 73–76 (2003)
Posttraumatic Deformity
P. Suchomel and R. Fricˇ
16
Posttraumatic spinal deformity has always been a
problem inevitably related to spinal trauma, although
relatively small number of spine fractures, with the
majority located in the thoracolumbar region, have
been described in paleopathological studies [9]. Weber
et al. [26] reported observation of a pseudarthrosis
after Anderson-Alonzo type III odontoid fracture in
skeletal remnants of a medieval man. Posttraumatic
deformity may be encountered in all parts of upper cervical spine (UCS) where fractures and dislocations
typically occur, although pseudoarthrosis of the odontoid has been reported most frequently [1, 3, 15, 20,
22, 24, 25].
The deformity of UCS results in sagittal and/or
frontal dysbalance and can easily become a significant
pain generator due to excessive mobility of UCS.
Moreover, healing failure of important stabilizing elements such as the odontoid may represent a critical and
potentially life-threatening instability.
Patients presenting with intractable pain related to
posttraumatic UCS deformity or instability usually have
to be treated surgically, although old patients and/or
those with high risk of medical complications may be
acceptable exceptions. Decompression of neural structures, sagittal and frontal spinal realignment, and stabilization are the primary goals of surgery.
16.1 Etiology
Generally, the UCS deformity is a result of healing
failure after trauma. This can be caused by a missed
diagnosis, inappropriate treatment, and/or failure of an
otherwise appropriate treatment.
Some types of fractures can easily be overlooked on
initial plain films, in particular those with hairline
appearance and without dislocation (Figs. 11.3 and 11.9,
Chap. 11) [4]. Deformity and instability following conservative treatment are often related to insufficient or
failed external immobilization (Fig. 11.11, Chap. 11;
Fig. 10.9, Chap. 10). If fracture healing is not confirmed
by radiological studies and the brace is withdrawn too
early, a deformity may develop consequently. Another
cause might be an inappropriate choice of conservative
treatment in cases obviously requiring surgery due to
present instability (Fig. 16.1). On the other hand, falsely
indicated or poorly performed surgical intervention
(Fig. 16.2) may lead to deformity of UCS as well. Even
an adequately indicated and preformed treatment of
UCS trauma can fail, and posttraumatic spinal deformity
or instability may develop anyway [7].
16.2 Clinical Symptoms
The clinical picture of posttraumatic UCS deformity is
not specific and does not differ from other causes of
P. Suchomel
Department of Neurosurgery,
Neurocenter, Regional Hospital Liberec,
Husova St. 10, 46063 Liberec, Czech Republic
R. Fricˇ
Department of Neurosurgery,
Rikshospitalet, Oslo University Hospital,
Sognsvannsveien 20, 0027 Oslo, Norway
P. Suchomel and O. Choutka, Reconstruction of Upper Cervical Spine and Craniovertebral Junction,
DOI: 10.1007/978-3-642-13158-5_16, © Springer-Verlag Berlin Heidelberg 2011
UCS instability. Patients can be completely asymptomatic. However, the majority of them present with
pain dependent on head rotation, occipital pain, neck
stiffness, and reduced mobility of the neck. The symptoms relates to the type of UCS injury and the treatment performed. Though not often, myelopathy signs
due to prolonged spinal cord compression and/or
219
220
a
cd
b
a
cd
b
Fig. 16.1 14-year-old boy
with Marphan’s syndrome
referred to our hospital from
abroad after 3 months of
unsuccessful treatment with
halo vest, presenting with
progressive quadrisymptomatology. Unclear history of
spine injury 1 year ago.
(a) C2-3 kyphotic deformity
on plain radiogram.
(b) Sagittal MRI scan
showing spinal cord
compression. (c, d) Pressure
sores caused by wearing the
halo vest, note the general
exhaustion appearance
16 Posttraumatic Deformity
Fig. 16.2 Inadequately
performed Goel-Harms
fixation of type II odontoid
fracture with posterior AA
subluxation and posterior
angulation of the odontoid
process with spinal cord
compression. (a) Midsagittal
CT scan. (b) Sagittal MRI
scan in T2-weighted images.
(c) CT reconstruction in the
plane of subluxed AA joint.
(d) Postoperative CT after
satisfactory transoral
decompression
16.4 Treatment Strategy
a b
ab
Fig. 16.3 AA instability as
shown on dynamic lateral
radiograms in a case of
odontoid pseudarthrosis
following treatment of type II
fracture with external brace.
(a) Extension. (b) Flexion
221
Fig. 16.4 Imaging of the
odontoid process pseudarthrosis in two different
patients. (a) Coronal
CT reconstruction.
(b) Midsagittal CT scan
in 3D format
vascular compromise may develop even several years
after the injury [18, 19].
16.3 Radiology
Plain films usually reveal significant deformity or
malunion, and dynamic radiographs will show its
potential instability (Fig. 16.3). Nonetheless, a CT
scan with adequate reconstruction is necessary if the
distortion of UCS anatomy shall be clearly depicted
(Fig. 16.4). MRI can show the capacity of spinal canal
and extent of neural compression (Fig. 16.5).
16.4 Treatment Strategy
Conservative treatment with external immobilization,
activity restriction, and analgesics can be justified only
in mild and stable deformities without any neurological
Fig. 16.5 MRI depicting the spinal cord compression consequent
with odontoid pseudarthrosis, the same patient as on Fig. 16.4b
222
16 Posttraumatic Deformity
symptoms, particularly in patients with sufficient pain
relief. Conservative treatment is also an option in
elderly patients and/or those with significant medical
comorbidities that unacceptably increases the risk of
surgical treatment. Nevertheless, the vast majority of
patients with symptomatic posttraumatic deformity/
instability are treated surgically. As in case of any other
UCS pathology, the decompression of neural structures
is the primary goal of surgical treatment, although correction of the deformity and adequate spinal reconstruction with concomitant fixation are the inherent
parts of the posttraumatic deformity surgery.
16.5 Odontoid Pseudarthrosis
As odontoid pseudoarthrosis appears to be the most
frequent reason to surgical intervention among posttraumatic deformities in our department, we wish to
focus on this topic in detail.
The rate of odontoid pseudarthrosis, as reported in literature, varies between 1 and 64% and depends on the
type of fracture and the treatment modality [12]. Failure
in bone healing after type II odontoid fracture, according
to Anderson and D’Alonso, is the most frequent cause.
There are similar reasons to development of pseudoarthrosis as in other treatment failures of UCS injuries.
Fractures initially overlooked and those not treated at all
are still common [4] and can lead to non-union in up to
100% of cases [2]. Type II odontoid fracture is highly
unstable and the treatment with external fixation fail in
30–50% of cases [8, 10, 13, 14, 23]. If patients older than
60 years are included in the series, the failure rate increases
dramatically up to 77–86% [10, 21]. Conversely, in fractures adequately treated with anterior compressive osteosynthesis, the malunion occurs only in up to 15% [7].
Diagnosis of odontoid pseudarthrosis is usually
based on the history of injury, clinical symptoms, and
radiological findings. Cervical spine radiographs in
lateral, AP, and Sandberg (transoral) projections along
with CT scan with bone windows and 3D reconstructions confirm the diagnosis. Stability of the odontoid
process can best be assessed on flexion-extension
views (Figs. 16.3 and 16.8).
Capacity of the spinal canal can be evaluated by
MRI, particularly in cases where hypertrophic callus
due to pseudoarthrosis is present. Dynamic MRI can
be of value in patients where conservative treatment is
considered.
Exceptionally, the diagnosis of pseudoarthrosis may
be difficult as demonstrated in the case of a 55-year-old
man reported by Rudzki et al. [19]. After a long asymptomatic period, signs of cervical myelopathy had developed and pseudoarthrosis following type II fracture
was diagnosed 39 years after the original injury.
Blauth et al. suggested a classification of odontoid
pseudarthrosis based on their extensive experience with
spine injuries [1]. In type I, called “fixed pseudarthrosis,” the fracture line is not bridged by osseous fusion
but there is no dislocation on flexion-extension radiographs. The patients are usually asymptomatic and can
be followed up with serial imaging. In type II, grossly
dislocated but “stable pseudoarthrosis,” the proximal
fragment is usually ventrally dislocated along with
the atlas. Dynamic films usually confirm this finding.
Reduction is not possible. As the patient can develop
symptoms and risk of neurological deterioration is
real, the surgical treatment is indicated. In type III,
referred to as “unstable pseudoarthrosis,” dynamic
radiographs show marked displacement. The patient
can be symptomatic and surgery is always indicated.
Type IV, “posttraumatic os odontoideum,” is distinguished by a high degree of instability. It may also be
found as an incidental finding. Indication for surgery
depends on clinical symptoms, general health, and
age of the patient.
As pseudoarthrosis of the odontoid process can
become a cause of chronic myelopathy and/or acute
spinal cord injury, the majority of authors recommend
performing AA stabilization even in asymptomatic
patients [2, 3, 5, 16]. Nonetheless, some authors advocate the conservative approach, particularly in patient
with high risk of complications owing to age, immobilization, or general health [11, 17]. In case of surgical
AA stabilization, the posterior C1-2 fixation is usually
performed [1, 3, 6, 18]. Use of transoral decompression
in cases of hypertrophic fibrous malunion was also
reported [3, 5]. In order to preserve AA motion, Ruf
et al. recommended a transorally performed debridement of pseudarthrosis, with cancellous bone grafting
accompanied by simultaneous anterior or posterior
temporary screw AA fixation for 3–4 months [20].
16.6 Our Preference
Depending on the type of deformity and instability,
surgery is indicated for those patients who can
benefit from decompression, reconstruction, and
16.6 Our Preference
a
b
a b
cd
223
stabilization. In asymptomatic patients, an estimation of potential risk related to the type of instability is crucial for surgical indication. Neurologically
compromised individuals with apparent symptoms
of spinal cord compression, but also those suffering
from continuous intractable pain as a result of malalignment, should definitely be considered for surgical
Fig. 16.6 The same patient
as shown on Fig. 16.1.
Simple manual traction
allowed lordotization of the
deformity from 41° to 20°,
thus giving evidence of
incompetence of the
halo-vest. (a) Lateral
fluoroscopy. (b) Manual
traction the angle changed
from
release and reconstruction. As an example, deformity
consequent with conservative treatment of hangman’s
fracture causing only temporary pain may be treated
conservatively (Fig. 12.11, Chap. 12); however, a
similar situation causing neurological deficit represents an absolute indication for surgery in our opinion
(Figs. 16.6 and 16.7).
Fig. 16.7 The same patient as on Figs. 16.1 and 16.6. CT scan
in 3D reconstruction revealed old C2/3 luxation on the right side
which together with elongated pars interarticularis led to diagnosis of type III inveterate hangman’s fracture. Because of general health condition of the patient but also due to partial
reducibility of the kyphosis, only a single stage C3 somatectomy
with graft and plate fixation was performed. (a) 3D CT scan in
sagittal plane demonstrating C2/3 facet dislocation on the rightside. (b) Postoperative plain laterogram. (c) CT scan of anterior
graft and plate fusion. Note bicortical screw insertion. (d) Patient
walking with hard collar fixation a week later
224
a
c d
b
16 Posttraumatic Deformity
As the actual risk of progressive neurological symptoms in case of odontoid pseudarthrosis is not known
and cases of significant clinical deterioration have been
reported, we favor an active surgical approach in the
majority of cases.
We definitely operate on patients with AA instability and those with neurological symptoms related to
compression caused by deformity (Fig. 16.8). We prefer stabilization also in patients with stable pseudoarthrosis developed after conservative treatment,
particularly in active and young individuals (Fig. 16.9),
while conservative approach with careful radiological
follow-up can be an alternative when age and/or medical risks do not allow the surgical treatment. In cases
where odontoid screw compressive osteosynthesis fails
to create continuous bone bridge across the fracture
line as confirmed by CT, we also choose an active
approach, particularly if the fracture gap is documented
(Fig. 6.38, Chap. 6).
The hardware failure may have catastrophic consequences. Occasionally, we see patients with inadequately performed odontoid screw fixation where the
risk of hardware failure is obvious (Fig. 16.10).
We usually perform posterior AA stabilization
according to techniques described by Magerl or GoelHarms, supplemented by an interlaminar graft. In rare
cases of hypertrophic pseudoarthrosis directly causing
anterior compression of neural structures, we perform
transoral odontoidectomy with removal of fibrous tissue,
followed by posterior AA stabilization (Fig. 16.11).
Fig. 16.8 A case of unstable
non-union of the odontoid
treated with posterior
transarticular screw and graft
fusion. (a) Classical
tomogram of a pseudarthrosis.
Dynamic radiograph in
flexion (b) and extension (c).
(d) Result of fusion one year
after surgery
16.6 Our Preference
ab
ab
abc
Fig. 16.9 Stable odontoid
pseudarthrosis in a 40 years
old active sportsman, treated
with posterior transarticular
screw and graft fusion. (a)
Sagittal CT reconstruction.
(b) Posterior AA fusion
Fig. 16.10 Failure of
inadequately performed
anterior double-screw
osteosynthesis of type II
odontoid fracture. Lag screw
is not compressing the
fracture and the antirotational
screw is too short, not
passing through but probably
distracting the fracture. This
instability was treated with
posterior fusion according to
Magerl with interlaminar
autologous graft.
(a) Transoral projection.
(b) Laterogram
225
Fig. 16.11 Irreducible odontoid malunion creating a deformity
with spinal cord compression; treated with transoral decompression, cage support, and posterior fusion in a single stage surgery.
(a) Sagittal CT scan showing the bone deformation. (b) Spinal
cord compression as shown on MRI. (c) Anterior Harms cage
fixed to C3 caudally and with a fork notch to clivus, posterior
O-C3 screw fusion
226
16 Posttraumatic Deformity
References
1. Blauth, M., Richter, M., Kiesewetter, B., et al.: Operative
versus non operative treatment of odontoid non unions. How
dangerous is it not to stabilize a non union of the dens?
Chirurg 70, 1225–1238 (1999)
2. Clark, C.R., White 3rd, A.A.: Fractures of the dens. A multicenter study. J Bone Joint Surg Am 67, 1340–1348 (1985)
3. Crockard, H.A., Heilman, A.E., Stevens, J.M.: Progressive
myelopathy secondary to odontoid fractures: clinical, radiological, and surgical features. J Neurosurg 78, 579–586 (1993)
4. Cusmano, F., Ferrozzi, F., Uccelli, M., et al.: Upper cervical
spine fracture: sources of misdiagnosis. Radiol Med 98,
230–235 (1999)
5. Fairholm, D., Lee, S.T., Lui, T.N.: Fractured odontoid: the
management of delayed neurological symptoms. Neurosurgery
38, 38–43 (1996)
6. Finn, M.A., Apfelbaum, R.I.: Atlantoaxial transarticular
screw fixation: update on technique and outcomes in 269
patients. Neurosurgery 66, A184–A192 (2010)
7. Fountas, K.N., Kapsalaki, E.Z., Karampelas, I., et al.: Results
of long-term follow-up in patients undergoing anterior screw
fixation for type II and rostral type III odontoid fractures.
Spine (Phila Pa 1976) 30, 661–669 (2005)
8. Fujii, E., Kobayashi, K., Hirabayashi, K.: Treatment in fractures of the odontoid process. Spine (Phila Pa 1976) 13,
604–609 (1988)
9. Gerszten, P.C., Gerszten, E., Allison, M.J.: Diseases of the
spine in South American mummies. Neurosurgery 48, 208–
213 (2001)
10. Greene, K.A., Dickman, C.A., Marciano, F.F.: Acute axis
fractures. Analysis of management and outcome in 340 consecutive cases. Spine (Phila Pa 1976) 22, 1843–1852 (1997)
11. Hart, R., Saterbak, A., Rapp, T., et al.: Nonoperative management of dens fracture nonunion in elderly patients without
myelopathy. Spine (Phila Pa 1976) 25, 1339–1343 (2000)
12. Knoller, S., Jeszenszky, D., Willms, R., et al.: Transaxial
spongiosa-plasty and ventral, temporary atlanto-axial fixation for therapy of dens pseudarthrosis. Z Orthop Ihre
Grenzgeb 137, 232–235 (1999)
13. Koivikko, M.P., Kiuru, M.J., Koskinen, S.K., et al.: Factors
associated with nonunion in conservatively-treated type-II
fractures of the odontoid process. J Bone Joint Surg Br 86,
1146–1151 (2004)
14. Lennarson, P.J., Mostafavi, H., Traynelis, V.C., et al.:
Management of type II dens fractures: a case-control study.
Spine (Phila Pa 1976) 25, 1234–1237 (2000)
15. Muller, E.J., Wick, M., Russe, O., et al.: Accident-induced
pseudarthroses of the dens axis. Etiology, follow-up and
therapy. Unfallchirurg 101, 750–754 (1998)
16. Paradis, G.R., Janes, J.M.: Posttraumatic atlantoaxial instability: the fate of the odontoid process fracture in 46 cases.
J Trauma 13, 359–367 (1973)
17. Pepin, J.W., Bourne, R.B., Hawkins, R.J.: Odontoid fractures, with special reference to the elderly patient. Clin
Orthop Relat Res 193, 178–183 (1985)
18. Platzer, P., Vecsei, V., Thalhammer, G., et al.: Posterior
atlanto-axial arthrodesis for fixation of odontoid nonunions.
Spine (Phila Pa 1976) 33, 624–630 (2008)
19. Rudzki, J.R., Lenke, L.G., Blanke, K., et al.: Pseudarthrosis of
a thirty-nine-year-old dens fracture causing myelopathy.
A case report. J Bone Joint Surg Am 86-A, 2509–2513 (2004)
20. Ruf, M., Welk, T., Muller, M., et al.: Ventral cancellous bone
augmentation of the dens and temporary instrumentation C1/
C2 as a function-preserving option in the treatment of dens
pseudarthrosis. J Spinal Disord Tech 23, 285–292 (2010)
21. Ryan, M.D., Taylor, T.K.: Odontoid fractures in the elderly.
J Spinal Disord 6, 397–401 (1993)
22. Schwarz, N., Bauer, J.: Post-traumatic os odontoideum.
Unfallchirurg 98, 483–486 (1995)
23. Seybold, E.A., Bayley, J.C.: Functional outcome of surgically
and conservatively managed dens fractures. Spine (Phila Pa
1976) 23, 1837–1845 (1998). discussion 1845–1836
24. Suchomel, P., Stulik, J., Klezl, Z., et al.: Transarticular fixation of C1-C2: a multicenter retrospective study. Acta Chir
Orthop Traumatol Cech 71, 6–12 (2004)
25. Wang, G.J., Mabie, K.N., Whitehill, R., et al.: The nonsurgical management of odontoid fractures in adults. Spine (Phila
Pa 1976) 9, 229–230 (1984)
26. Weber, J., Vieweg, U., Dollhopf, K.D., et al.: Type III odontoid fracture with pseudarthrosis in a skeleton from the early
Middle Ages. Acta Neurochir (Wien) 146, 1379–1381
(2004). discussion 1381
Non Specific Inflammation
P. Suchomel and O. Choutka
17
Pyogenic infections of the UCS are very rare; nevertheless, they can have a major impact on the health of
the patient and therefore, we feel that it is important to
share our experience with the reader. The purulent
destruction of bone and ligaments can lead to lifethreatening AA instability [1]. Whereas the rate of
specific spine inflammation is growing in the European
countries as a result of increased migration from
developing countries, the growing rate of non-specific,
infective AA osteomyelitis stems from population
aging and overall decreased immunocompetency. This
is mainly due to a growing number of immunodeficient people, uncontrolled use of broad-spectrum antibiotics, and an increasing number of people suffering
from diseases of our civilization (atherosclerosis, diabetes). Further, the substantial development in diagnostic technology enables us to detect a greater
number of pathologies. Last but not the least, a significant amount of people worldwide suffer from HIV
and/or are drug users, heavy smokers, and alcoholics
[20, 21, 27].
Despite an increased frequency of UCS tuberculosis detected not only in Asia but currently also in those
countries where a lot of immigrants have settled (UK),
we have not seen such a case so far. Nevertheless, this
P. Suchomel
Department of Neurosurgery,
Neurocenter, Regional Hospital Liberec,
Husova St. 10, 46063 Liberec, Czech Republic
O. Choutka
University of Cincinnati, Medical Center,
Department of Neurosurgery,
Albert Sabin Way 231,
Cincinnati, OH 45267-0515, USA
possibility must be entertained in every differential
diagnosis of an UCS pyogenic process.
During the last 15 years, we have encountered an
increasing amount of patients presenting with pyogenic spondylitis. Five of them suffered from a dangerous infection involving the UCS and requiring surgical
intervention.
17.1 Incidence
When considering the entire skeleton, cervical spine
is affected by pyogenic osteomyelitis relatively
infrequently (3–6%) [6, 7, 15]. The first report of atlan-
toaxial osteomyelitis in three patients is credited to
Malkins and Abbott, in 1896 [16]. All of the reported
patients died because of unavailability of antibiotics at
that time. In the modern times, only individual cases
[13, 14, 27] or very small series [24, 29] of the UCS
pyogenic inflammation were reported. In 1994,
Gormley and Rock [8] reviewed 17 case reports published previously and revealed that majority of the
reports had not been older than 10 years and thus concluded that UCS osteomyelitis is a growing contemporary problem.
Most frequently, AA osteomyelitis occurs as a
result of previous orofacial infection (primary or
secondary e.g.: after tonsillectomy, dental surgery).
The infection reaches the UCS bones either directly
or via venous drainage, although hematogenous
dissemination is also possible. Pathogens detected in
UCS conform to those causing osteomyelitis in other
parts of axial skeleton. Staphylococcus aureus was
confirmed in the majority of reported cases followed
by Pseudomonas aeruginosa, Escherichia coli, and
Proteus mirabilis.
P. Suchomel and O. Choutka, Reconstruction of Upper Cervical Spine and Craniovertebral Junction,
DOI: 10.1007/978-3-642-13158-5_17, © Springer-Verlag Berlin Heidelberg 2011
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