Tải bản đầy đủ (.pdf) (10 trang)

Spinal Disorders: Fundamentals of Diagnosis and Treatment Part 89 pptx

Bạn đang xem bản rút gọn của tài liệu. Xem và tải ngay bản đầy đủ của tài liệu tại đây (217.84 KB, 10 trang )

118. Julien TD, Frankel B, Traynelis VC, Ryken TC (2000) Evidence-based analysis of odontoid
fracture management. Neurosurg Focus 8:1–6
119. Koivikko MP, Myllynen P, Karjalainen M, Vornanen M, Santavirta S (2000) Conservative
and operative treatment in cervical burst fractures. Arch Orthop Trauma Surg 120:448–51
120. Kricun M (1988) Imaging modalities in spinal disorders. WB Saunders, Philadelphia
121. Labler L, Eid K, Platz A, Trentz O, Kossmann T (2004) Atlanto-occipital dislocation: four
case reports of survival in adults and review of the literature. Eur Spine J 13:172–80
122. Lammertse DP (2004) Update on pharmaceutical trials in acute spinal cord injury. J Spinal
Cord Med 27:319–25
123. Larson SJ, Holst RA, Hemmy DC, Sances A, Jr. (1976) Lateral extracavitary approach to
traumatic lesions of the thoracic and lumbar spine. J Neurosurg 45:628–37
124. Lee AS, MacLean JC, Newton DA (1994) Rapid traction for reduction of cervical spine dis-
locations. J Bone Joint Surg Br 76:352–6
125. Lennarson PJ, Mostafavi H, Traynelis VC, Walters BC (2000) Management of type II dens
fractures: a case-control study. Spine 25:1234–7
126. Lerman JA, Dickman CA, Haynes RJ (2001) Penetration of cranial inner table with Gard-
ner-Wells tongs. J Spinal Disord 14:211–3
127. Levine AM, Edwards CC (1985) The management of traumatic spondylolisthesis of the
axis. J Bone Joint Surg Am 67:217–26
128. Levine AM, Edwards CC (1989) Traumatic lesions of the occipitoatlantoaxial complex. Clin
Orthop Relat Res:53–68
129. Levine AM, Edwards CC (1991) Fractures of the atlas. J Bone Joint Surg Am 73:680–91
130. Lewis LM, Docherty M, Ruoff BE, Fortney JP, Keltner RA, Jr., Britton P (1991) Flexion-
extension views in the evaluation of cervical-spine injuries. Ann Emerg Med 20:117–21
131. Licina P, Nowitzke AM (2005) Approach and considerations regarding the patient with spi-
nal injury. Injury 36 Suppl 2:B2–12
132. Lieberman IH, Webb JK (1994) Cervical spine injuries in the elderly. J Bone Joint Surg Br
76:877–81
133. Lifeso RM, Colucci MA (2000) Anterior fusion for rotationally unstable cervical spine frac-
tures. Spine 25:2028–34
134. Lind B, Sihlbom H, Nordwall A (1988) Halo-vest treatment of unstable traumatic cervical


spine injuries. Spine 13:425–32
135. Louis R (1983) Surgery of the spine. Surgical anatomy and operative approaches. Springer,
Heidelberg
136. Lysell E (1969) Motion in the cervical spine. An experimental study on autopsy specimens.
Acta Orthop Scand: Suppl 123
137. MaimanDJ,SancesA,Jr.,MyklebustJB,LarsonSJ,HoutermanC,ChilbertM,El-GhatitAZ
(1983) Compression injuries of the cervical spine: a biomechanical analysis. Neurosurgery
13:254–60
138. Malik H, Lovell M (2004) Soft tissue neck symptoms following high-energy road traffic
accidents. Spine 29:E315–7
139. Maynard FM, Jr., Bracken MB, Creasey G, Ditunno JF, Jr., Donovan WH, Ducker TB, Gar-
ber SL, Marino RJ, Stover SL, Tator CH, Waters RL, Wilberger JE, Young W (1997) Interna-
tional Standards for Neurological and Functional Classification of Spinal Cord Injury.
American Spinal Injury Association. Spinal Cord 35:266–74
140. Mayou R, Radanov BP (1996) Whiplash neck injury. J Psychosom Res 40:461–74
141. Menezes AH (1999) Pathogenesis, dynamics, and management of os odontoideum. Neuro-
surg Focus 6:e2
142. Merriam WF, Taylor TK, Ruff SJ, McPhail MJ (1986) A reappraisal of acute traumatic cen-
tral cord syndrome. J Bone Joint Surg Br 68:708–13
143. Mills H, Horne G (1986) Whiplash – manmade disease? N Z Med J 99:373–4
144. Nacimiento W, Noth J (1999) What, if anything, is spinal shock? Arch Neurol 56:1033–5
145. Nickel VL, Perry J, Garrett A, Heppenstall M (1968) The halo. A spinal skeletal traction fix-
ation device. J Bone Joint Surg Am 50:1400–9
146. Nickel VL, Perry J, Garrett A, Heppenstall M (1989) The halo. A spinal skeletal traction fix-
ation device. In: Nickel VL, Perry J, Garrett A, Heppenstall M, 1968. Clin Orthop Relat
Res:4 –11
147. Nordgren RE, Markesbery WR, Fukuda K, Reeves AG (1971) Seven cases of cerebromedul-
lospinal disconnection: the “locked-in” syndrome. Neurology 21:1140–8
148. Nordin M, Carragee EJ, Hogg-Johnson S, Weiner SS, Hurwitz EL, Peloso PM, Guzman J,
vanderVeldeG,CarrollLJ,HolmLW,CoteP,CassidyJD,HaldemanS(2008)Assessment

of neck pain and its associated disorders: results of the Bone and Joint Decade 2000–2010
Task Force on Neck Pain and Its Associated Disorders. Spine 33:S101–22
149. Norris SH, Watt I(1983) The prognosis of neck injuries resulting from rear-end vehicle col-
lisions. J Bone Joint Surg Br 65:608–11
150. Oda T, Panjabi MM, Crisco JJ, 3rd, Oxland TR (1992) Multidirectional instabilities of
experimental burst fractures of the atlas. Spine 17:1285–90
878 Section Fractures
151. Paeslack V, Frankel H, Michaelis L (1973) Closed injuries of the cervical spine and spinal
cord: results of conservative treatment of flexion fractures and flexion rotation fracture
dislocation of the cervical spine with tetraplegia. Proc Veterans Adm Spinal Cord Inj
Conf:39–42
152. Pepin JW, Bourne RB, Hawkins RJ (1985) Odontoid fractures, with special reference to the
elderly patient. Clin Orthop Relat Res 193:178–83
153. Pfirrmann CW, Binkert CA, Zanetti M, Boos N, Hodler J (2000) Functional MR imaging of
the craniocervical junction. Correlation with alar ligaments and occipito-atlantoaxial joint
morphology: a study in 50 asymptomatic subjects. Schweiz Med Wochenschr 130:645–51
154. Pfirrmann CW, Binkert CA, Zanetti M, Boos N, Hodler J (2001) MR morphology of alar lig-
aments and occipitoatlantoaxial joints: study in 50 asymptomatic subjects. Radiology
218:133–7
155. Podolsky S, Baraff LJ, Simon RR, Hoffman JR, Larmon B, Ablon W (1983) Efficacy of cervi-
cal spine immobilization methods. J Trauma 23:461–5
156. Polin RS, Szabo T, Bogaev CA, Replogle RE, Jane JA (1996) Nonoperative management of
Types II and III odontoid fractures: the Philadelphia collar versus the halo vest. Neurosur-
gery 38:450–6; discussion 456–7
157. Qian T, Cai Z, Yang MS (2004) Determination of adenosine nucleotides in cultured cells by
ion-pairing liquid chromatography-electrospray ionization mass spectrometry. Anal Bio-
chem 325:77–84
158. Quinlan KP, Annest JL, Myers B, Ryan G, Hill H (2004) Neck strains and sprains among
motor vehicle occupants – United States, 2000. Accid Anal Prev 36:21–7
159. Radanov BP, di Stefano G, Schnidrig A, Ballinari P (1991) Role of psychosocial stress in

recovery from common whiplash [see comment]. Lancet 338:712–5
160. Radanov BP, Dvorak J (1996) Spine update. Impaired cognitive functioning after whiplash
injury of the cervical spine. Spine 21:392–7
161. Radanov BP, Sturzenegger M, Di Stefano G, Schnidrig A, Aljinovic M (1993) Factors influ-
encing recovery from headache after common whiplash. BMJ 307:652–5
162. Razack N, Green BA, Levi AD (2000) The management of traumatic cervical bilateral facet
fracture – dislocations with unicortical anterior plates. J Spinal Disord 13:374–81
163. Reid DC, Henderson R, Saboe L, Miller JD (1987) Etiology and clinical course of missed
spine fractures. J Trauma 27:980–6
164. Richards PJ (2005) Cervical spine clearance: a review. Injury 36:248–69; discussion 270
165. Richter D, Latta LL, Milne EL, Varkarakis GM, Biedermann L, Ekkernkamp A, Ostermann
PA (2001) The stabilizing effects of different orthoses in the intact and unstable upper cer-
vical spine: a cadaver study. J Trauma 50:848–54
166. Rokkanen P, Alho A, Avikainen V, Karaharju E, Kataja J, Lahdensuu M, Lepisto P, Tervo T
(1974) The efficacy of corticosteroids in severe trauma. Surg Gynecol Obstet 138:69–73
167. Ryan MD, Taylor TK (1993) Odontoid fractures in the elderly. J Spinal Disord 6:397–401
168. Sauerland S, Nagelschmidt M, Mallmann P, Neugebauer EA (2000) Risks and benefits of
preoperative high dose methylprednisolone in surgical patients: a systematic review. Drug
Saf 23:449–61
169. Schmand B, Lindeboom J, Schagen S, Heijt R, Koene T, Hamburger HL (1998) Cognitive
complaints in patients after whiplash injury: the impact of malingering. J Neurol Neuro-
surg Psychiatry 64:339–43
170. Schneider RC, Cherry G, Pantek H (1954) The syndrome of acute central cervical spinal
cord injury; with special reference to the mechanisms involved in hyperextension injuries
of cervical spine. J Neurosurg 11:546–77
171. Schneider RC, Kahn EA (1956) Chronic neurological sequelae of acute trauma to the cervi-
cal spine and spinal cord. J Bone Joint Surg Am 38A:985
172. Schneider RC, Livingston KE, Cave AJ, Hamilton G (1965) “Hangman’s fracture” of the cer-
vical spine. J Neurosurg 22:141–54
173. Schneider RC, Schemm GW (1961) Vertebral artery insufficiency in acute and chronic spi-

nal trauma, with special reference to the syndrome of acute central cervical spinal cord
injury. J Neurosurg 18:348–60
174. Schneider RC, Thompson JM, Bebin J (1958) The syndrome of acute central cervical spinal
cord injury. J Neurol Neurosurg Psychiatry 21:216–27
175. Scholten-Peeters GG, Verhagen AP, Bekkering GE, van der Windt DA, Barnsley L, Oosten-
dorp RA, Hendriks EJ (2003) Prognostic factors of whiplash-associated disorders: a sys-
tematic review of prospective cohort studies. Pain 104:303–22
176. Schuler TC, Kurz L, Thompson DE, Zemenick G, Hensinger RN, Herkowitz HN (1991) Nat-
ural history of os odontoideum. J Pediatr Orthop 11:222–5
177. Seferiadis A, Rosenfeld M, Gunnarsson R (2004) A review of treatment interventions in
whiplash-associated disorders. Eur Spine J 13:387–97
178. Sharpe KP, Rao S, Ziogas A (1995) Evaluation of the effectiveness of the Minerva cervico-
thoracic orthosis. Spine 20:1475–9
179. Sherk HH, Nicholson JT (1970) Fractures of the atlas. J Bone Joint Surg Am 52:1017–24
Cervical Spine Injuries Chapter 30 879
180. Short D (2001) Is the role of steroids in acute spinal cord injury now resolved? Curr Opin
Neurol 14:759–63
181. Skovron ML (1998) Epidemiology of whiplash. In: Gunzburg R, Szpalski M (eds) Lippin-
cott-Raven, Philadelphia, pp 61–67
182. Sonntag VK, Hadley MN (1988) Nonoperative management of cervical spine injuries. Clin
Neurosurg 34:630–49
183. Spence KF, Jr., Decker S, Sell KW (1970) Bursting atlantal fracture associated with rupture
ofthetransverseligament.JBoneJointSurgAm52:543–9
184. Spitzer WO, Skovron ML, Salmi LR, Cassidy JD, Duranceau J, Suissa S, Zeiss E (1995) Scien-
tific monograph of the Quebec Task Force on Whiplash-Associated Disorders: redefining
“whiplash” and its management. Spine 20:1S–73S
185. Sponseller PD, Cass JR (1997) Atlanto-occipital fusion for dislocation in children with neu-
rologic preservation. A case report. Spine 22:344 –7
186.StiellIG,WellsGA,VandemheenKL,ClementCM,LesiukH,DeMaioVJ,LaupacisA,
Schull M, McKnight RD, Verbeek R, Brison R, Cass D, Dreyer J, Eisenhauer MA, Greenberg

GH, MacPhail I, Morrison L, Reardon M, Worthington J (2001) The Canadian C-spine rule
for radiography in alert and stable trauma patients. JAMA 286:1841–8
187. Streitwieser DR, Knopp R, Wales LR, Williams JL, Tonnemacher K (1983) Accuracy of stan-
dard radiographic views in detecting cervical spine fractures. Ann Emerg Med 12:538–42
188. Subach BR, Morone MA, Haid RW, Jr., McLaughlin MR, Rodts GR, Comey CH (1999) Man-
agement of acute odontoid fractures with single-screw anterior fixation. Neurosurgery
45:812–9; discussion 819–20
189. Suechting RL, French LA (1955) Posterior inferior cerebellar artery syndrome; following a
fracture of the cervical vertebra. J Neurosurg 12:187–9
190. Svennevig JL, Bugge-Asperheim B, Vaage J, Geiran O, Birkeland S (1984) Corticosteroids in
the treatment of blunt injury of the chest. Injury 16:80–4
191. Taylor AE, Cox CA, Mailis A (1996) Persistent neuropsychological deficits following whip-
lash: evidence for chronic mild traumatic brain injury? Arch Phys Med Rehabil 77:529–35
192. Toh E, Nomura T, Watanabe M, Mochida J (2006) Surgical treatment for injuries ofthemid-
dle and lower cervical spine. Int Orthop 30:54–8
193. Transfeldt EE, White D, Bradford DS, Roche B (1990) Delayed anterior decompression in
patients with spinal cord and cauda equina injuries of the thoracolumbar spine. Spine
15:953–7
194. Travlos A, Hirsch G (1993) Steroid psychosis: a cause of confusion on the acute spinal cord
injury unit. Arch Phys Med Rehabil 74:312–5
195. Traynelis VC (1997) Evidence-based management of type II odontoid fractures. Clin Neu-
rosurg 44:41–9
196. Traynelis VC, Marano GD, Dunker RO, Kaufman HH (1986) Traumatic atlanto-occipital
dislocation. Case report. J Neurosurg 65:863–70
197. Vaccaro AR, Daugherty RJ, Sheehan TP, Dante SJ, Cotler JM, Balderston RA, Herbison GJ,
Northrup BE (1997) Neurologic outcome of early versus late surgery for cervical spinal
cord injury. Spine 22:2609–13
198. Verhagen AP, Peeters GG, de Bie RA, Oostendorp RA (2001) Conservative treatment for
whiplash. Cochrane Database Syst Rev:CD003338
199. Verhagen AP, Scholten-Peeters GG, van Wijngaarden S, de Bie RA, Bierma-Zeinstra SM

(2007) Conservative treatments for whiplash. Cochrane Database Syst Rev:CD003338
200. Versteegen GJ, Kingma J, Meijler WJ, ten Duis HJ (1998) Neck sprain in patients injured in
car accidents: a retrospective study covering the period 1970–1994. Eur Spine J 7:195–200
201. Versteegen GJ, Kingma J, Meijler WJ, ten Duis HJ (1998) Neck sprain not arising from car
accidents: a retrospective study covering 25 years. Eur Spine J 7:201–5
202. Werne S (1957) Studies in spontaneous atlas dislocation. Acta Orthop Scand Suppl
23:1–150
203. White AA, 3rd, Panjabi MM (1978) The basic kinematics of the human spine. A review of
past and current knowledge. Spine 3:12–20
204. White AA, 3rd, Panjabi MM (1990) Kinematics of the spine. In: White AA, 3rd, Panjabi MM
(eds) Clinical biomechanics of the spine. JB Lippincott, Philadelphia, pp 85–125
205. White AA, 3rd, Panjabi MM (1990) Practical biomechanics of spine trauma. In: White AA,
3rd, Panjabi MM (eds) Clinical biomechanics of the spine. JB Lippincott, Philadelphia, pp
169–275
206. White AA, 3rd, Panjabi MM (1990) The problem of clinical instability in the human spine:
a systematic approach. In: White AA, 3rd, Panjabi MM (eds) Clinical biomechanics of the
spine. JB Lippincott, Philadelphia, pp 277–378
207. Williamson E, Williams M, Gates S, Lamb SE (2008) A systematic literature review of psy-
chological factors and the development of late whiplash syndrome. Pain 135:20–30
208. Willis BK, Greiner F, Orrison WW, Benzel EC (1994) The incidence of vertebral artery
injury after midcervical spine fracture or subluxation. Neurosurgery 34:435–41; discus-
sion 441–2
880 Section Fractures
209. Woltmann A, Buhren V (2004) [Shock trauma room management of spinal injuries in the
framework of multiple trauma. A systematic review of the literature]. Unfallchirurg
107:911–8
210. Wood-Jones F (1913) The ideal lesion produced by judicial hanging. Lancet 1
211. Yablon IG, Palumbo M, Spatz E, Mortara R, Reed J, Ordia J (1991) Nerve root recovery in
complete injuries of the cervical spine. Spine 16:S518–21
212. Young WF, Rosenwasser RH, Getch C, Jallo J (1994) Diagnosis and management of occipi-

tal condyle fractures. Neurosurgery 34:257–60; discussion 260–1
Cervical Spine Injuries Chapter 30 881
31
Thoracolumbar Spinal Injuries
Michael Heinzelmann, Guido A. Wanner
Core Messages

Spinal fractures are frequently located at the
thoracolumbar junction for biomechanical rea-
sons

The AO classification has gained widespread
acceptance in Europe for the grading of thora-
columbar fractures: Type A: vertebral compres-
sion fractures; Type B: anterior and posterior
column injuries with distraction; Type C: ante-
rior and posterior element injury with rotation

The initial focus of the physical examination of
a patient with a spinal injury is on the vital and
neurological functions, because effective resus-
citation is critical to the management of poly-
traumatized patients and patients with spinal
cord injury

The imaging modalities of choice are standard
radiographs and CT scans. A CT scan should
routinely be made to visualize bony injury. MRI
is helpful to diagnose discoligamentous injuries
and to identify a possible cord lesion


Primary goals of treatment are prevention and
limitation of neurological injury as well as res-
toration of spinal stability, regardless of
whether operative or non-operative therapy is
chosen

Secondary goals consist of correction of defor-
mities, minimizing the loss of motion, and facili-
tating rapid rehabilitation

Early stabilization and fusion is generally
accepted for patients with unstable fractures
and neurological deficits

The optimal treatment for patients with less
instability, moderate deformity and absence of
neurological compromise is not based on
scientific evidence and remains a matter of
debate.

Good clinical outcome can be achieved with
non-operative as well as operative treatment
Epidemiology
Fractures most frequently
affect the thoracolumbar
junction
Systematic epidemiologic data on traumatic thoracolumbar fractures are rare and
differ depending on the area studied and on the treating center. The studies avail-
able from western countries reveal typical and comparable data on incidence, local-

ization, and mechanisms of injury. Thoracolumbar fractures are more frequent in
men (2/3) than in women (1/3) and peak between the ages of 20 and 40 years [30, 47,
65, 81, 94]. Approximately, 160000 patients/year sustain an injury of the spinal col-
umn in the United States. The majority of these injuries comprise cervical and lum-
bar (L3–L5) spine fractures. However, between 15% and 20% of traumatic fractures
occur at the thoracolumbar junction (T11–L2), whereas 9–16% occur in the tho-
racic spine (T1–T10) [36, 46]. Hu and coworkers [56] studied the total population of
a Canadian province over a period of 3 years. The incidence of spine injuries was 64/
100000 inhabitants per year, predominantly younger men and older women. A total
of 2063 patients were registered and 944 patients were treated in hospital: 182
patients (20%) with a cervical spine injury, 286 patients (30%) with a thoracic spine
injury and 403 patients (50%) with an injury of the lumbosacral spine. Traumatic
cross-section spinal cord injury occurred in 40 out of 1 million inhabitants. About
Fractures Section 883
a bc d
ef gh
ijkl
Case Introduction
This 23-year-old female sustained a motor vehicle accident as an unrestrained passenger. Clinically, she presented with
an incomplete paraplegia (ASIA C) and an incomplete conus-cauda syndrome. The initial CT (
a–d) scan demonstrates an
unstable complete burst fracture of L1 (Type A3.3). The 3D reconstruction (
a, b)givesagoodoverviewofthedegreeof
comminution and the deformity; the posterior fragment is best visualized in the lateral 2D reconstruction (
c)andthe
axial view (
d). In an emergency procedure, the myelon was decompressed by laminectomy and the fracture was reduced
andstabilizedwithaninternalfixator(
e–h). Interestingly, the prone position alone (e) reduced the fracture to a certain
degree when compared to the CT scan taken with the patient in a supine position. With the internal fixator (RecoFix), the

anatomical height and physiological alignment was restored (
f) and the posterior fragment was partially reduced (g, h).
This indirect reduction of bony fragments, called ligamentotaxis, is possible if the posterior ligaments and the attach-
ment to the anulus fibrosus are intact. We performed a complete clearance of the spinal canal by an anterior approach
5dayslater(
i–l). In this minimally invasive technique, the spine is approached by a small thoracotomy from the left, the
ruptured disc and bony fragments are removed, and an expandable cage is inserted. One of the first steps in this tech-
nique is the positioning of a K-wire in the upper disc space of the fractured vertebra (
i). In this figure, the four retractors
of the Synframe and the endoscopic light source are seen. The final result after 9 months (
j–l) demonstrates the cage
(Synex), the physiological alignment without signs of implant failure or kyphosis, a good clearance of the spinal canal
from anterior and the laminectomy from posterior (
k), and a bony healing of the local bone transplant of the lateral side
of the cage (
l). Fortunately, the patient completely recovered from her neurological deficit (ASIA E).
50–60% of thoracolumbar fractures affect the transition T11–L2, 25–40% the
thoracic spine and 10–14% the lower lumbar spine and sacrum [80, 86].
In a study by Magerl and Engelhardt [81] on 1446 thoracolumbar fractures,
most injuries concerned the first lumbar vertebra, i.e., 28% (n=402), followed by
T12 (17%, n=246) and L2(14%,n=208). The epidemiologic multicenter study
on fractures of the thoracolumbar transition (T10–L2) by the German Trauma
Society studied 682 patients and revealed 50% (n =336) L1 fractures, 25%
884 Section Fractures
(n=170) T12 fractures, and 21% (n=141) L2 fractures [65].Our own series at the
University Hospital in Zürich demonstrated a very similar distribution for oper-
ated spine fractures (1992–2004, n=1744): 20% cervical spine (n =350),8%tho-
racic spine T1–T10 (n=142), 62% thoracolumbar spine T11–L2 (n=1075), and
10% lumbosacral spine L3-sacrum (n=176). The susceptibility of the thoraco-
lumbar transition is attributed mainly to the following anatomical reasons:

The transition from a relatively rigid thoracic kyphosis to a more mobile
lumbar lordosis occurs at T11–12.
Thelowestthoracicribs(T11andT12)providelessstabilityatthethoraco-
lumbar junction region compared to the rostral thoracic region, because
they do not connect to the sternum and are free floating.
The facet joints of the thoracic region are oriented in the coronal (frontal)
plane, limiting flexion and extension while providing substantial resistance
to anteroposterior translation [36]. In the lumbosacral region, the facet
joints are oriented in a more sagittal alignment, which increases the degree
of potential flexion and extension at the expense of limiting lateral bending
and rotation.
Spinal cord injury occurs in
about 10– 30 % of traumatic
fractures
Spinal cord inj ury occurs in about 10–30% of traumatic spinal fractures [37, 56].
In thoracolumbar spine fractures (T1–L5), Magerl et al. [81] and Gertzbein [47]
reported 22% and 35.8% neurological deficiencies, respectively. The epidemio-
logic multicenter study on fractures of the thoracolumbar transition (T10–L2) by
the German Society of Traumatology [65] revealed neurological deficiencies in
22–51%, depending on the fracture type (22% in Type A fractures, 28% in Type
B fractures, and 51% in Type C fractures, according to the AO classification).
Complete paraplegia was found in 5% of the patients with fractures of the thora-
columbar transition.
Pathomechanisms
At the time of injury, several forces may act together to produce structural dam-
age to the spine. However, most frequently, one or two major forces, defining the
major injury vector, account for most of the bony and ligamentous damage. The
most relevant forces are:
axial compression
flexion/distraction

hyperextension
rotation
shear
Axial Compression
Axial load may result
in a burst fracture
While axial loading of the body results in anterior flexion forces in the kyphotic tho-
racic spine, mainly compressive forces occur in the straight thoracolumbar region
[64]. Axial loading of a vertebra produces endplate failure followed by vertebral
body compression [98]. Depending on the energy, the axial load may result in
incomplete or complete bu rst fractures, i.e., vertical fractures with centripetal dis-
placement of the fragments [12, 33]. The posterior elements are usually intact; how-
ever, with severe compression, significant disruption of these elements may occur.
The combination of an axially directed central compressive force with an eccentric
compressive force anterior to the axis of rotation (center of nucleus pulposus) typi-
cally leads to wedge compression fractures. Herein, the vertebral body fails in
(wedge) compression, while the posterior ligamentous and osseous elements may
Thoracolumbar Spinal Injuries Chapter 31 885
remain intact or fail in tension, depending on the energy level of the injury. In the
latter case, the injury is classified as flexion-distraction injury. Violent trauma is the
most common cause of compression fractures in young and middle-aged adults.
The most frequent causes are motor vehicle accidents and falls from a height, fol-
lowed by sports and recreational activity injuries. In the elderly population, osteo-
porotic compression fractures following low-energy trauma are most common.
Flexion/Distraction
Flexion forces cause eccentric compression of the vertebral bodies and discs and
cause tension to the posterior elements. If the anterior wedging exceeds 40–50%,
rupture of the posterior ligaments and facet joint capsules must be assumed
[117]. In flexion/distraction injuries, the axis of flexion is moved anteriorly
(towards the anterior abdominal wall), and the entire vertebral column is sub-

jected to large tensile forces. These forces can produce:
pure osseous lesion
mixed osteoligamentous lesion
pure soft tissue (ligamentous or disc) lesion
In flexion/distraction
injuries, the posterior
ligamentous and osseous
elements fail in tension
Distraction leads to a horizontal disrupture of the anterior and/or posterior ele-
ments. A distraction fracture that extends through the bone was first described
by Chance [22]. This lesion involves a horizontal fracture, which begins in the
spinous process, progresses through the lamina, transverse processes, and pedi-
cles, and extends into the vertebral body. Depending on the axis of flexion the
vertebralbodyanddiscmayruptureormaybecompressedanteriorlyas
described above. Although any accident providing significant forward flexion
combined with distraction can produce this type of injury, the typical cause is a
motor vehicle accident with the victim wearing a lap seat belt. These injuries are
associated with a high rate of hollow visceral organ lesions, typically of the small
bowel, colon or stomach, but also pancreatic injuries have been reported [3, 13].
Hyperextension
Hyperextension may result
in anterior discoligamentous
disruption and posterior
compression fractures
of facets, laminae,
or spinous processes
Extension forces occur when the upper part of the trunk is thrust posteriorly. This
produces an injury pattern that is the reverse of that seen with flexion. Tension is
applied anteriorly to the strong anterior longitudinal ligaments and anterior por-
tion of the anulus fibrosus, whereas compression forces are transmitted to the

posterior elements. This mechanism results in a rupture from anterior to poste-
rior and may result in facet, lamina, and spinous process fractures [43]. Denis and
Burks reported on a hyperextension injury pattern that they termed lumberjack
fracture-dislocation [32]. The mechanism of this injury is a falling mass, often
timber, striking the midportion of the patient’s back. The injury involves com-
plete disruption of the anterior ligaments and is an extremely unstable injury pat-
tern. These injuries are the result of a reversed trauma mechanism. The interver-
tebral disc ruptures from anterior to posterior. The lesion may proceed into the
posterior column and is then unstable against extension and shearing forces.
Rotational Injuries
Rotational injuries combine
compressive forces and flex-
ion/distraction mechanisms
and are highly unstable
Both compressive forces and flexion-distraction mechanisms may be combined
with rotational forces and lead to rotational fracture dislocations. As rotational
forces increase, ligaments and facet capsules fail and lead to subsequent disrup-
tion of both the anterior and posterior elements. A highly unstable injury pattern
will develop, i.e., the posterior ligaments and joint capsule will rupture and the
886 Section Fractures
anterior disc and vertebral body will disrupt obliquely or will be compressed.
Rotational forces may further be combined with shearing forces and lead to most
unstable fractures (slice fractures, Holdsworth) [54]. These patients have often
been thrown against an obstacle or hit by a heavy device. Thus, the patients often
have widespread dermabrasions and contusions on the back.
Shear
Shear forces produce severe
ligamentous disruption and
are often associated with
spinal cord injury

Shear forces produce severe ligamentous disruption and may result in anterior, pos-
terior or lateral vertebral displacement [98]. The most frequent type is traumatic
anterior spondylolisthesis that usually results in a complete spinal cord injury.
Classification
Vertebral spine injuries are very heterogeneous in nature. Most important for the
understanding and treatment of these injuries is the evaluation of spinal stability
or instability, respectively. However, the conclusive evaluation of this question is
difficult because the term “instability” is not yet clearly defined in the context of
spinal disorders.
Several classifications of spinal injuries have been introduced based primarily
on fracture morphology and different stability concepts. White and Panjabi [118]
defined clinical instability of the spine as shown in
Table 1:
Table 1. Definition of spinal instability
Loss of the ability of the spine under physiologic loads to maintain relationships
between vertebrae in such a way that there is neither damage nor subsequent irrita-
tion to the spinal cord or nerve root and, in addition, there is no development of
incapacitating deformity or pain from structural changes
Physiologic loads are defined as loads during normal activity, incapacitating
deformity as gross deformity unacceptable to the patient, and incapacitating
pain as discomfort uncontrolled by non-narcotic analgesics.
Presently, there is no generally used classification for thoracolumbar injuries.
However, the most important classification of spinal injuries aims to differenti-
ate between:
stable fractures
unstable fractures
This concept was first introduced by Nicoll in 1949 [89] and is still the most
widely accepted differentiation. However, this classification is insufficient to give
detailed treatment recommendations.
Holdsworth [54] was the first to stress the mechanism of injury to classify spi-

nal injuries and described five different injury types. Kelly and Whitesides [61,
119] reorganized the mechanistic classification and defined the two column con-
cept, which became the basis of the AO classification (see below). Louis further
modified this structural classification scheme and suggested the posterior facet
joint complex of each side to become a separate column [79]. The ventral column
consists of the vertebral body; the two dorsal columns involve the facet articula-
tions of both sides. Roy-Camille was concerned about the relationship of the
injury to vertebra, especially the neural ring, and the spinal cord. He described
the “segment moyen,” referring to the neural ring, and related injury of the seg-
ment moyen to instability [99]. This aspect led to the term of the so-called “mid-
dle column,” which is not a distinct anatomic column.
Thoracolumbar Spinal Injuries Chapter 31 887
Denis Classification
The middle column became a central part of the classification of spinal injuries
according to Denis [30], which is in widespread use in the United States. Accord-
ingly, the vertebral column is divided into three columns [30]:
anterior column
middle column
posterior column
The anterior column consists of the ventral longitudinal ligament (VLL), the
anterior anulus fibrosus, and the anterior halfof the vertebral bodies. Themiddle
column consists of the posterior longitudinal ligament (PLL), the dorsal anulus
fibrosus, and the dorsal half of the vertebral bodies. Finally, the posterior column
consists of the bony neural arch, posterior spinous ligaments and ligamentum
flavum,aswellasthefacetjoints.
Denis considered the middle column to be the key structure. A relevant injury
to the middle column was therefore the essential criterion for instability. Accord-
ing to the Denis classification, rupture of the posterior ligamentous complex only
creates instability if there is concomitant disruption of at least the PLL and dorsal
anulus. However, the middle column is not clearly defined either anatomically or

biomechanically, i.e., the middle column bony part resists compression forces,
The Denis classification
does not allow for a detailed
fracture classification
and the ligamentous part resists distraction forces. Although the three column
concept by Denis raised several concerns, his classification is still frequently
used, because it is simple and includes all the injury patterns most commonly
seen. Denis distinguished minor and major injuries: minor injuries included
fracturesofthearticular,transverse,andspinousprocessesaswellasthepars
interarticularis. Major spinal injuries were divided into compression fractures,
burst fractures, flexion-distraction (seat-belt) injuries, and fracture dislocations.
AO Classification
The AO/ASIF (Arbeitsgemeinschaft für Osteosynthesefragen/Association for the
Study of Internal Fixation) classification introduced by Magerl et al. in 1994 [80]
is increasingly being accepted as the gold standard for documentation and treat-
ment of injuries of the vertebral spine.
The AO classification is based on the “two column theory”describedby
Holdsworth [54, 55] and Kelly and Whitesides [61, 119]. The AO classification
considers the spine to comprise two functionally separate supportive columns.
The anterior column consists of the vertebral body and the intervertebral discs
and is loaded in compression. The posterior column consists of the pedicles, the
laminae, the facet joints, and the posterior ligamentous complex, and is loaded in
tension. According to the common AO classification system, injuries are catego-
rized with increasing severity into types (
Fig. 1):
Type A: compression injuries
Type B: distraction injuries
Type C: rotational injuries
Type A injuries are the result of compression by axial loading (e.g., compression
and burst fractures). Type B injuries are flexion-distraction or hyperextension

injuries and involve the anterior and posterior column. Disruption may occur in
the posterior or anterior structures. Type C fractures are the result of a compres-
sion or flexion/distraction force in combination with a rotational force in the
horizontal plane (e.g., fracture dislocations with a rotatory component). Each
type is classified into three major groups (1–3) of increasing severity (
Fig. 2)and
can further be divided into subgroups and specifications (
Table 2).
888 Section Fractures

×