XIII Contents - bücher.de · Acute Low Back Pain Without Radicular Symptoms,WithoutTrauma ........

Contents

1 History of Spinal DisordersPhilipp Gruber, Thomas Boeni

Core Messages . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1A Brief Etymology . . . . . . . . . . . . . . . . . . . . . . . . . 1Historical Case Introduction . . . . . . . . . . . . . . . . . 2Spinal Anatomy and Physiology . . . . . . . . . . . . . . 4Anesthesia and Supportive Techniques . . . . . . . . 6

Laughing Gas, Chloroform and Cocaine . . . . . 6Antisepsis and Antibiotics . . . . . . . . . . . . . . . . . 6Diagnostic Imaging . . . . . . . . . . . . . . . . . . . . . . 8

Scoliosis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 8Pathogenesis . . . . . . . . . . . . . . . . . . . . . . . . . . . . 9Assessment . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 9Non-operative Treatment . . . . . . . . . . . . . . . . . . 11Scoliosis Surgery . . . . . . . . . . . . . . . . . . . . . . . . . 13

Juvenile Kyphosis . . . . . . . . . . . . . . . . . . . . . . . . . . 13Spondylolisthesis . . . . . . . . . . . . . . . . . . . . . . . . . . 14

An Obstetrical Problem . . . . . . . . . . . . . . . . . . . 14Surgery . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 14

Back Pain and Sciatica . . . . . . . . . . . . . . . . . . . . . . 15A Wrong Mixture of Fluids . . . . . . . . . . . . . . . . 15Disc Herniation . . . . . . . . . . . . . . . . . . . . . . . . . . 17Historical Case Study . . . . . . . . . . . . . . . . . . . . . 19The Facet Syndrome . . . . . . . . . . . . . . . . . . . . . . 21Spinal Stenosis . . . . . . . . . . . . . . . . . . . . . . . . . . 21

Spinal Infections . . . . . . . . . . . . . . . . . . . . . . . . . . . 22Egyptian Mummies and Sir Percival Pott . . . . 22Treatment . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 24

Ankylosing Spondylitis . . . . . . . . . . . . . . . . . . . . . 24Discovery of a New Disease . . . . . . . . . . . . . . . . 25

Spinal Injuries . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 27First Reports . . . . . . . . . . . . . . . . . . . . . . . . . . . . 27Spinal Injuries as a Socioeconomic Problem . . 28Traction Table and Laminectomy . . . . . . . . . . . 29The Advent of Internal Spinal Fixation . . . . . . 29

Recapitulation . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 30Appendix: History of spinal disorders . . . . . . . . . 31Key Articles . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 33References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 34

Basic Science

2 Biomechanics of the SpineStephen Ferguson

Core Messages . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 41The Human Spine . . . . . . . . . . . . . . . . . . . . . . . . . . 41The Motion Segment . . . . . . . . . . . . . . . . . . . . . . . 42

Anterior Structures . . . . . . . . . . . . . . . . . . . . . . . 42Posterior Elements . . . . . . . . . . . . . . . . . . . . . . . 46Ligaments of the Spine . . . . . . . . . . . . . . . . . . . . 47Motion Segment Stiffness . . . . . . . . . . . . . . . . . 48

Muscles . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 48Spinal Stability Through Muscular Activity . . 52Muscle Activity During Flexion and Extension 54Muscle Activity During Lateral Flexion andRotation . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 54

Spine Kinematics . . . . . . . . . . . . . . . . . . . . . . . . . . . 54Range of Motion . . . . . . . . . . . . . . . . . . . . . . . . . 55Mechanical Response of the Spinal MotionSegment . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 55Clinical Instability . . . . . . . . . . . . . . . . . . . . . . . 57

Kinetics (Spinal Loading) . . . . . . . . . . . . . . . . . . . 58Static Loading . . . . . . . . . . . . . . . . . . . . . . . . . . . 58Loads During Lifting . . . . . . . . . . . . . . . . . . . . . 59Dynamic Loading . . . . . . . . . . . . . . . . . . . . . . . . 60

Recapitulation . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 61Key Articles . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 62References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 63

3 Spinal InstrumentationDaniel Haschtmann, Stephen J. Ferguson

Core Messages . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 67Goals of Spinal Instrumentation . . . . . . . . . . . . . . 67Basic Biomechanics of Spinal Instrumentation . . 69

Loading and Load Sharing Characteristics . . . 69Posterior Stabilization Principles . . . . . . . . . . . 71Anterior Stabilization Principles . . . . . . . . . . . . 74Anterior Tension Band Technique . . . . . . . . . . 78

Biomechanics of the “Adjacent Segment” . . . . . . 79Non-Fusion Principles . . . . . . . . . . . . . . . . . . . . . . 80

Disc Arthroplasty . . . . . . . . . . . . . . . . . . . . . . . . 80Nucleoplasty . . . . . . . . . . . . . . . . . . . . . . . . . . . . 82Posterior Dynamic Stabilization Technique . . 82

XIII

Interspinous Process Distraction Technique 83Recapitulation . . . . . . . . . . . . . . . . . . . . . . . . . . . . 84Key Articles . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 85References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 86

4 Age-Related Changes of the SpineAtul Sukthankar, Andreas G. Nerlich,

Günther Paesold

Core Messages . . . . . . . . . . . . . . . . . . . . . . . . . . . . 91Epidemiology . . . . . . . . . . . . . . . . . . . . . . . . . . . . 91Case Introduction . . . . . . . . . . . . . . . . . . . . . . . . . 92General Age-Related Changes . . . . . . . . . . . . . . . 92Functional Spine Unit . . . . . . . . . . . . . . . . . . . . . . 93The Intervertebral Disc and Cartilage Endplate 95

Intervertebral Disc . . . . . . . . . . . . . . . . . . . . . . 95The Cartilage Endplate . . . . . . . . . . . . . . . . . . . 107

The Facet Joints . . . . . . . . . . . . . . . . . . . . . . . . . . . 109Normal Anatomy . . . . . . . . . . . . . . . . . . . . . . . 109Age-Related Changes . . . . . . . . . . . . . . . . . . . . 109

Vertebral Bodies . . . . . . . . . . . . . . . . . . . . . . . . . . 110Normal Anatomy and Composition . . . . . . . . 110Age-Related Changes . . . . . . . . . . . . . . . . . . . . 110

Spinal Ligaments . . . . . . . . . . . . . . . . . . . . . . . . . . 111Normal Anatomy and Composition . . . . . . . . 111Age-Related Changes . . . . . . . . . . . . . . . . . . . . 111

Spinal Muscles . . . . . . . . . . . . . . . . . . . . . . . . . . . . 112Normal Anatomy and Structure . . . . . . . . . . . 112Age-Related Changes . . . . . . . . . . . . . . . . . . . . 112

Recapitulation . . . . . . . . . . . . . . . . . . . . . . . . . . . . 114Key Articles . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 115References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 116

5 Pathways of Spinal PainHeike E. Künzel, Norbert Boos

Core Messages . . . . . . . . . . . . . . . . . . . . . . . . . . . . 123Historical Background . . . . . . . . . . . . . . . . . . . . . 123

Precartesian Theories . . . . . . . . . . . . . . . . . . . . 123Cartesian Theory . . . . . . . . . . . . . . . . . . . . . . . 124Gate Control Theory . . . . . . . . . . . . . . . . . . . . . 124Modern Pain Theories . . . . . . . . . . . . . . . . . . . 124

Epidemiology of Chronic Pain . . . . . . . . . . . . . . 125Definition and Classification . . . . . . . . . . . . . . . . 125

Temporal Course . . . . . . . . . . . . . . . . . . . . . . . . 126Contemporary Pain Classification . . . . . . . . . 126

Pathways of Pain . . . . . . . . . . . . . . . . . . . . . . . . . . 128Transduction . . . . . . . . . . . . . . . . . . . . . . . . . . . 129Conduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . 130Transmission and Modulation . . . . . . . . . . . . 130Pain Projection . . . . . . . . . . . . . . . . . . . . . . . . . 133Pain Perception . . . . . . . . . . . . . . . . . . . . . . . . . 134

Neuroplasticity . . . . . . . . . . . . . . . . . . . . . . . . . . . 135Peripheral Sensitization . . . . . . . . . . . . . . . . . . 135Transcriptional DRG Changes . . . . . . . . . . . . . 136Central Sensitization . . . . . . . . . . . . . . . . . . . . 136

Disinhibition . . . . . . . . . . . . . . . . . . . . . . . . . . . 137Endogenous and Environmental Influenceson Pain Perception . . . . . . . . . . . . . . . . . . . . . . . . 137Clinical Assessment of Pain . . . . . . . . . . . . . . . . . 138

Differentiating Inflammatory and NeuropathicPain . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 138

General Concepts of Pain Treatment . . . . . . . . . 141Pharmacological Treatment . . . . . . . . . . . . . . . 141Non-pharmacological Treatment of SpinalPain . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 143Biopsychosocial Interventions . . . . . . . . . . . . 143Surgical Treatment . . . . . . . . . . . . . . . . . . . . . . 144


6 Epidemiology and Risk Factors of SpinalDisorders

Achim Elfering, Anne F. Mannion

Core Messages . . . . . . . . . . . . . . . . . . . . . . . . . . . . 153General Scope . . . . . . . . . . . . . . . . . . . . . . . . . . . . 153

Objectives in Spinal Disorders . . . . . . . . . . . . 154Classification of Spinal Disorders . . . . . . . . . . . . 155

Etiology . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 155Time Course . . . . . . . . . . . . . . . . . . . . . . . . . . . 155Low Back Pain . . . . . . . . . . . . . . . . . . . . . . . . . . 156Neck Pain . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 157Pain, Impairment and Disability . . . . . . . . . . . 157

Burden of Spinal Disorders . . . . . . . . . . . . . . . . . 159Economic Costs . . . . . . . . . . . . . . . . . . . . . . . . . 159

Risk Factors . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 161Individual Risk Factors . . . . . . . . . . . . . . . . . . 161Morphological Risk Factors . . . . . . . . . . . . . . . 162Psychosocial Factors . . . . . . . . . . . . . . . . . . . . . 162Occupational Physical Risk Factors . . . . . . . . 163Occupational Psychological Risk Factors . . . . 163Absence of Evidence for Certain Risk Factors 164

Geographical Variation . . . . . . . . . . . . . . . . . . . . 164Flag System for the Risk Factors . . . . . . . . . . . . . 165

Red Flags . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 165Yellow Flags . . . . . . . . . . . . . . . . . . . . . . . . . . . . 166Blue Flags . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 166Black Flags . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 166

Direction for Future Epidemiological Research 167Recapitulation . . . . . . . . . . . . . . . . . . . . . . . . . . . . 167Key Articles . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 168References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 169

7 Predictors of Surgical OutcomeAnne F. Mannion, Achim Elfering

Core Messages . . . . . . . . . . . . . . . . . . . . . . . . . . . . 175Epidemiology . . . . . . . . . . . . . . . . . . . . . . . . . . . . 175Outcome Measures . . . . . . . . . . . . . . . . . . . . . . . . 179

What Constitutes a “Successful Outcome” . . . 180

XIV Contents

The Outcome of Common Spine SurgicalProcedures . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 182Predictors of Outcome of Spinal Surgery . . . . . . 183

Medical Factors . . . . . . . . . . . . . . . . . . . . . . . . . 184Biological and Demographic Variables . . . . . 186Health Behavioral and Lifestyle Factors . . . . . 187Psychological Factors . . . . . . . . . . . . . . . . . . . . 187Sociological Factors . . . . . . . . . . . . . . . . . . . . . 189Work-Related Factors . . . . . . . . . . . . . . . . . . . . 189

Risk Factor Assessment in Clinical Practice . . . 190Recapitulation . . . . . . . . . . . . . . . . . . . . . . . . . . . . 192Key Articles . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 193References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 194

Patient Assessment

8 History and Physical ExaminationClement M.L. Werner, Norbert Boos

Core Messages . . . . . . . . . . . . . . . . . . . . . . . . . . . . 201Epidemiology . . . . . . . . . . . . . . . . . . . . . . . . . . . . 201Case Introduction . . . . . . . . . . . . . . . . . . . . . . . . . 202History . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 203

Pain . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 204Function . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 210Spinal Deformity . . . . . . . . . . . . . . . . . . . . . . . . 210

Physical Examination . . . . . . . . . . . . . . . . . . . . . . 211Walking . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 211Standing . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 211Sitting . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 216Lying Supine . . . . . . . . . . . . . . . . . . . . . . . . . . . 220Lying on Left/Right Side . . . . . . . . . . . . . . . . . 220Lying Prone . . . . . . . . . . . . . . . . . . . . . . . . . . . . 221Abnormal Illness Behavior . . . . . . . . . . . . . . . 221Reproducibility . . . . . . . . . . . . . . . . . . . . . . . . . 221

Differential Diagnosis of Spinal Pain Syndromes 222Recapitulation . . . . . . . . . . . . . . . . . . . . . . . . . . . . 222Key Articles . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 223References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 224

9 Imaging StudiesMarius R. Schmid, Jürg Hodler

Core Messages . . . . . . . . . . . . . . . . . . . . . . . . . . . . 227Imaging Methods . . . . . . . . . . . . . . . . . . . . . . . . . 227

Standard Radiographs . . . . . . . . . . . . . . . . . . . 227Magnetic Resonance Imaging . . . . . . . . . . . . . 229Computed Tomography . . . . . . . . . . . . . . . . . . 241Additional Imaging Methods . . . . . . . . . . . . . 244

Indications for Spinal Imaging . . . . . . . . . . . . . . 247Acute Low Back Pain Without RadicularSymptoms, Without Trauma . . . . . . . . . . . . . . 247Acute Low Back Pain With RadicularSymptoms . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 248

Spinal Cord and Cauda CompressionSyndromes . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 249

Acute Trauma . . . . . . . . . . . . . . . . . . . . . . . . . . 249Chronic Low Back Pain . . . . . . . . . . . . . . . . . . 251Postoperative Imaging . . . . . . . . . . . . . . . . . . . 251Whiplash-Associated Disorders . . . . . . . . . . . 252Pain Relating to the Sacroiliac Joint . . . . . . . . 253Disease of the Spinal Cord . . . . . . . . . . . . . . . . 255


10 Spinal InjectionsMassimo Leonardi, Christian W. Pfirrmann

Core Messages . . . . . . . . . . . . . . . . . . . . . . . . . . . . 261Rationale for Spinal Injections . . . . . . . . . . . . . . 261Lumbar and Cervical Nerve Root Blocks . . . . . . 262

Indications . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 262Technique . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 263Complications . . . . . . . . . . . . . . . . . . . . . . . . . . 265Diagnostic and Therapeutic Efficacy . . . . . . . 265

Epidural and Caudal Blocks . . . . . . . . . . . . . . . . . 267Indications . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 267Technique . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 268Complications . . . . . . . . . . . . . . . . . . . . . . . . . . 268Therapeutic Efficacy . . . . . . . . . . . . . . . . . . . . . 268

Provocative Discography . . . . . . . . . . . . . . . . . . . 271Indications . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 271Technique . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 272Complications . . . . . . . . . . . . . . . . . . . . . . . . . . 273Diagnostic Efficacy . . . . . . . . . . . . . . . . . . . . . . 273

Facet Joint Blocks . . . . . . . . . . . . . . . . . . . . . . . . . 275Indications . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 275Technique . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 276Complications . . . . . . . . . . . . . . . . . . . . . . . . . . 277Diagnostic and Therapeutic Efficacy . . . . . . . 278

Sacroiliac Joint Blocks . . . . . . . . . . . . . . . . . . . . . 280Indications . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 280Technique . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 280Complications . . . . . . . . . . . . . . . . . . . . . . . . . . 280Diagnostic Efficacy . . . . . . . . . . . . . . . . . . . . . . 281

Contraindications for Spinal Injections . . . . . . . 281Algorithm for Spinal Injections . . . . . . . . . . . . . . 282Recapitulation . . . . . . . . . . . . . . . . . . . . . . . . . . . . 283Key Articles . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 284References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 285

11 Neurological Assessment in Spinal DisordersUta Kliesch, Armin Curt

Core Messages . . . . . . . . . . . . . . . . . . . . . . . . . . . . 291Epidemiology . . . . . . . . . . . . . . . . . . . . . . . . . . . . 291Case Introduction . . . . . . . . . . . . . . . . . . . . . . . . . 292Anatomy and Somatotopic Background . . . . . . . 294Classification . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 295Neurological Assessment . . . . . . . . . . . . . . . . . . . 298

Pain . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 298

Contents XV

Sensory Deficits . . . . . . . . . . . . . . . . . . . . . . . . 298Motor Deficits . . . . . . . . . . . . . . . . . . . . . . . . . . 299Reflex Deficits . . . . . . . . . . . . . . . . . . . . . . . . . . 299Gait Disorders . . . . . . . . . . . . . . . . . . . . . . . . . . 301Bowel and Bladder Dysfunction . . . . . . . . . . . 303Disorders of the Autonomic System . . . . . . . . 303Spinal Cord Injury . . . . . . . . . . . . . . . . . . . . . . 304Spinal Cord Syndrome . . . . . . . . . . . . . . . . . . . 304

Differential Diagnosis . . . . . . . . . . . . . . . . . . . . . . 306Differentiation of Central and PeripheralParesis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 306Differentiation of Radicular and PeripheralNerve Lesions . . . . . . . . . . . . . . . . . . . . . . . . . . 306Differential Diagnosis of Spinal CordCompression Syndromes . . . . . . . . . . . . . . . . . 311Miscellaneous Differential Diagnoses . . . . . . 311


12 Neurophysiological InvestigationsArmin Curt, Uta Kliesch

Core Messages . . . . . . . . . . . . . . . . . . . . . . . . . . . . 319Historical Background . . . . . . . . . . . . . . . . . . . . . 319Neuroanatomy . . . . . . . . . . . . . . . . . . . . . . . . . . . . 320Neurophysiological Modalities . . . . . . . . . . . . . . 321

Electromyography . . . . . . . . . . . . . . . . . . . . . . 321Nerve Conduction Studies . . . . . . . . . . . . . . . . 322F-Wave Recordings . . . . . . . . . . . . . . . . . . . . . . 324H-Reflex . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 325Somatosensory Evoked Potentials . . . . . . . . . 326Motor Evoked Potentials (TranscranialMagnetic Stimulation) . . . . . . . . . . . . . . . . . . . 328Intraoperative Neuromonitoring . . . . . . . . . . 329

Role of Neurophysiology in Specific Disorders . . 330Spinal Cord Injury . . . . . . . . . . . . . . . . . . . . . . 330Cervical/Lumbar Radiculopathy . . . . . . . . . . . 330Cervical Myelopathy . . . . . . . . . . . . . . . . . . . . . 331Lumbar Spinal Canal Stenosis . . . . . . . . . . . . . 331

Neurophysiology in Differential Diagnosis . . . . 332Peripheral Nerve Lesion Versus Radiculopathy 332Neuropathy Versus Spinal Canal Stenosis . . . 332Myopathy and Myotonic Disorders . . . . . . . . . 333Hereditary and Neurodegenerative Disease . 333


13 Surgical ApproachesNorbert Boos, Claudio Affolter,

Martin Merkle, Frank J. Ruehli

Core Messages . . . . . . . . . . . . . . . . . . . . . . . . . . . . 337Surgery and Planning . . . . . . . . . . . . . . . . . . . . . . 337

Anterior Medial Approach to Cervical Spine . . . 337Indications . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 338Patient Positioning . . . . . . . . . . . . . . . . . . . . . . 338Surgical Exposure . . . . . . . . . . . . . . . . . . . . . . . 339Pitfalls and Complications . . . . . . . . . . . . . . . . 341

Posterior Approach to the Cervical Spine . . . . . 342Indications . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 342Patient Positioning . . . . . . . . . . . . . . . . . . . . . . 342Surgical Exposure . . . . . . . . . . . . . . . . . . . . . . . 343Pitfalls and Complications . . . . . . . . . . . . . . . . 345

Right-Sided Thoracotomy . . . . . . . . . . . . . . . . . . 345Indications . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 346Patient Positioning . . . . . . . . . . . . . . . . . . . . . . 346Surgical Exposure . . . . . . . . . . . . . . . . . . . . . . . 346Pitfalls and Complications . . . . . . . . . . . . . . . . 349

Left-Sided Thoraco-Phrenico-Lumbotomy . . . . 350Indications . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 350Patient Positioning . . . . . . . . . . . . . . . . . . . . . . 350Surgical Exposure . . . . . . . . . . . . . . . . . . . . . . . 350Pitfalls and Complications . . . . . . . . . . . . . . . . 353

Anterior-Lateral Retroperitoneal Approachto L2–L5 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 353

Indications . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 353Patient Positioning . . . . . . . . . . . . . . . . . . . . . . 353Surgical Exposure . . . . . . . . . . . . . . . . . . . . . . . 353Pitfalls and Complications . . . . . . . . . . . . . . . . 355

Anterior Lumbar Retroperitoneal Approach . . . 355Indications . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 355Patient Positioning . . . . . . . . . . . . . . . . . . . . . . 355Surgical Exposure . . . . . . . . . . . . . . . . . . . . . . . 356Pitfalls and Complications . . . . . . . . . . . . . . . . 358

Posterior Approach to the Thoracolumbar Spine 358Indications . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 358Patient Positioning . . . . . . . . . . . . . . . . . . . . . . 358Surgical Exposure . . . . . . . . . . . . . . . . . . . . . . . 359Pitfalls and Complications . . . . . . . . . . . . . . . . 361

Landmarks for Screw Insertion . . . . . . . . . . . . . . 361Cervico-occipital Spine . . . . . . . . . . . . . . . . . . 361


Peri- and Postoperative Management

14 Preoperative AssessmentStephan Blumenthal, Youri Reiland,

Alain Borgeat

Core Messages . . . . . . . . . . . . . . . . . . . . . . . . . . . . 373Aim of Preanesthetic Evaluation . . . . . . . . . . . . . 373

Information and Instructions . . . . . . . . . . . . . 374Patient Assessment . . . . . . . . . . . . . . . . . . . . . . . . 374

History . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 374Physical Examination . . . . . . . . . . . . . . . . . . . . 375Laboratory Studies . . . . . . . . . . . . . . . . . . . . . . 375

XVI Contents

Organ-Specific Assessment . . . . . . . . . . . . . . . . . 376Airway Assessment . . . . . . . . . . . . . . . . . . . . . . 376Respiratory System . . . . . . . . . . . . . . . . . . . . . . 376Cardiovascular Assessment . . . . . . . . . . . . . . . 378Neurological Assessment . . . . . . . . . . . . . . . . . 379

Perioperative Drug Therapy . . . . . . . . . . . . . . . . 379What to Stop, to Continue and to Add? . . . . . 379Premedication . . . . . . . . . . . . . . . . . . . . . . . . . . 380Thromboembolic Prophylaxis . . . . . . . . . . . . . 380

Special Conditions Requiring Spinal Surgery . . 382Spinal Deformity . . . . . . . . . . . . . . . . . . . . . . . . 382Neuromuscular Disease . . . . . . . . . . . . . . . . . . 383Cerebral Palsy . . . . . . . . . . . . . . . . . . . . . . . . . . 383Malignancy . . . . . . . . . . . . . . . . . . . . . . . . . . . . 384Spinal Cord Injury . . . . . . . . . . . . . . . . . . . . . . 384


15 Intraoperative Anesthesia ManagementJuan Francisco Asenjo

Core Messages . . . . . . . . . . . . . . . . . . . . . . . . . . . . 389Historical Background . . . . . . . . . . . . . . . . . . . . . 389Goals of Anesthesia in Spinal Surgery . . . . . . . . 389Preoperative Patient Assessment . . . . . . . . . . . . . 390Induction of Anesthesia . . . . . . . . . . . . . . . . . . . . 390

Airway Control and Endotracheal Intubation 391Antibiotic Prophylaxis . . . . . . . . . . . . . . . . . . . 393Patient Positioning . . . . . . . . . . . . . . . . . . . . . . 394Maintenance of Anesthesia . . . . . . . . . . . . . . . 396

Intraoperative Monitoring Techniques . . . . . . . . 397Advanced Monitoring of Vital Functions . . . . 397Monitoring Depth of Anesthesia(Consciousness) . . . . . . . . . . . . . . . . . . . . . . . . 400

Intraoperative Blood Preserving Techniques . . . 400Controlled Hypotensive Anesthesia . . . . . . . . 401Intrathecal Opiates . . . . . . . . . . . . . . . . . . . . . . 402Blood Predeposit and ErythropoietinInjection . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 402Cell Salvage . . . . . . . . . . . . . . . . . . . . . . . . . . . . 402Pharmacological Measures . . . . . . . . . . . . . . . 403Blood Transfusion and Coagulation FactorSubstitution . . . . . . . . . . . . . . . . . . . . . . . . . . . . 403

Intraoperative Spinal Cord Monitoring . . . . . . . 405Anesthetic Effects on SSEPs . . . . . . . . . . . . . . . 406Anesthetic Effects on MEPs . . . . . . . . . . . . . . . 407Nerve Root Monitoring . . . . . . . . . . . . . . . . . . 408Wake-up Test . . . . . . . . . . . . . . . . . . . . . . . . . . . 408

End of Anesthesia . . . . . . . . . . . . . . . . . . . . . . . . . 409Postoperative Pain Management . . . . . . . . . . . . . 409Recapitulation . . . . . . . . . . . . . . . . . . . . . . . . . . . . 411Key Articles . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 411References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 412

16 Postoperative Care and Pain ManagementStephan Blumenthal, Alain Borgeat

Core Messages . . . . . . . . . . . . . . . . . . . . . . . . . . . . 417Postoperative Care . . . . . . . . . . . . . . . . . . . . . . . . 417

Postoperative Ventilation or Extubation . . . . 418Hemodynamic Assessment . . . . . . . . . . . . . . . 419Neurological Assessment . . . . . . . . . . . . . . . . . 419Gastrointestinal Function . . . . . . . . . . . . . . . . 420Thromboembolic Prophylaxis . . . . . . . . . . . . . 420

Postoperative Pain Management . . . . . . . . . . . . . 420Consequences of Pain . . . . . . . . . . . . . . . . . . . . 420Non-narcotics . . . . . . . . . . . . . . . . . . . . . . . . . . 421Non-steroidal Drugs . . . . . . . . . . . . . . . . . . . . . 421Opioids . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 421Local Anesthetics . . . . . . . . . . . . . . . . . . . . . . . 422N-Methyl-D-aspartate Antagonists . . . . . . . . . 422


Degenerative Disorders

17 Degenerative Disorders of the Cervical SpineMassimo Leonardi, Norbert Boos

Core Messages . . . . . . . . . . . . . . . . . . . . . . . . . . . . 429Case Introduction . . . . . . . . . . . . . . . . . . . . . . . . . 430Epidemiology . . . . . . . . . . . . . . . . . . . . . . . . . . . . 430Pathogenesis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 432

Neck Pain . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 432Cervical Disc Herniation . . . . . . . . . . . . . . . . . 432Cervical Spondylotic Radiculopathy . . . . . . . 433Cervical Spondylotic Myelopathy . . . . . . . . . . 433

Clinical Presentation . . . . . . . . . . . . . . . . . . . . . . . 435History . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 436Physical Findings . . . . . . . . . . . . . . . . . . . . . . . 437Functional Assessment . . . . . . . . . . . . . . . . . . . 439

Diagnostic Work-up . . . . . . . . . . . . . . . . . . . . . . . 439Imaging Studies . . . . . . . . . . . . . . . . . . . . . . . . 439Neurophysiological Assessment . . . . . . . . . . . 444Differential Diagnosis . . . . . . . . . . . . . . . . . . . 444

Non-operative Treatment . . . . . . . . . . . . . . . . . . . 444Natural History . . . . . . . . . . . . . . . . . . . . . . . . . 445Conservative Treatment Modalities . . . . . . . . 446

Operative Treatment . . . . . . . . . . . . . . . . . . . . . . . 448General Principles . . . . . . . . . . . . . . . . . . . . . . 448Surgical Techniques . . . . . . . . . . . . . . . . . . . . . 449Case Study 1 . . . . . . . . . . . . . . . . . . . . . . . . . . . 451Case Study 2 . . . . . . . . . . . . . . . . . . . . . . . . . . . 454Case Study 3 . . . . . . . . . . . . . . . . . . . . . . . . . . . 456Surgical Decision-Making . . . . . . . . . . . . . . . . 459Complications . . . . . . . . . . . . . . . . . . . . . . . . . . 463


Contents XVII

18 Disc Herniation and RadiculopathyMassimo Leonardi, Norbert Boos

Core Messages . . . . . . . . . . . . . . . . . . . . . . . . . . . . 481Epidemiology . . . . . . . . . . . . . . . . . . . . . . . . . . . . 481Case Introduction . . . . . . . . . . . . . . . . . . . . . . . . . 482Pathogenesis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 483

Risk Factors . . . . . . . . . . . . . . . . . . . . . . . . . . . . 483Radiculopathy . . . . . . . . . . . . . . . . . . . . . . . . . . 484

Clinical Presentation . . . . . . . . . . . . . . . . . . . . . . . 486History . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 486Physical Findings . . . . . . . . . . . . . . . . . . . . . . . 487

Diagnostic Work-up . . . . . . . . . . . . . . . . . . . . . . . 488Imaging Studies . . . . . . . . . . . . . . . . . . . . . . . . 488Neurophysiologic Assessment . . . . . . . . . . . . . 490Urologic Assessment . . . . . . . . . . . . . . . . . . . . 490Differential Diagnosis . . . . . . . . . . . . . . . . . . . 491

Classification . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 491Non-operative Treatment . . . . . . . . . . . . . . . . . . . 493

Natural History . . . . . . . . . . . . . . . . . . . . . . . . . 494Conservative Measures . . . . . . . . . . . . . . . . . . . 494

Operative Treatment . . . . . . . . . . . . . . . . . . . . . . . 496General Principles . . . . . . . . . . . . . . . . . . . . . . 496Case Study 1 . . . . . . . . . . . . . . . . . . . . . . . . . . . 497Surgical Techniques . . . . . . . . . . . . . . . . . . . . . 497Case Study 2 . . . . . . . . . . . . . . . . . . . . . . . . . . . 499Conservative Versus Operative Treatment . . . 503Complications . . . . . . . . . . . . . . . . . . . . . . . . . . 504


19 Lumbar Spinal StenosisPatrick O. Zingg, Norbert Boos


Anatomy . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 515Pathogenesis . . . . . . . . . . . . . . . . . . . . . . . . . . . 515Spinal Claudication Syndrome . . . . . . . . . . . . 517

Classification . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 517Clinical Presentation . . . . . . . . . . . . . . . . . . . . . . . 519

History . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 519Physical Findings . . . . . . . . . . . . . . . . . . . . . . . 520

Diagnostic Work-up . . . . . . . . . . . . . . . . . . . . . . . 520Imaging Studies . . . . . . . . . . . . . . . . . . . . . . . . 520Neurophysiologic Studies . . . . . . . . . . . . . . . . 523Differential Diagnosis . . . . . . . . . . . . . . . . . . . 524

Non-operative Treatment . . . . . . . . . . . . . . . . . . . 524Natural History . . . . . . . . . . . . . . . . . . . . . . . . . 525Non-operative Options . . . . . . . . . . . . . . . . . . . 525

Operative Treatment . . . . . . . . . . . . . . . . . . . . . . . 526General Principles . . . . . . . . . . . . . . . . . . . . . . 526Surgical Techniques . . . . . . . . . . . . . . . . . . . . . 526

Case Study 1 . . . . . . . . . . . . . . . . . . . . . . . . . . . 527Case Study 2 . . . . . . . . . . . . . . . . . . . . . . . . . . . 529Operative Risks and Complications . . . . . . . . 530


20 Degenerative Lumbar SpondylosisMartin Merkle, Beat Wälchli,

Norbert Boos


Disc Degeneration and Discogenic Back Pain 542Facet Joint Osteoarthritis . . . . . . . . . . . . . . . . . 543Segmental Instability . . . . . . . . . . . . . . . . . . . . 544

Clinical Presentation . . . . . . . . . . . . . . . . . . . . . . . 545History . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 546Case Study 1 . . . . . . . . . . . . . . . . . . . . . . . . . . . 547Physical Findings . . . . . . . . . . . . . . . . . . . . . . . 548

Diagnostic Work-up . . . . . . . . . . . . . . . . . . . . . . . 548Imaging Studies . . . . . . . . . . . . . . . . . . . . . . . . 549Case Study 2 . . . . . . . . . . . . . . . . . . . . . . . . . . . 550Injection Studies . . . . . . . . . . . . . . . . . . . . . . . . 551Temporary Stabilization . . . . . . . . . . . . . . . . . . 552Patient Selection for Treatment . . . . . . . . . . . . 552

Non-operative Treatment . . . . . . . . . . . . . . . . . . . 553Operative Treatment . . . . . . . . . . . . . . . . . . . . . . . 554

General Principles . . . . . . . . . . . . . . . . . . . . . . 554Biology of Spinal Fusion . . . . . . . . . . . . . . . . . 555Surgical Techniques . . . . . . . . . . . . . . . . . . . . . 558Comparison of Treatment Modalities . . . . . . . 568Complications . . . . . . . . . . . . . . . . . . . . . . . . . . 569


21 Non-specific Low Back PainFlorian Brunner, Sherri Weiser,

Annina Schmid, Margareta Nordin

Core Messages . . . . . . . . . . . . . . . . . . . . . . . . . . . . 585Epidemiology . . . . . . . . . . . . . . . . . . . . . . . . . . . . 585Case Introduction . . . . . . . . . . . . . . . . . . . . . . . . . 586Classification of Back Pain . . . . . . . . . . . . . . . . . . 587Pathogenesis of NSLBP . . . . . . . . . . . . . . . . . . . . . 587Patient Assessment and Triage for Non-operativeTreatment . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 588Management of NSLBP . . . . . . . . . . . . . . . . . . . . . 590

Management of Acute NSLBP (<4 weeks) . . . 590Management of Subacute NSLBP (4– 12 weeks) 592Management of Chronic Non-specific LBP(>12 weeks) . . . . . . . . . . . . . . . . . . . . . . . . . . . . 595

Recapitulation . . . . . . . . . . . . . . . . . . . . . . . . . . . . 596

XVIII Contents

Key Articles . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 596References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 598

22 Postoperative RehabilitationFlorian Brunner, Shira Schecter-Weiner,

Annina Schmid, Rudolf Kissling

Core Messages . . . . . . . . . . . . . . . . . . . . . . . . . . . . 603Epidemiology . . . . . . . . . . . . . . . . . . . . . . . . . . . . 603Conceptional Background . . . . . . . . . . . . . . . . . . 604

Theoretical Considerations . . . . . . . . . . . . . . . 604Anatomical and Surgical Considerations . . . . 605Individual and Societal Considerations . . . . . 606

Indications for Postoperative SpinalRehabilitation . . . . . . . . . . . . . . . . . . . . . . . . . . . . 606

General Goals . . . . . . . . . . . . . . . . . . . . . . . . . . 607Specific Goals . . . . . . . . . . . . . . . . . . . . . . . . . . 607

Principles of Postoperative Rehabilitation . . . . . 607Preoperative Assessment . . . . . . . . . . . . . . . . . 607Postoperative Rehabilitation . . . . . . . . . . . . . . 608

Obstacles for Rehabilitation . . . . . . . . . . . . . . . . . 616Morphological Obstacles and General MedicalObstacles . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 616Psychosocial Obstacles . . . . . . . . . . . . . . . . . . . 617Work-Related Obstacles . . . . . . . . . . . . . . . . . . 617


Spinal Deformities and Malformations

23 Idiopathic ScoliosisMathias Haefeli, Kan Min


Genetic Factors . . . . . . . . . . . . . . . . . . . . . . . . . 625Connective Tissue and Skeletal MuscleAbnormalities . . . . . . . . . . . . . . . . . . . . . . . . . . 625Thrombocyte Abnormalities, Calmodulinand Melatonin . . . . . . . . . . . . . . . . . . . . . . . . . . 626

Classification . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 626Age-Related Classification . . . . . . . . . . . . . . . . 626Radiological Classification . . . . . . . . . . . . . . . 627

Clinical Presentation . . . . . . . . . . . . . . . . . . . . . . . 627History . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 627Physical Examination . . . . . . . . . . . . . . . . . . . . 629

Diagnostic Work-up . . . . . . . . . . . . . . . . . . . . . . . 632Imaging Studies . . . . . . . . . . . . . . . . . . . . . . . . 632Neurophysiologic Evaluation . . . . . . . . . . . . . . 637

Treatment . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 637General Considerations . . . . . . . . . . . . . . . . . . 637Natural History . . . . . . . . . . . . . . . . . . . . . . . . . 637Non-operative Options . . . . . . . . . . . . . . . . . . . 639

Operative Treatment . . . . . . . . . . . . . . . . . . . . . . . 641Indications for Surgery . . . . . . . . . . . . . . . . . . 641General Principles . . . . . . . . . . . . . . . . . . . . . . 642Case Study 1 . . . . . . . . . . . . . . . . . . . . . . . . . . . 646Surgical Decision Making . . . . . . . . . . . . . . . . 647Case Study 2 . . . . . . . . . . . . . . . . . . . . . . . . . . . 651Complications . . . . . . . . . . . . . . . . . . . . . . . . . . 651


24 Neuromuscular ScoliosisJean A. Ouellet, Vincent Arlet

Core Messages . . . . . . . . . . . . . . . . . . . . . . . . . . . . 663Epidemiology . . . . . . . . . . . . . . . . . . . . . . . . . . . . 663

Case Introduction . . . . . . . . . . . . . . . . . . . . . . . 664Disease Specific Spinal Deformity . . . . . . . . . 666

Pathogenesis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 667Classification . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 667Clinical Presentation . . . . . . . . . . . . . . . . . . . . . . . 669

History . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 669Physical Examination . . . . . . . . . . . . . . . . . . . . 670Case Study 1 . . . . . . . . . . . . . . . . . . . . . . . . . . . 671

Diagnostic Work-up . . . . . . . . . . . . . . . . . . . . . . . 673Medical Assessment . . . . . . . . . . . . . . . . . . . . . 673Case Study 2 . . . . . . . . . . . . . . . . . . . . . . . . . . . 674Imaging Studies . . . . . . . . . . . . . . . . . . . . . . . . 675

Non-operative Treatment . . . . . . . . . . . . . . . . . . . 677Natural History . . . . . . . . . . . . . . . . . . . . . . . . . 677Non-operative Treatment Options . . . . . . . . . 678

Operative Treatment . . . . . . . . . . . . . . . . . . . . . . . 678Surgical Indications . . . . . . . . . . . . . . . . . . . . . 678General Principles . . . . . . . . . . . . . . . . . . . . . . 679Surgical Techniques . . . . . . . . . . . . . . . . . . . . . 680Case Study 3 . . . . . . . . . . . . . . . . . . . . . . . . . . . 680Case Study 4 . . . . . . . . . . . . . . . . . . . . . . . . . . . 686


25 Congenital ScoliosisFrancis H. Shen, Vincent Arlet

Core Messages . . . . . . . . . . . . . . . . . . . . . . . . . . . . 693Epidemiology . . . . . . . . . . . . . . . . . . . . . . . . . . . . 693Case Introduction . . . . . . . . . . . . . . . . . . . . . . . . . 694Pathogenesis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 694Classification . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 695Clinical Presentation . . . . . . . . . . . . . . . . . . . . . . . 696

History . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 696Physical Findings . . . . . . . . . . . . . . . . . . . . . . . . . 697Diagnostic Work-up . . . . . . . . . . . . . . . . . . . . . . . 698

Imaging Studies . . . . . . . . . . . . . . . . . . . . . . . . 698Specific Investigations . . . . . . . . . . . . . . . . . . . 700

Non-operative Treatment . . . . . . . . . . . . . . . . . . . 700

Contents XIX

Natural History and Progression . . . . . . . . . . 700Operative Treatment . . . . . . . . . . . . . . . . . . . . . . . 701

General Principles . . . . . . . . . . . . . . . . . . . . . . 701Surgical Techniques . . . . . . . . . . . . . . . . . . . . . 702Corrective Surgery Procedures . . . . . . . . . . . . 702Case Study 1 . . . . . . . . . . . . . . . . . . . . . . . . . . . 703Case Study 2 . . . . . . . . . . . . . . . . . . . . . . . . . . . 704Miscellaneous Surgical Techniques . . . . . . . . . 707


26 Degenerative ScoliosisMax Aebi



Diagnostic Workup . . . . . . . . . . . . . . . . . . . . . . . . 720Imaging Studies . . . . . . . . . . . . . . . . . . . . . . . . 720Interventional Radiological Procedure . . . . . 721Additional Diagnostic Tools . . . . . . . . . . . . . . 722

Non-operative Treatment . . . . . . . . . . . . . . . . . . . 722Operative Treatment . . . . . . . . . . . . . . . . . . . . . . . 723

Decompression Procedure . . . . . . . . . . . . . . . . 724Correction Procedures . . . . . . . . . . . . . . . . . . . 724Surgical Techniques . . . . . . . . . . . . . . . . . . . . . 725Case Study 1 . . . . . . . . . . . . . . . . . . . . . . . . . . . 728Case Study 2 . . . . . . . . . . . . . . . . . . . . . . . . . . . 729


27 SpondylolisthesisClayton N. Kraft, Rüdiger Krauspe


History . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 736Physical Findings . . . . . . . . . . . . . . . . . . . . . . . 738Differential Diagnosis . . . . . . . . . . . . . . . . . . . 738

Diagnostic Work-up . . . . . . . . . . . . . . . . . . . . . . . 739Imaging . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 739Case Study 1 . . . . . . . . . . . . . . . . . . . . . . . . . . . 742Invasive Imaging Studies . . . . . . . . . . . . . . . . . 743

Non-operative Treatment . . . . . . . . . . . . . . . . . . . 745Natural History . . . . . . . . . . . . . . . . . . . . . . . . . 745

Conservative Treatment Options . . . . . . . . . . 745Operative Treatment . . . . . . . . . . . . . . . . . . . . . . . 747

General Principles . . . . . . . . . . . . . . . . . . . . . . 747Surgical Techniques . . . . . . . . . . . . . . . . . . . . . 748Case Study 2 . . . . . . . . . . . . . . . . . . . . . . . . . . . 751Complications . . . . . . . . . . . . . . . . . . . . . . . . . . 756


28 Juvenile Kyphosis (Scheuermann’s Disease)Dietrich Schlenzka, Vincent Arlet

Core Messages . . . . . . . . . . . . . . . . . . . . . . . . . . . . 765Epidemiology . . . . . . . . . . . . . . . . . . . . . . . . . . . . 765Case Introduction . . . . . . . . . . . . . . . . . . . . . . . . . 766Pathogenesis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 767Normal Sagittal Profile . . . . . . . . . . . . . . . . . . . . . 768Definition and Classification . . . . . . . . . . . . . . . . 771Clinical Presentation . . . . . . . . . . . . . . . . . . . . . . . 773


Diagnostic Work-up . . . . . . . . . . . . . . . . . . . . . . . 775Imaging Studies . . . . . . . . . . . . . . . . . . . . . . . . 775Neurophysiological Tests . . . . . . . . . . . . . . . . . 777Lung Function Test . . . . . . . . . . . . . . . . . . . . . . 777Differential Diagnosis . . . . . . . . . . . . . . . . . . . 777

Non-operative Treatment . . . . . . . . . . . . . . . . . . . 779Natural History . . . . . . . . . . . . . . . . . . . . . . . . . 779Bracing and Casting . . . . . . . . . . . . . . . . . . . . . 780Case Study 1 . . . . . . . . . . . . . . . . . . . . . . . . . . . 780

Operative Treatment . . . . . . . . . . . . . . . . . . . . . . . 782Preoperative Assessment . . . . . . . . . . . . . . . . . 782General Principles . . . . . . . . . . . . . . . . . . . . . . 783Operative Technique . . . . . . . . . . . . . . . . . . . . . 784Case Study 2 . . . . . . . . . . . . . . . . . . . . . . . . . . . 786Results of Operative Treatment . . . . . . . . . . . . 788Complications . . . . . . . . . . . . . . . . . . . . . . . . . . 790


29 Malformations of the Spinal CordDilek Könü-Leblebicioglu, Yasuhiro

Yonekawa


Embryological Aspects . . . . . . . . . . . . . . . . . . . 799Relevant Embryogenetic Steps . . . . . . . . . . . . 800Risk Factors . . . . . . . . . . . . . . . . . . . . . . . . . . . . 801Pathophysiology of Tethered Cord Syndrome 802

Terminology and Classification . . . . . . . . . . . . . . 802Classification of Spinal Malformation . . . . . . 803

XX Contents

Case Study 1 . . . . . . . . . . . . . . . . . . . . . . . . . . . 805Classification of Tethered Spinal Cord . . . . . . 811


Diagnostic Work-up . . . . . . . . . . . . . . . . . . . . . . . 814Prenatal Diagnosis . . . . . . . . . . . . . . . . . . . . . . 814Postnatal Diagnostic Tests . . . . . . . . . . . . . . . . 815

Treatment . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 815In Utero Treatment . . . . . . . . . . . . . . . . . . . . . . 816Postnatal Surgery . . . . . . . . . . . . . . . . . . . . . . . 816


Fractures

30 Cervical Spine InjuriesMichael Heinzelmann, Karim Eid,

Norbert Boos

Core Messages . . . . . . . . . . . . . . . . . . . . . . . . . . . . 825Case Introduction . . . . . . . . . . . . . . . . . . . . . . . . . 826Epidemiology . . . . . . . . . . . . . . . . . . . . . . . . . . . . 827Pathomechanisms . . . . . . . . . . . . . . . . . . . . . . . . . 828

Normal Anatomy . . . . . . . . . . . . . . . . . . . . . . . 828Biomechanics of Cervical Spine Trauma . . . . 830Spinal Cord Injury . . . . . . . . . . . . . . . . . . . . . . 832Pathomechanism of Whiplash-AssociatedDisorders . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 833

Clinical Presentation . . . . . . . . . . . . . . . . . . . . . . . 834History . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 834Physical Findings . . . . . . . . . . . . . . . . . . . . . . . 835Classification of Whiplash-AssociatedDisorders . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 836

Diagnostic Work-up . . . . . . . . . . . . . . . . . . . . . . . 836Imaging Studies . . . . . . . . . . . . . . . . . . . . . . . . 836Neurophysiology . . . . . . . . . . . . . . . . . . . . . . . . 842Vascular Assessment . . . . . . . . . . . . . . . . . . . . . 842Synopsis of Assessment Recommendations . . 842

General Treatment Principles . . . . . . . . . . . . . . . 844Whiplash-Associated Disorders . . . . . . . . . . . 844Non-operative Treatment Modalities . . . . . . . 845Spinal Cord Injuries . . . . . . . . . . . . . . . . . . . . . 848

Specific Treatment of Upper Cervical SpineInjuries . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 850

Fractures of the Occipital Condyle . . . . . . . . . 850Atlanto-occipital Dislocation . . . . . . . . . . . . . . 851Fractures of the Atlas . . . . . . . . . . . . . . . . . . . . 852Atlantoaxial Instabilities . . . . . . . . . . . . . . . . . 853Dens Fractures . . . . . . . . . . . . . . . . . . . . . . . . . 854Case Study 1 . . . . . . . . . . . . . . . . . . . . . . . . . . . 858Traumatic Spondylolisthesis of the Axis . . . . 860Case Study 2 . . . . . . . . . . . . . . . . . . . . . . . . . . . 862Combined Atlas/Axis Fractures . . . . . . . . . . . 863

Classification and Treatment of Subaxial Injuries 863Classification . . . . . . . . . . . . . . . . . . . . . . . . . . . 864Treatment . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 866Case Study 3 . . . . . . . . . . . . . . . . . . . . . . . . . . . 870Complications . . . . . . . . . . . . . . . . . . . . . . . . . . 871


31 Thoracolumbar Spinal InjuriesMichael Heinzelmann, Guido A. Wanner

Core Messages . . . . . . . . . . . . . . . . . . . . . . . . . . . . 883Epidemiology . . . . . . . . . . . . . . . . . . . . . . . . . . . . 883Case Introduction . . . . . . . . . . . . . . . . . . . . . . . . . 884Pathomechanisms . . . . . . . . . . . . . . . . . . . . . . . . . 885

Axial Compression . . . . . . . . . . . . . . . . . . . . . . 885Flexion/Distraction . . . . . . . . . . . . . . . . . . . . . . 886Hyperextension . . . . . . . . . . . . . . . . . . . . . . . . . 886Rotational Injuries . . . . . . . . . . . . . . . . . . . . . . 886Shear . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 887

Classification . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 887Denis Classification . . . . . . . . . . . . . . . . . . . . . 888AO Classification . . . . . . . . . . . . . . . . . . . . . . . 888

Clinical Presentation . . . . . . . . . . . . . . . . . . . . . . . 892Spinal Injuries . . . . . . . . . . . . . . . . . . . . . . . . . . 892Neurological Deficit . . . . . . . . . . . . . . . . . . . . . 892Concomitant Non-spinal Injuries . . . . . . . . . . 893History . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 893Physical Findings . . . . . . . . . . . . . . . . . . . . . . . 894

Diagnostic Work-up . . . . . . . . . . . . . . . . . . . . . . . 895Imaging Studies . . . . . . . . . . . . . . . . . . . . . . . . 895

Non-operative Treatment . . . . . . . . . . . . . . . . . . . 898Steroid Treatment of Spinal Cord Injury . . . . 899Non-operative Treatment Modalities . . . . . . . 899Case Study 1 . . . . . . . . . . . . . . . . . . . . . . . . . . . 900

Operative Treatment . . . . . . . . . . . . . . . . . . . . . . . 903General Principles . . . . . . . . . . . . . . . . . . . . . . 903Surgical Techniques . . . . . . . . . . . . . . . . . . . . . 905Case Study 2 . . . . . . . . . . . . . . . . . . . . . . . . . . . 906Case Study 3 . . . . . . . . . . . . . . . . . . . . . . . . . . . 911Outcome of Operative Versus Non-operativeTreatment . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 914


32 Osteoporotic Spine FracturesPaul F. Heini, Albrecht Popp

Core Messages . . . . . . . . . . . . . . . . . . . . . . . . . . . . 925Epidemiology . . . . . . . . . . . . . . . . . . . . . . . . . . . . 925Case Introduction . . . . . . . . . . . . . . . . . . . . . . . . . 926Pathogenesis and Definition . . . . . . . . . . . . . . . . 926Classification of Vertebral Body CompressionFractures . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 929

Contents XXI


Diagnostic Work-up . . . . . . . . . . . . . . . . . . . . . . . 933Imaging Studies . . . . . . . . . . . . . . . . . . . . . . . . 933Radionuclide Studies . . . . . . . . . . . . . . . . . . . . 934Densitometry . . . . . . . . . . . . . . . . . . . . . . . . . . 934Bone Biopsy . . . . . . . . . . . . . . . . . . . . . . . . . . . . 935Laboratory Investigations . . . . . . . . . . . . . . . . 935

Non-operative Treatment . . . . . . . . . . . . . . . . . . . 936Conservative Fracture Management . . . . . . . . 936Medical Treatment . . . . . . . . . . . . . . . . . . . . . . 936

Operative Treatment . . . . . . . . . . . . . . . . . . . . . . . 937General Principles . . . . . . . . . . . . . . . . . . . . . . 937Surgical Principles . . . . . . . . . . . . . . . . . . . . . . 937


Tumors and Inflammation

33 Primary Tumors of the SpineBruno Fuchs, Norbert Boos

Core Messages . . . . . . . . . . . . . . . . . . . . . . . . . . . . 951Epidemiology . . . . . . . . . . . . . . . . . . . . . . . . . . . . 951Case Introduction . . . . . . . . . . . . . . . . . . . . . . . . . 952Tumor Biology . . . . . . . . . . . . . . . . . . . . . . . . . . . . 953

Molecular Tumor Biology . . . . . . . . . . . . . . . . 953Pathways of Metastasis . . . . . . . . . . . . . . . . . . . 954Histology and Biology of Spinal Tumors . . . . 956


Diagnostic Work-up . . . . . . . . . . . . . . . . . . . . . . . 958Imaging Studies . . . . . . . . . . . . . . . . . . . . . . . 958Case Study 1 . . . . . . . . . . . . . . . . . . . . . . . . . . . 960Case Study 2 . . . . . . . . . . . . . . . . . . . . . . . . . . . 961Biopsy . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 964Laboratory Investigations . . . . . . . . . . . . . . . 964

Tumor Staging . . . . . . . . . . . . . . . . . . . . . . . . . . . 964Benign Tumors . . . . . . . . . . . . . . . . . . . . . . . . 965Malignant Tumors . . . . . . . . . . . . . . . . . . . . . 966

Non-operative Treatment . . . . . . . . . . . . . . . . . . 967Non-steroidal Anti-inflammatory Drugs . . . 967Adjuvant Therapy . . . . . . . . . . . . . . . . . . . . . . 967

Operative Treatment . . . . . . . . . . . . . . . . . . . . . . 968General Principles . . . . . . . . . . . . . . . . . . . . . 968Surgical Techniques . . . . . . . . . . . . . . . . . . . . 969Case Study 3 . . . . . . . . . . . . . . . . . . . . . . . . . . . 971

Recapitulation . . . . . . . . . . . . . . . . . . . . . . . . . . . 973Key Articles . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 974References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 974

34 Spinal MetastasisDante G. Marchesi

Core Messages . . . . . . . . . . . . . . . . . . . . . . . . . . . 977Epidemiology . . . . . . . . . . . . . . . . . . . . . . . . . . . 977Case Introduction . . . . . . . . . . . . . . . . . . . . . . . . . 978Pathogenesis . . . . . . . . . . . . . . . . . . . . . . . . . . . . 978Clinical Presentation . . . . . . . . . . . . . . . . . . . . . . 980

History . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 980Physical Findings . . . . . . . . . . . . . . . . . . . . . . 980

Diagnostic Work-up . . . . . . . . . . . . . . . . . . . . . . 981Imaging Studies . . . . . . . . . . . . . . . . . . . . . . . 981Biopsy . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 983Laboratory Investigation . . . . . . . . . . . . . . . . 983

Classification . . . . . . . . . . . . . . . . . . . . . . . . . . . . 984Non-operative Treatment . . . . . . . . . . . . . . . . . . 985

Steroids . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 985Radiotherapy . . . . . . . . . . . . . . . . . . . . . . . . . . 985

Operative Treatment . . . . . . . . . . . . . . . . . . . . . . 986General Principles . . . . . . . . . . . . . . . . . . . . . 986General Surgical Techniques . . . . . . . . . . . . . 987Specific Surgical Techniques . . . . . . . . . . . . . 988Case Study 1 . . . . . . . . . . . . . . . . . . . . . . . . . . . 989Case Study 2 . . . . . . . . . . . . . . . . . . . . . . . . . . . 992Case Study 3 . . . . . . . . . . . . . . . . . . . . . . . . . . . 993Postoperative Patient Management . . . . . . . 993


35 Intradural TumorsYashuhiro Yonekawa, Richard Marugg

Core Messages . . . . . . . . . . . . . . . . . . . . . . . . . . . 997Epidemiology . . . . . . . . . . . . . . . . . . . . . . . . . . . 997Case Introduction . . . . . . . . . . . . . . . . . . . . . . . . . 998Etiology and Pathogenesis . . . . . . . . . . . . . . . . . 998Classification of Intradural Tumors . . . . . . . . . 999

Intradural-Extramedullary Tumors . . . . . . . 999Differential Diagnosis . . . . . . . . . . . . . . . . . . 1000Case Study 1 . . . . . . . . . . . . . . . . . . . . . . . . . . 1001Intradural-Intramedullary Tumors . . . . . . . . 1002Case Study 2 . . . . . . . . . . . . . . . . . . . . . . . . . . 1004

Clinical Presentation . . . . . . . . . . . . . . . . . . . . . . 1005History . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1005Physical Findings . . . . . . . . . . . . . . . . . . . . . . 1006

Diagnostic Work-up . . . . . . . . . . . . . . . . . . . . . . 1006Imaging Studies . . . . . . . . . . . . . . . . . . . . . . . 1007Lumbar Puncture . . . . . . . . . . . . . . . . . . . . . . 1008

Treatment . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1009Non-surgical Treatment . . . . . . . . . . . . . . . . . 1009Surgical Treatment . . . . . . . . . . . . . . . . . . . . . 1009Surgical Techniques . . . . . . . . . . . . . . . . . . . . 1010Intrinsic Spinal Cord Tumor Resection . . . . 1012Case Study 3 . . . . . . . . . . . . . . . . . . . . . . . . . . 1013

Recapitulation . . . . . . . . . . . . . . . . . . . . . . . . . . . 1016

XXII Contents

Key Articles . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1017References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1018

36 Infections of the SpineNorbert Boos

Core Messages . . . . . . . . . . . . . . . . . . . . . . . . . . . 1021Epidemiology . . . . . . . . . . . . . . . . . . . . . . . . . . . 1021Case Introduction . . . . . . . . . . . . . . . . . . . . . . . . 1022Pathogenesis . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1023Classification . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1023Clinical Presentation . . . . . . . . . . . . . . . . . . . . . . 1024


Diagnostic Work-up . . . . . . . . . . . . . . . . . . . . . . 1025Labaratory Investigations . . . . . . . . . . . . . . . 1025Imaging Studies . . . . . . . . . . . . . . . . . . . . . . . 1026Biopsy . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1028

Nonoperative Treatment . . . . . . . . . . . . . . . . . . 1029Case Study 1 . . . . . . . . . . . . . . . . . . . . . . . . . . 1030

Operative Treatment . . . . . . . . . . . . . . . . . . . . . . 1031General Principles . . . . . . . . . . . . . . . . . . . . . 1031Surgical Techniques . . . . . . . . . . . . . . . . . . . . 1031Case Study 2 . . . . . . . . . . . . . . . . . . . . . . . . . . 1035


37 Rheumatoid ArthritisDieter Grob

Core Messages . . . . . . . . . . . . . . . . . . . . . . . . . . . 1041Epidemiology . . . . . . . . . . . . . . . . . . . . . . . . . . . 1041Pathogenesis . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1041Case Introduction . . . . . . . . . . . . . . . . . . . . . . . . 1042Classification . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1044Clinical Presentation . . . . . . . . . . . . . . . . . . . . . . 1045


Diagnostic Work-up . . . . . . . . . . . . . . . . . . . . . . 1045Imaging Studies . . . . . . . . . . . . . . . . . . . . . . . 1045Case Study 1 . . . . . . . . . . . . . . . . . . . . . . . . . . 1047Injection Studies . . . . . . . . . . . . . . . . . . . . . . . 1048Neurophysiological Investigations . . . . . . . . 1048

Non-operative Treatment . . . . . . . . . . . . . . . . . . 1048Operative Treatment . . . . . . . . . . . . . . . . . . . . . . 1048

General Principles . . . . . . . . . . . . . . . . . . . . . 1048Indications . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1049Surgical Techniques . . . . . . . . . . . . . . . . . . . . 1050Case Study 2 . . . . . . . . . . . . . . . . . . . . . . . . . . 1053


38 Ankylosing SpondylitisThomas Liebscher, Kan Min, Norbert Boos

Core Messages . . . . . . . . . . . . . . . . . . . . . . . . . . . 1057Epidemiology . . . . . . . . . . . . . . . . . . . . . . . . . . . 1057Case Introduction . . . . . . . . . . . . . . . . . . . . . . . . 1058Pathogenesis . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1060Clinical Presentation . . . . . . . . . . . . . . . . . . . . . . 1061


Diagnostic Work-up . . . . . . . . . . . . . . . . . . . . . . 1063Laboratory Investigations . . . . . . . . . . . . . . . 1063Imaging Studies . . . . . . . . . . . . . . . . . . . . . . . 1063Diagnostic Criteria . . . . . . . . . . . . . . . . . . . . . 1066

Non-operative Treatment . . . . . . . . . . . . . . . . . . 1067Natural History . . . . . . . . . . . . . . . . . . . . . . . . 1067Non-operative Management . . . . . . . . . . . . . 1068Physiotherapy . . . . . . . . . . . . . . . . . . . . . . . . . 1069Treatment Recommendations . . . . . . . . . . . . 1069

Operative Treatment . . . . . . . . . . . . . . . . . . . . . . 1070General Principles . . . . . . . . . . . . . . . . . . . . . 1070Planning of Osteotomies . . . . . . . . . . . . . . . . 1071Surgical Techniques . . . . . . . . . . . . . . . . . . . . 1072Case Study 1 . . . . . . . . . . . . . . . . . . . . . . . . . . 1076Case Study 2 . . . . . . . . . . . . . . . . . . . . . . . . . . 1078Complications . . . . . . . . . . . . . . . . . . . . . . . . . 1080


39 Treatment of PostoperativeComplications

Martin Krismer, Norbert Boos

Core Messages . . . . . . . . . . . . . . . . . . . . . . . . . . . 1087Frequency of Complications . . . . . . . . . . . . . . . 1087

Cervical Spine Surgery . . . . . . . . . . . . . . . . . . 1087Case Introduction . . . . . . . . . . . . . . . . . . . . . . 1088Anterior Spinal Surgery . . . . . . . . . . . . . . . . . 1089Disc Herniation and Spinal Stenosis . . . . . . 1089Lumbar Spinal Fusion . . . . . . . . . . . . . . . . . . 1090Comparison of Complications . . . . . . . . . . . 1090

Preventive Measures . . . . . . . . . . . . . . . . . . . . . . 1090Screening of Risk Factors . . . . . . . . . . . . . . . . 1091Preoperative Planning . . . . . . . . . . . . . . . . . . 1093Profound Knowledge of Anatomy . . . . . . . . . 1094Patient Positioning . . . . . . . . . . . . . . . . . . . . . 1094Neuromonitoring . . . . . . . . . . . . . . . . . . . . . . 1095

Approach-Related Complications . . . . . . . . . . . 1095Anteromedial Cervical Approach . . . . . . . . . 1096Case Study 1 . . . . . . . . . . . . . . . . . . . . . . . . . . 1097Anterior Approach to the CervicothoracicJunction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1098Thoracotomy . . . . . . . . . . . . . . . . . . . . . . . . . . 1098Thoracolumbar Approach . . . . . . . . . . . . . . . 1100

Contents XXIII

Anterior Lumbar and LumbosacralApproach . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1100Posterior Approach to the Cervical Spine . . 1103Posterior Approaches to the Thoracic andLumbar Spine . . . . . . . . . . . . . . . . . . . . . . . . . 1104

Procedure Related Complications . . . . . . . . . . . 1104Decompressive Cervical and LumbarSurgery . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1104Deformity Correction . . . . . . . . . . . . . . . . . . . 1106Reduction of High-Grade Spondylolisthesis 1108Corpectomy/Osteotomy . . . . . . . . . . . . . . . . . 1108

Postoperative Complications . . . . . . . . . . . . . . . 1109Homeostasis Related Complications . . . . . . 1109Neurological Complications . . . . . . . . . . . . . 1110Postoperative Wound Problems . . . . . . . . . . 1110Cerebrospinal Fluid Fistula . . . . . . . . . . . . . . 1112Vascular Complications . . . . . . . . . . . . . . . . . 1112Pulmonary Problems . . . . . . . . . . . . . . . . . . . 1113Gastrointestinal Problems . . . . . . . . . . . . . . . 1113Urogenital Complications . . . . . . . . . . . . . . . 1114Retrograde Ejaculation . . . . . . . . . . . . . . . . . 1114


40 Outcome Assessment in SpinalSurgery

Mathias Haefeli, Norbert Boos

Core Messages . . . . . . . . . . . . . . . . . . . . . . . . . . . 1123General Concepts of Outcome Assessment . . . 1123Pain . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1125

General Aspects . . . . . . . . . . . . . . . . . . . . . . . 1125Instruments . . . . . . . . . . . . . . . . . . . . . . . . . . . 1126

Disability . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1128General Aspects . . . . . . . . . . . . . . . . . . . . . . . 1128Instruments . . . . . . . . . . . . . . . . . . . . . . . . . . . 1128

Quality of Life . . . . . . . . . . . . . . . . . . . . . . . . . . . 1130General Aspects . . . . . . . . . . . . . . . . . . . . . . . 1130Instruments . . . . . . . . . . . . . . . . . . . . . . . . . . . 1130

Psychosocial Aspects, Work Situation and FearAvoidance Beliefs . . . . . . . . . . . . . . . . . . . . . . . . 1133

General Aspects . . . . . . . . . . . . . . . . . . . . . . . 1133Instruments . . . . . . . . . . . . . . . . . . . . . . . . . . . 1133

Clinical Feasibility and Practicability . . . . . . . . 1134Recapitulation . . . . . . . . . . . . . . . . . . . . . . . . . . . 1135References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1136

Subject Index . . . . . . . . . . . . . . . . . . . . . . . . . . . 1143

The Editors . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1163

The Medical Illustrator . . . . . . . . . . . . . . . . . . . 1164

The Artist . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1165

XXIV Contents

31Thoracolumbar Spinal Injuries

Michael Heinzelmann, Guido A. Wanner

Core Messages

✔ Spinal fractures are frequently located at thethoracolumbar junction for biomechanical rea-sons

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

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

✔ The imaging modalities of choice are standardradiographs and CT scans. A CT scan shouldroutinely be made to visualize bony injury. MRIis helpful to diagnose discoligamentous injuriesand to identify a possible cord lesion

✔ Primary goals of treatment are prevention andlimitation of neurological injury as well as res-toration of spinal stability, regardless ofwhether operative or non-operative therapy ischosen

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

✔ Early stabilization and fusion is generallyaccepted for patients with unstable fracturesand neurological deficits

✔ The optimal treatment for patients with lessinstability, moderate deformity and absence ofneurological compromise is not based onscientific evidence and remains a matter ofdebate.

✔ Good clinical outcome can be achieved withnon-operative as well as operative treatment

Epidemiology

Fractures most frequently

affect the thoracolumbar

junction

Systematic epidemiologic data on traumatic thoracolumbar fractures are rare anddiffer 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 inmen (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 fracturesoccur 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 ofa 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 totalof 2063 patients were registered and 944 patients were treated in hospital: 182patients (20%) with a cervical spine injury, 286 patients (30%) with a thoracic spineinjury and 403 patients (50%) with an injury of the lumbosacral spine. Traumaticcross-section spinal cord injury occurred in 40 out of 1 million inhabitants. About

Fractures Section 883

a b c d

e f g h

i j k l

Case Introduction

This 23-year-old female sustained a motor vehicle accident as an unrestrained passenger. Clinically, she presented withan incomplete paraplegia (ASIA C) and an incomplete conus-cauda syndrome. The initial CT (a–d) scan demonstrates anunstable complete burst fracture of L1 (Type A3.3). The 3D reconstruction (a, b) gives a good overview of the degree ofcomminution and the deformity; the posterior fragment is best visualized in the lateral 2D reconstruction (c) and theaxial view (d). In an emergency procedure, the myelon was decompressed by laminectomy and the fracture was reducedand stabilized with an internal fixator (e–h). Interestingly, the prone position alone (e) reduced the fracture to a certaindegree when compared to the CT scan taken with the patient in a supine position. With the internal fixator (RecoFix), theanatomical 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 approach5 days later (i–l). In this minimally invasive technique, the spine is approached by a small thoracotomy from the left, theruptured 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 retractorsof 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 canalfrom anterior and the laminectomy from posterior (k), and a bony healing of the local bone transplant of the lateral sideof 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% thethoracic 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 byT12 (17%, n =246) and L2 (14%, n =208). The epidemiologic multicenter studyon fractures of the thoracolumbar transition (T10–L2) by the German TraumaSociety 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 theUniversity 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), and10% 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 mobilelumbar lordosis occurs at T11–12.) The lowest thoracic ribs (T11 and T12) provide less stability at the thoraco-

lumbar junction region compared to the rostral thoracic region, becausethey 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 resistanceto anteroposterior translation [36]. In the lumbosacral region, the facetjoints are oriented in a more sagittal alignment, which increases the degreeof potential flexion and extension at the expense of limiting lateral bendingand rotation.

Spinal cord injury occurs in

about 10 – 30 % of traumatic

fractures

Spinal cord injury 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) bythe German Society of Traumatology [65] revealed neurological deficiencies in22–51%, depending on the fracture type (22% in Type A fractures, 28% in TypeB 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 themajor injury vector, account for most of the bony and ligamentous damage. Themost 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 vertebralbody compression [98]. Depending on the energy, the axial load may result inincomplete or complete burst 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 eccentriccompressive 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 thelatter case, the injury is classified as flexion-distraction injury. Violent trauma is themost 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 andcause 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 describedby Chance [22]. This lesion involves a horizontal fracture, which begins in thespinous process, progresses through the lamina, transverse processes, and pedi-cles, and extends into the vertebral body. Depending on the axis of flexion thevertebral body and disc may rupture or may be compressed anteriorly asdescribed above. Although any accident providing significant forward flexioncombined with distraction can produce this type of injury, the typical cause is amotor vehicle accident with the victim wearing a lap seat belt. These injuries areassociated with a high rate of hollow visceral organ lesions, typically of the smallbowel, 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. Thisproduces an injury pattern that is the reverse of that seen with flexion. Tension isapplied anteriorly to the strong anterior longitudinal ligaments and anterior por-tion of the anulus fibrosus, whereas compression forces are transmitted to theposterior elements. This mechanism results in a rupture from anterior to poste-rior and may result in facet, lamina, and spinous process fractures [43]. Denis andBurks reported on a hyperextension injury pattern that they termed lumberjackfracture-dislocation [32]. The mechanism of this injury is a falling mass, oftentimber, 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 theposterior 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 combinedwith rotational forces and lead to rotational fracture dislocations. As rotationalforces increase, ligaments and facet capsules fail and lead to subsequent disrup-tion of both the anterior and posterior elements. A highly unstable injury patternwill develop, i.e., the posterior ligaments and joint capsule will rupture and the


anterior disc and vertebral body will disrupt obliquely or will be compressed.Rotational forces may further be combined with shearing forces and lead to mostunstable fractures (slice fractures, Holdsworth) [54]. These patients have oftenbeen thrown against an obstacle or hit by a heavy device. Thus, the patients oftenhave 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 traumaticanterior spondylolisthesis that usually results in a complete spinal cord injury.

Classification

Vertebral spine injuries are very heterogeneous in nature. Most important for theunderstanding and treatment of these injuries is the evaluation of spinal stabilityor instability, respectively. However, the conclusive evaluation of this question isdifficult because the term “instability” is not yet clearly defined in the context ofspinal disorders.

Several classifications of spinal injuries have been introduced based primarilyon 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 relationshipsbetween 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 ofincapacitating deformity or pain from structural changes

Physiologic loads are defined as loads during normal activity, incapacitatingdeformity as gross deformity unacceptable to the patient, and incapacitatingpain 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 mostwidely accepted differentiation. However, this classification is insufficient to givedetailed 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 furthermodified this structural classification scheme and suggested the posterior facetjoint complex of each side to become a separate column [79]. The ventral columnconsists of the vertebral body; the two dorsal columns involve the facet articula-tions of both sides. Roy-Camille was concerned about the relationship of theinjury to vertebra, especially the neural ring, and the spinal cord. He describedthe “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.


Denis Classification

The middle column became a central part of the classification of spinal injuriesaccording 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), theanterior anulus fibrosus, and the anterior half of the vertebral bodies. The middlecolumn consists of the posterior longitudinal ligament (PLL), the dorsal anulusfibrosus, and the dorsal half of the vertebral bodies. Finally, the posterior columnconsists of the bony neural arch, posterior spinous ligaments and ligamentumflavum, as well as the facet joints.

Denis considered the middle column to be the key structure. A relevant injuryto the middle column was therefore the essential criterion for instability. Accord-ing to the Denis classification, rupture of the posterior ligamentous complex onlycreates instability if there is concomitant disruption of at least the PLL and dorsalanulus. However, the middle column is not clearly defined either anatomically orbiomechanically, 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 columnconcept by Denis raised several concerns, his classification is still frequentlyused, because it is simple and includes all the injury patterns most commonlyseen. Denis distinguished minor and major injuries: minor injuries includedfractures of the articular, transverse, and spinous processes as well as the parsinterarticularis. 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 theStudy 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” described byHoldsworth [54, 55] and Kelly and Whitesides [61, 119]. The AO classificationconsiders the spine to comprise two functionally separate supportive columns.The anterior column consists of the vertebral body and the intervertebral discsand is loaded in compression. The posterior column consists of the pedicles, thelaminae, the facet joints, and the posterior ligamentous complex, and is loaded intension. 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., compressionand burst fractures). Type B injuries are flexion-distraction or hyperextensioninjuries and involve the anterior and posterior column. Disruption may occur inthe 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 thehorizontal plane (e.g., fracture dislocations with a rotatory component). Eachtype is classified into three major groups (1 – 3) of increasing severity (Fig. 2) andcan further be divided into subgroups and specifications (Table 2).


Figure 1. Algorithmfor AO fracture typeclassification

According to Magerl et al.[80].

Figure 2. AO fracture classification – fracture types and groups

According to Magerl et al. [80].


Table 2. AO fracture classification

Type A: vertebral bodycompression

Type B: anterior and posteriorelement injury with distraction

Type C: anterior and posterior element injurywith rotation

A1. Impaction fracturesA1.1. Endplate impactionA1.2. Wedge impaction fracturesA1.2.1. Superior wedge impaction

fractureA1.2.2. Lateral wedge impaction

fractureA1.2.3. Inferior wedge impaction

fracture

B1. Posterior disruption pre-dominantly ligamentous(flexion-distraction injury)

B1.1. With transverse disruptionof the disc

B1.1.1. Flexion-subluxationB1.1.2. Anterior dislocationB1.1.3. Flexion-subluxation/anterior

dislocation with fracture ofthe articular processes

B1.2. With Type A fracture of thevertebral body

B1.2.1. Flexion-subluxation +Type A fracture

B1.2.2. Anterior dislocation +Type A fracture

B1.2.3. Flexion-subluxation/anteriordislocation with fracture ofthe articular processes +Type A fracture

C1. Type A injuries with rotation (compres-sion injuries with rotation)

C1.1. Rotational wedge fractureC1.2. Rotational split fracturesC1.2.1. Rotational sagittal split fractureC1.2.2. Rotational coronal split fractureC1.2.3. Rotational pincer fractureC1.2.4. Vertebral body separationC1.3. Rotational burst fracturesC1.3.1. Incomplete rotational burst fracturesC1.3.2. Rotational burst-split fractureC1.3.3. Complete rotational burst fracture

A2. Split fracturesA2.1. Sagittal split fractureA2.2. Coronal split fractureA2.3. Pincer fracture

B2. Posterior disruption pre-dominantly osseous (flexion-distraction injury)

B2.1. Transverse bicolumn frac-ture

B2.2. With transverse disruptionof the disc

B2.2.1. Disruption through thepedicle and disc

B2.2.2. Disruption through the parsinterarticularis and disc(flexion-spondylolysis)

B2.3. With Type A fracture of thevertebral body

B2.3.1. Fracture through the pedicle+ Type A fracture

B2.3.2. Fracture through the parsinterarticularis (flexion-spon-dylolysis) + Type A fracture

C2. Type B injuries with rotationC2.1. B1 injuries with rotation (flexion-

distraction injuries with rotation)C2.1.1. Rotational flexion subluxationC2.1.2. Rotational flexion subluxation with

unilateral articular process fractureC2.1.3. Unilateral dislocationC2.1.4. Rotational anterior dislocation without/

with fracture of articular processesC2.1.5. Rotational flexion subluxation without/

with unilateral articular process + Type Afracture

C2.1.6. Unilateral dislocation + Type A fractureC2.1.7. Rotational anterior dislocation without/

with fracture of articular processes +Type A fracture

C2.2. B2 injuries with rotation (flexiondistraction injuries with rotation)

C2.2.1. Rotational transverse bicolumn fractureC2.2.2. Unilateral flexion spondylolysis with

disruption of the discC2.2.3. Unilateral flexion spondylolysis +

Type A fractureC2.3. B3 injuries with rotation (hyperexten-

sion-shear injuries with rotation)C2.3.1. Rotational hyperextension-subluxation

without/with fracture of posterior ver-tebral elements

C2.3.2. Unilateral hyperextension-spondylolysisC2.3.3. Posterior dislocation with rotation

A3. Burst fracturesA3.1. Incomplete burst fractureA3.1.1. Superior incomplete burst

fractureA3.1.2. Lateral incomplete burst

fractureA3.1.3. Inferior incomplete burst

fractureA3.2. Burst-split fractureA3.2.1. Superior burst-split fractureA3.2.2. Lateral burst-split fractureA3.2.3. Inferior burst-split fractureA3.3. Complete burst fractureA3.3.1. Pincer burst fractureA3.3.2. Complete flexion burst fractureA3.3.3. Complete axial burst fracture

B3. Anterior disruption throughthe disc (hyperextension-shear injury)

B3.1. Hyperextension-subluxa-tions

B3.1.1. Without injury of the poste-rior column

B3.1.2. With injury of the posteriorcolumn

B3.2. Hyperextension-spondylo-lysis

B3.3. Posterior dislocation

C3. Rotational-shear injuriesC3.1. Slice fractureC3.2. Oblique fracture

Types, groups, subgroups and specifications allow for a morphology based classification of thoracolumbar fractures accordingto Magerl et al. [80]


Table 3. Frequency of fracture types and groups

Case Percentage of total Percentage of type

Type A 956 66.16A1 502 34.74 52.51A2 50 3.46 5.23A3 404 27.96 42.26

Type B 209 14.46B1 126 8.72 60.29B2 80 5.54 38.28B3 3 0.21 1.44

Type C 280 19.38C1 156 10.80 55.71C2 108 7.47 38.57C3 16 1.11 5.71

Based on an analysis of 1 445 cases (Magerl et al. [80])

a b c

Figure 3. Burst fracture subgroups

According to Magerl et al. [80].

Impaction and burst

fracture are the most

frequent fracture types

Second to simple impaction fractures (A1), the most frequent injury types areburst fractures, which can be divided into three major subgroups (Table 3,Fig. 3). The likelihood of neurological deficit increases in the higher subgroups(Table 4).

The important morphological criteria of instability according to the AO clas-sification are injuries to the ligaments and discs. A graded classification is usefulbecause there is a range from “definitely stable” to “definitely unstable” frac-tures.

Fractures are considered stable if no injury to ligaments or discs is evident,e.g., pure impaction fractures (Type A1). Structural changes of the spine underphysiologic loads are unlikely. Slightly unstable fractures reveal partial damageof ligaments and intervertebral discs, but heal under functional treatment with-out gross deformity and without additional neurological deficit. This is the casein a frequent type (A3), the so-called incomplete superior burst fracture (A3.1.1).Highly unstable implicates a severe damage of the ligaments and intervertebraldiscs, as it occurs in the fracture Types A3, B, and C.


Table 4. Frequency of neurological deficits

Types and groups Number of injuries Neurological deficit (%)

Type A 890 14A1 501 2A2 45 4A3 344 32

Type B 145 32B1 61 30B2 82 33B3 2 50

Type C 177 55C1 99 53C2 62 60C3 16 50

Total 1 212 22

Based on an analysis of 1 212 cases (Magerl et al. [80])

Clinical Presentation

The clinical assessment of patients with a putative trauma to the spine has threemajor objectives, i.e., to identify:

) the spinal injury) neurological deficits) concomitant non-spinal injuries

Spinal Injuries

About 30 % of

polytraumatized patients

have a spinal injury

It is obvious that the management and the priorities differ between a life-threat-ening polytrauma that includes a spinal injury and a monotrauma of the spine. Inthe case of a polytrauma, about one-fourth to one-third of patients have a spinalinjury [120]. In our institution, we found spinal injuries in 22% of polytrauma-tized patients. In a series of 147 consecutive patients with multiple trauma, Dai etal. [24] found a delayed diagnosis of thoracolumbar fractures in 19%, confirmingan earlier study by Anderson et al. [5], in which 23% of patients with major tho-racolumbar fractures were diagnosed after the patient had left the emergencydepartment. A delay in the diagnosis of thoracolumbar fractures is frequentlyassociated with an unstable patient condition that necessitates higher-priorityprocedures than thoracolumbar spine radiographs in the emergency depart-ment. However, with the routine use of multi-slice computed tomography (CT) in

Polytraumatized patients

should be screened

for spinal fracture by CT

polytraumatized patients, the diagnostic work-up is usually adequate [57, 106]and delayed diagnosis of spine fractures should become rare. Multiple burst frac-tures occur in approximately 10–34% [10, 11, 53].

Neurological Deficit

Sacral sparing indicates

an incomplete lesion

with a better prognosis

An accurate and well-documented neurological examination is of great impor-tance. With an inaccurate or incomplete examination and a subsequent variation ofthe patient’s neurological deficit, it will be unclear if the situation has changed or ifthe initial assessment was simply inappropriate. In the case of a progressive neuro-logical deficit, this may hinder urgent further management, i.e., the need for a sur-gical intervention with spinal decompression. Neurological assessment is usuallydone according to the guidelines of the American Spinal Injury Association (seeChapter 11 ). Importantly, the examination has to include the “search for a sacralsparing” which will determine the completeness of the deficit and the prognosis.


Concomitant Non-spinal Injuries

About one-third of all spine injuries have concomitant injuries [65, 100, 120]. Ina review of 508 consecutive hospital admissions of patients with spinal injuries,Saboe et al. [100] identified the presence of associated injuries in 240 (47%) indi-viduals. Most frequently found concomitant injuries were:

) head injuries (26%)) chest injuries (24%)) long bone injuries (23%)

About one-third of all spinal

injuries have concomitant

injuries

One associated injury was found in 22%, two injuries in 15%, and 10% of thepatients had three or more associated injuries. Most spine fractures involved thelower cervical spine (29%) or the thoracolumbar junction (21%). Eighty-twopercent of thoracic fractures and 72% of lumbar fractures had associated injuriescompared to 28% of lower cervical spine fractures [100]. There is an association

Flexion injuries are

frequently associated

with abdominal injuries

between flexion injuries of the lumbar spine (Chance type) and abdominal inju-ries in seat belt injuries. Anderson et al. [2] reviewed 20 cases of Chance-typethoracolumbar flexion-distraction fractures and found that 13 patients (65%)had associated life-threatening intra-abdominal trauma. Twelve of these patientshad bowel wall injury. Conversely, specific injury mechanisms and fracture pat-terns should lead to a targeted search for concomitant spinal injuries. It is wellestablished that calcaneus or tibia plateau fractures following a fall from a greatheight are associated with spinal burst fractures. Also, sternal injuries may beassociated with spinal fractures. Injury to the sternum, when due to indirect vio-lence, is almost always associated with a severe spinal column injury [48].

History

The history of a patient who sustained a thoracolumbar spinal injury is usuallyobvious. The cardinal symptoms are:

) pain) loss of function (inability to move)) sensorimotor deficit) bowel and bladder dysfunction

History should include

the trauma type

and injury mechanism

The history should include a detailed assessment of the injury, i.e.:

) type of trauma (high vs. low energy)) mechanism of injury (compression, flexion/distraction, hyperextension,

rotation, shear injury)

Fractures of the thoracolumbar spine usually result from high-energy traumasuch as traffic accidents and falls from a great height. Recreational activities fre-quently associated with spinal injuries are skiing, snowboarding, paragliding orhorseriding. A spinal fracture should be suspected in any patient who has had ahigh-energy trauma. Consequently, patients should be treated as if they have aspinal injury unless proven otherwise [97]. On the contrary, vertebral compres-sion fractures can also occur in less severe accidents or more or less spontane-ously in elderly patients with osteoporotic bones (see Chapter 32 ) [63].

In patients with neurological deficits, the history must be detailed regarding:

) time of onset) course (unchanged, progressive, or improving)

The time course of the

neurological deficit matters

As outlined in Chapter 30 , polytraumatized and unconscious (head-injured)patients are difficult to assess. Polytraumatized patients carry a high risk (up to


30%) of having suffered a spinal fracture and must be scrutinized for such aninjury. Assessing the history is not possible in unconscious patients and the diag-nosis must therefore be based on thorough imaging studies.

Physical Findings

Similarly to the assessment of the patient with a cervical spine injury (see Chap-ter 30 ), the initial focus of the physical examination is on the assessment of:

) vital functions) neurological deficits

Assess vital functions

and neurological deficits

The goal is to immediately secure vital functions, which can be compromised inpolytraumatized patients and patients with a spinal cord injury. Often hypoten-sion and hypovolemia is encountered both in polytraumatized and spinal cordinjured patients. Importantly, secondary deterioration of spinal cord functionthat results from hypotension and inadequate tissue oxygenization has to beavoided by timely and appropriate treatment.

Neurological deficits due

to thoracolumbar fractures

vary considerably

A thorough neurological examination is indispensable (see Chapter 11 ). Thespinal cord usually terminates at the level of L1 in adults, although it may extendto L2 in some patients. Therefore, fractures at the thoracolumbar junction mayresult in a variety of neurological injury types and symptoms, i.e., damage to:

) distal spinal cord with complete/incomplete paraplegia) conus medullaris with malfunction of the vegetative system) cauda equina) thoracolumbar nerve roots

Consider a spinal shock in

patients with neurological

deficits

In the case of a neurological deficit, the differentiation between a complete andincomplete paraplegia is of great importance for the prognosis, because approxi-mately 60% of patients with an incomplete lesion have the potential to make afunctionally relevant improvement. In thoracolumbar fractures, the clinical pic-ture of a complete neurogenic shock will not develop, because only the caudalparts of the sympathetic system are possibly damaged. However, a spinal shockmay be present (see Chapter 30 ). It is mandatory to exclude a spinal shockbecause spinal shock can disguise remaining neural function and has an impacton the treatment decision and timing.

Thoracolumbar factures may damage the parasympathic centers located inthe conus medullaris. This injury will lead to bladder dysfunction, bowel dys-function as well as sexual dysfunction. In the case of damage to the cauda equinaor in a combination with damage to the conus medullaris, a more diffuse distri-bution of lower extremity paresthesia, weakness and loss of reflexes is found.Radiculopathy can be identified by a segmental pattern of sensory alterationsthat do not have to be combined with motor dysfunction. As outlined in the pre-vious chapter, the neurological function must be precisely documented. TheASIA protocol [84] has become an assessment standard for this objective (seeChapter 11 ).

The inspection and palpation of the spine should include the search for:

) skin bruises, lacerations, ecchymoses) open wounds) swellings) hematoma) spinal (mal)alignment) gaps


Diagnostic Work-up

Imaging Studies

The radiographic examination is an extension of the physical examination thatconfirms clinical suspicions and documents the presence and the extent of manyinjuries. Similarly to the “clearance of the cervical spine” [97], the clinical assess-ment is of great importance to evaluate the necessity of imaging studies. In thealert patient who has no distracting injuries, and is not affected by sedativedrugs, alcohol, or neurological deficit, the requirement for imaging is guided byclinical symptoms. The absence of back pain and tenderness has been shown toexclude a thoracolumbar injury [101].

Modern imaging studies such as computed tomography (CT) and magneticresonance imaging (MRI) have substantially improved the diagnosis of osseousand discoligamentous injuries after spinal trauma. Thus, changes such asimprovement in scan availability, image quality, acquisition time, and imagereformatting have changed commonly used algorithms [6]. However, plain filmsare still helpful, because they allow a quick overview of the bony deformity. Also,standard radiographs are important for analyzing long-term results and defor-mities at follow-up.

Static imaging studies

may disguise the real extent

of displacement at the time

of impact

It is important to remember that any static imaging study is a “snapshot intime” that is taken after the major impact has hit the spine. Thus, even CT scansor MRI do not reveal the actual degree of spinal displacement that may have hap-pened during the injury. Also, routine plain X-rays, CT and MRI studies are takenwith the patient in a prone position, i.e., in a position that lacks physiologicalload, and may therefore lead to a misjudgement of the severity and instability ofthe spine injury.

Standard Radiographs

Supine radiographs

underestimate the kyphotic

deformity

In most institutions, anterior-posterior and lateral radiographs of the entirespine are standard imaging studies after a spinal trauma. If there is a clinical sus-picion of a spinal injury, plain radiographs (anterior-posterior and lateral view)should be obtained. Radiographs taken with the patient in the prone positionunderestimate the extent of kyphotic deformity. Films taken with the patient inthe standing position can demonstrate a possible loss of integrity of the posteriortension band under axial loading and should be done in equivocal cases.

Emergency radiographs

often do not suffice because

of their poor quality

Krueger and coworkers [74] studied 28 patients with fractures of the lumbartransverse process and found that three patients (11%) had a lumbar spine frac-ture that was identified by CT but was overlooked on plain radiographs. They con-cluded that patients with acute trauma and fractures of the transverse processshould be examined with CT, because CT scanning decreases the risk of missingpotentially serious injuries. In a prospective series, Hauser et al. [52] comparedplain films and initial CT of the chest, abdomen, and pelvis with thin cut CT scans.The authors found that all unstable fractures were diagnosed with plain radio-

CT has replaced radiographs

for the assessment

of seriously injured patients

graphs. However, the initial CT detected acute fractures that were missed with theconventional X-rays and correctly classified old fractures that plain films read as“possibly” acute. The total misclassification rate for plain films was 12.6% com-pared to 1.4% for the initial CT. In an emergency situation radiographs are oftenof poor quality and CT is prompted if a fracture cannot be ruled out with certainty.

Measurements should be made at the level of injury and be compared with thevertebrae at the more cranial and caudal levels. Any posterior cortical disruptionseen in the lateral view or any interpedicular widening seen in the anteroposte-rior view suggests a burst fracture that should be further analyzed by CT scan.


When analyzing plain films, the following signs and points have to be consideredand searched for [13] in the anteroposterior view:

) loss of lateral vertebral body height (i.e., scoliotic deformity) (Fig. 4a)) changes in horizontal and vertical interpedicular distance (Fig. 4a)) asymmetry of the posterior structures (Fig. 4b)) luxation of costotransverse articulations (Fig. 4b)) perpendicular or oblique fractures of the dorsal elements) irregular distance between the spinous processes (equivocal sign)

In the lateral view, the following features should be investigated:

) sagittal profile (Fig. 4c)) degree of vertebral body compression (Fig. 4c)) interruption or bulging of the posterior line of the vertebral body (Fig. 4d)) dislocation of a dorsoapical fragment (Fig. 4d)) height of the intervertebral space

Computed TomographyThere is an increasing trend in trauma management, especially polytrauma man-agement, to exclude visceral injuries with a multislice spiral CT scan of the chest,abdomen and pelvis [77]. In a systematic review of the literature in polytraumapatients, Woltmann and Bühren [120] advocate that imaging diagnostics, prefer-ably as multislice spiral CT, should be performed after stabilization of thepatient’s general condition and before admission to the intensive care unit.Because CT has a better sensitivity and specificity compared to standard radio-graphs, Hauser et al. [52] point out that an initial CT scan should replace plain

a b

c

d

Figure 4. Radiographic fracture assessment

The standard anteroposterior radiographs demonstrate: a widening of theinterpedicular distance as evidence for a burst fracture and unilateral loss of ver-tebral body height (scoliosis); b asymmetry of the spinal alignment (arrows)with luxation of the costotransverse articulations (arrowheads). Standard lateralradiographs demonstrate: c the altered sagittal profile with segmental kypho-sis; d disruption of the posterior vertebral body wall and dislocation of a dorsoa-pical fragment


a b c

d

Figure 5. CT fracture assessment

The axial CT scan reveals: a significant spinal canal compromise bya retropulsed bony fragment. Note the double contour of the ver-tebral body indicating a “burst” component. b Sagittal 2D imagereformation demonstrating fracture subluxation. Note the bonyfragment behind the vertebral body which may cause neuralcompression when the fracture is reduced. c Severe luxation frac-ture of the spine. d The 3D CT reformation nicely demonstratesthe rotation component indicating a Type C lesion

radiographs in high-risk trauma patients who require screening. In their pro-spective series of 222 patients with 63 thoracic and lumbar injuries, the results ofconventional X-ray compared to initial CT scan were as follows: sensitivity 58%vs. 97%, specificity 93% vs. 99%, positive predictive value 64% vs. 97%, negativepredictive value 92% vs. 99%, respectively.

CT is the imaging study

of choice to demonstrate

bony injuries

The axial view allows an accurate assessment of the comminution of the frac-ture and dislocation of fragments into the spinal canal (Fig. 5a). Sagittal andcoronal 2D or 3D reconstructions are helpful for determining the fracture pat-tern (Fig. 5b–d). The canal at the injured segment should be measured in theanteroposterior and transverse planes and compared with the cephalad and cau-dal segments.

Magnetic Resonance Imaging

MRI is helpful in ruling out

discoligamentous lesions

In the presence of neurological deficits, MRI is recommended to identify a possi-ble cord lesion or a cord compression that may be due to disc or fracture frag-ments or to an epidural hematoma (Fig. 6a). In the absence of neurological defi-cits, MRI of the thoracolumbar area is usually not necessary in the acute phase.However, MRI can be helpful in determining the integrity of the posterior liga-mentous structures and thereby differentiate between a Type A and an unstableType B lesion. For this purpose a fluid sensitive sequence (e.g., STIR) is fre-quently used to determine edema (Fig. 6b).


a b

Figure 6. MRI fracture assessment

a The T2 weighted MR scan reveals a fracture subluxation with disc material retropulsed behind the vertebral body. Notethe severe signal intensity alterations of the spinal cord as the morphological correlate for a complete spinal cord injury(arrowheads). b The parasagittal STIR image demonstrates a pincer fracture (black arrowheads). Note the joint effusion(white arrowheads) and the bright signal intensity alterations in the posterior elements indicating that this pincer frac-ture is combined with a posterior injury (Type B lesion)

Radionuclide Studies

Radionuclide studies are very infrequently used to diagnose acute vertebral frac-tures. However, skeletal scintigraphy may be useful for fracture screening in poly-traumatized patients, especially in a medicolegal context. Spitz et al. [109] foundthat after 10– 12 days, with the aim of skeletal scintigraphy, an additional fracturewas found in half of all patients, and was subsequently verified radiologically.Because skeletal scintigraphy can be employed with equal efficacy to reliablyexclude bone injuries, the authors advocate that skeletal scintigraphy is of partic-ular significance in the determination of the extent of bone injury in polytrauma-tized patients. However, bone scans have been surpassed by MRI using fluid-sen-sitive sequences which demonstrate the subtle lesions (e.g., bone bruise).

Non-operative Treatment

Progress in pre-hospital care has considerably improved outcomes for patientswith spinal injuries. This is in part due to the knowledge and awareness of the res-cue team, the adherence to the Advanced Trauma Life Support (ATLS) protocols,and the transportation on a backboard or a vacuum board (see Chapter 30 ).

The general objectives of the treatment of thoracolumbar injuries are the sameas for cervical injuries (Table 5):

Table 5. General objectives of treatment

) restoration of spinal alignment ) preservation or improvement of neurological function) restoration of spinal stability ) avoidance of collateral damage

The treatment should provide a biologically and biomechanically sound envi-ronment that allows accurate bone and soft-tissue healing and eventually creates


The main advantage

of non-operative treatment

is the avoidance of surgery-

related complications

a stable and pain-free spinal column. These goals should be accomplished with aminimal risk of morbidity. Hence, the main advantage of non-operative treatmentof thoracolumbar fracture is avoidance of surgery-related complications such as:

) infection) iatrogenic neurological injury) failure of instrumentation) anesthesia-related complications

The relationship between post-traumatic kyphotic deformity and chronic backpain is not well established in the literature. Most clinicians believe that kyphoticdeformity of the thoracolumbar area is synonymous with a poor clinical out-come. Although few studies provide some evidence that moderate kyphosis isassociated with either pain or disability [47], several studies suggest that there isno direct relationship between kyphosis and back pain or functional impairment[20, 73, 87, 89, 116].

Steroid Treatment of Spinal Cord Injury

High-dose steroid treatment

is highly controversial

The controversy over steroid treatment of thoracolumbar spinal cord injury isdiscussed in the previous chapter (see Chapter 30 ). The overall consensus isthat high-dose steroid treatment is regarded as an option for spinal monotraumain young patients but not as a guideline for standard of care.

Non-operative Treatment Modalities

As more and more data are collected, information emerges that supports bothsurgical and non-operative treatment. Non-operative treatment is still a viableand effective treatment for the vast majority of thoracolumbar fractures (Table 6)and should be part of the armamentarium available to all clinicians that treatthese patients [92].

Table 6. Favorable indications for non-operative treatment

) pure osseous lesions ) absence of malalignment) absence of neurological deficits ) absence of gross bony destruction) only mild to moderate pain on mobilization ) absence of osteopenia/osteoporosis

There are three different methods of non-operative treatment:

) repositioning and cast stabilization) functional treatment and bracing without repositioning) functional treatment without bracing

However, functional treatment without bracing is not applicable to all fracturetypes, while basically all fractures can be treated with repositioning and formalcasting (Böhler technique).

Repositioning and Cast Stabilization

Böhler [18] was one of the first to advocate a conservative treatment with reposi-tioning and retention in a cast. The correct technique of repositioning andimmobilization in a plaster of Paris cast is quite sophisticated and needs to beperformed perfectly to obtain good results [13, 58]. The fracture is reduced usinga fracture table with the abdomen hanging freely. The hyperextension results ina fracture reduction by ligamentotaxis (Case Study 1). As a general rule, Böhler


a b

c

d e f

Case Study 1

In 1988, a 33-year-old male sustained a motor vehicle accident and was admitted to hospital. On examination, thepatient had severe pain at the thoracolumbar junction and in his right foot (talus neck fracture). The neurological exami-nation was normal with some slight sensory deficit of L2 predominantly on the right side. Standard radiographs (a, b)revealed a burst fracture at the level of L2 with scoliotic deformity. The axial CT scan showed a burst fracture with severeretropulsion of a dorsoapical fragment and almost complete spinal canal stenosis (c). Despite this severe canal compro-mise, the patient was treated non-operatively for unknown reasons. The conservative treatment consisted of bed rest for3 – 4 weeks in conjunction with reduction on a fracture table and cast fixation. The patient was mobilized thereafter witha thoracolumbar cast. At 4 months the patient was treated with a functional brace for an additional 2 months. Thepatient was reevaluated 10 years later in a medicolegal context related to his injury. Standard radiographs (d, e) demon-strated significant disc height decrease (L1/2) but without segmental kyphosis. The scoliotic deformity remainedunchanged. An MRI scan revealed a complete resorption of the dorsoapical fragment with spontaneous canal clearance,and only mild to moderate disc degeneration at the level of L1/2 and L2/3 (f ). At the time of follow-up examination, thepatient was fully functional and only had very occasional back pain. This case nicely demonstrates that even severe burstfractures can be treated conservatively with excellent results although today we would suggest surgical treatment in thiscase to shorten the hospital stay and rehabilitation period. (Courtesy University Hospital Balgrist).


used the kyphosis angle in degrees to calculate the numbers of weeks of immobi-lization (minimum 12 weeks, maximum 5 months). Patients were allowed toambulate almost immediately and were discharged home after a couple of days.Regular clinical and radiological exams were performed, initially every 2 weeks,then every 4 weeks, and the cast had to be changed if it became loose. Impor-tantly, an intense and skillful physical therapy was, and still is, paramount toachieving good or satisfactory results.

Böhler’s fracture treatment

today is still a viable treat-

ment option

The disadvantage of the Böhler technique is that it is very uncomfortable andpainful for the patient and often requires sedation and strong analgesics. TheBöhler technique is also prone to plaster cast related pressure sores. In patientswith an indication for conservative treatment, we prefer to apply the cast in thestanding position in hyperextension. This is possible in the vast majority ofpatients after a few days post-trauma and after orthostatic training on a verticallytilted board (Fig. 7).

a

b c d

Figure 7. Non-operative treatment

a The patient with an orthostatic problem after a fracture is firstplaced on a motorized table which can be tilted vertically.b When the patient is able to stand upright for 15 – 20 min, he ispositioned between two vertical bars and moderately extendshis spine while the cast is applied. c, d The thoracolumbar castbuttresses onto the iliac crest and reaches up to the sternum


Functional Bracing

Reduced kyphotic fractures

are prone to return

to the initial deformity,

placing a questionmark

over reduction

Magnus [82] advocated early functional treatment without repositioning. Accord-ing to this concept, a thoracolumbar fracture is bound to return to the initialdeformity and repositioning is therefore not necessary. The functional treatmentconcept was initiated with a phase of prone position on a stable bed and, if neces-sary, with lordotic support. The time of immobilization in bed depended on thefracture type. The next phases of treatment consisted of physical therapy toenhance muscle strength, mobilization in a waterbath, mobilization with a threepoint orthesis to prevent flexion and to assure an upright position of the patient,and a discharge home after approximately 3 weeks. Outpatient treatment was con-tinued for another 3–4 months and physical therapy to enhance spine mobilitywas initiated after radiologic consolidation of the fracture, i.e., after 3–4 months.

Functional Treatment

Functional treatment is indi-

cated only in unequivocal

stable fractures

In contrast to Böhler’s repositioning and stabilization [18] or Magnus’ functionalbracing [82], functional treatment does not include any bracing device. Espe-cially patients with stable fractures will benefit from this treatment (Table 7).Some braces are rather cumbersome and will hinder the patient in many activi-ties of daily life. In fact, braces can be considered an “aide-memoire” and remindthe patient not to perform painful movements. With the functional treatment,patients are advised to mobilize freely according to their capabilities and accord-ing to the resulting pain. Importantly, qualified physical therapy and adequatepain medication are necessary to obtain optimal results.

Table 7. Outcome of conservative and operative treatment

Authors Cases Studydesign

Fracturetype(numbers)

Type oftreatment

Neuro-logicaldeficit

Follow-up(months)

Outcome Conclusions

Wein-steinet al.(1988)[116]

42 retro-spec-tive

burstfractures(T10–L5)

non-operative:treatmentranged fromimmediateambulation ina body cast orbrace to3 months bedrest

22 % 240 neurological deteriora-tion: noneable to return to work:88 %kyphotic angle 26.4° in

flexion and 16.8° inextension

average back pain score3.5 (0 – 10)

non-operative treat-ment of thoracolumbarburst fractures withoutneurological deficit canlead to acceptablelong-term results

Mum-fordtet al.(1993)[87]

41 retro-spec-tive

single levelthoracolum-bar burstfracturesT11–L5:type I: 5 %type II: 78 %type III: 5 %type V: 12 %(Denis classi-fication)

non-operative:bedrest mean:

31.3 (range,7 – 68 days)

bracing mean11.9 (range,2 – 24 weeks)

none 24 functional results:excellent 49 %good 17 %fair 22 %poor 12 %one patient developedneurological deteriora-tion that required sur-gery

for patients with burstfractures withoutneurological deficit:

non-operative manage-ment yields accept-able results

bony deformity progres-ses marginally relativeto the rate of canalarea remodeling

radiographic severity ofinjury or residualdeformity does notcorrelate with long-term symptoms

Chowet al.(1996)[23]

24 retro-spec-tive

unstableburstfractures(T11–L2)

non-operative:casting or brac-ing and earlyambulation

None 34 no correlation betweenpost-traumatic kypho-sis and outcome

little/no pain 79 %return to work 75 %no restrictions at work75 %

hyperextension castingor bracing is a safe andeffective method fortreatment of thoraco-lumbar burst fractures


Table 7. (Cont.)



Type oftreatment


Follow-up(months)

Outcome Conclusions

Kanedaet al.(1997)[60]

150 retro-spec-tive

FrankelgradesA (24 %)B (58 %)C (6 %)D (7 %)E (4 %)

operative:single stageanterior spinaldecompres-sion, strut graf-ting, and ante-rior instrumen-tation

100 % 96(60 – 156)

neurological functionimproved at least onegrade in 95 % ofpatients. 72 % ofpatients with bladderdysfunction recoveredcompletely. 96 %returned to work, 86 %to their previous jobwithout restrictions

anterior decompressionand stabilization inpatients with burst frac-tures and neurologicaldeficit yielded goodfunctional results

Knopet al.(2001)[67]

372 pro-spec-tive,multi-center

thoracolum-bar fractures(T12–L2)type:A (69 %)B (17 %)C (14 %)

operative:Posterior (59 %)combined

anterior-pos-terior (35 %)

anterior (6 %)stabilization

20 % 27(4 – 61)

for detailed descriptionsee text

all treatment methodsresulted in compara-ble clinical and func-tional outcome

one-third of all patientshad severe and persist-ing functional disabili-ties

Khooet al.(2002)[62]

371 retro-spec-tive

N/A 35 % stand-alone ante-rior thora-coscopic sta-bilization

65 % additionalposterior pedi-cle screwinstrumenta-tion

15 % 24(4 – 72)

low rate of severe com-plications (1.3 %); onecase each of aorticinjury, splenic contu-sion, neurologicaldeterioration, CSF fluidleak, and severewound infection

42 % less narcotics forpostoperative paintreatment comparedto a group of 30patients treated withopen thoracotomy

anterior thoracoscopic-assisted reconstructionof thoracolumbar frac-tures can be safelyaccomplished, reducingpain and morbidityassociated with openapproaches

DefinoandScar-paro(2005)[29]

18 retro-spec-tive

type B and Cfractures(AO classifi-cation), T10–L4

operative:posteriormonosegmen-tal fixation andarthrodesis

38.9 % 78(24 – 144)

low residual pain ratesand high level patientsatisfaction with finalresult. 95.5 % returnedto work and presentedwith a low disabilityindex (Oswestry Disabil-ity Index = 10.33 %)

posterior monoseg-mental fixation is anadequate and satisfac-tory procedure in spe-cific types of thoraco-lumbar spine fractures

Woodet al.(2005)[122]

38 pro-spec-tive,ran-domi-zed

isolatedburst frac-tures (T10–L2)

operative:18 posteriorfusion20 anterior sta-bilization

none 43(24 – 108)

17 minor complicationsin patients treatedposteriorly, includingimplant removal, 3minor complicationswith anterior stabiliza-tion

similar functional out-comes

anterior fusion andinstrumentation mayexhibit fewer complica-tions and fewer addi-tional surgeries

Operative Treatment

General Principles

There is a general trend towards operative treatment of unstable fractures [31,47], mostly because surgical stabilizing allows for:

) early mobilization of the patient) diminished pain) facilitated nursing care (polytraumatized patients)) earlier return to work) avoidance of late neurological complications


Despite theoretical

advantages, the superiority

of surgical fracture

treatment is not supported

by scientific evidence

However, evidence suggests that there is no difference as regards neurologicalrecovery (Frankel score) and no substantial difference in functional long-termoutcome between the operative and non-operative treatment [114]. This isclearly valid for compression fractures that are relatively stable, i.e., A1 and A2fractures, according to the AO classification. Quite frequently, however, studiespresented in the literature analyze a mixed cohort of fracture types without fur-ther differentiation, which leaves their results somewhat inconclusive.

In burst fractures, there is often some degree of canal compromise with apotential risk of neurological injury. Hence, progressive neurological deteriora-tion in the presence of substantial canal compromise is an indication for surgicaldecompression and stabilization. Importantly, neurological status, spinal stabil-ity, degree of deformity of the injured segment, degree of canal compromise, andassociated injuries are the most relevant factors that need to be considered when

Progressive neurological

deficit is an absolute

indication for surgery

deciding on operative or non-operative treatment for patients with a thoraco-lumbar spine fracture. Most surgeons agree on absolute indications for surgerywhile relative indications are debatable (Table 8):

Table 8. Indications for surgical treatment

Absolute Relative

) incomplete paraparesis ) pure osseous lesions) progressive neurological deficit ) desire for early return to regular activities) spinal cord compression w/o neurological deficit ) avoidance of secondary kyphosis) fracture dislocation ) concomitant injuries (thoracic, cerebral)) severe segmental kyphosis (> 30°) ) facilitating nursing in paraplegic patients) predominant ligamentous injuries

In the absence of class I or II level scientific evidence for the vast majority of frac-ture types, treatment guidelines remain controversial but a pragmatic approachas used in our center may be useful.

Spinal Cord Decompression

Decompression

of incomplete spinal cord

lesions with persistent

compression is generally

recommended

The severity of a spinal cord injury is related to the force and duration of com-pression, the displacement and the kinetic energy. Many animal models, includ-ing primates, have demonstrated that neurological recovery is enhanced by earlydecompression [40]. However, this compelling evidence has not been able to betranslated into patients with acute spinal cord injury. This may in part be due to:(1) heterogeneous injury patterns and to (2) the absence of thoroughly designedand well-performed randomized controlled trials. However, a number of studieshave documented recovery of neurological function after delayed decompressionof the spinal cord (months to years) after the injury [4, 14, 15, 76, 112]. Theimprovement in neurological function with delayed decompression in patientswith cervical or thoracolumbar spinal cord injury who have plateaued in theirrecovery is noteworthy and suggests that compression of the cord is an importantcontributing cause of neurological dysfunction. Although many clinical studiesdo not support the concept that surgery improves neurological deficits, mostinvestigators recommend early surgical decompression in cases of an incompletespinal cord injury and persistent compression of neurogenic structures.

Timing of Surgery

The timing of surgery remains controversial. While one randomized controlledtrial showed no benefit of early (< 72 h) decompression [113], several recent pro-


spective series suggest that early decompression (<12 h) can be performed safelyand may improve neurological outcomes [40].

Early rather than late

decompression

is recommended

La Rosa et al. [75] published a meta-analysis on the issue of early decompres-sion in acute spinal cord injury. They reviewed 1687 patients in studies publishedup to 2000. Patients were divided into three treatment groups: early decompres-sion (<24 h), delayed decompression (>24 h), and conservative treatment. Sta-tistically, early decompression resulted in better outcomes compared to bothdelayed decompression and conservative management. Because the analysis ofhomogeneity demonstrated that only data regarding patients with incompletespinal cord injury who underwent early decompression were reliable, the authorsconcluded that early decompression can only be considered a practice option.Currently, there are no standards regarding the role and timing of decompressionin acute spinal cord injury. Also, the presence and duration of a therapeutic win-dow, during which surgical decompression could attenuate the secondary mech-anisms of spinal cord injury, remains unclear. In a recent article, Fehlings et al.[40] provide evidence-based recommendations regarding spinal cord decom-pression in patients with acute spinal cord injury. Animal studies consistentlyshow that neurological recovery is enhanced by early decompression. One ran-domized controlled trial showed no benefit to early (<72 h) decompression. Sev-eral recent prospective series suggest that early decompression (< 12 h) can beperformed safely and may improve neurological outcomes. Currently, there areno standards regarding the role and timing of decompression in acute spinal cord

Early decompression

of progressive neurological

deficits is indicated

injury. On the other hand, no significant adverse effects of early decompressionhave been documented. In the absence of clear guidelines from the literature,early decompression of compressed neurological structures appears to be bestpractice.

Surgical Techniques

If surgical treatment is chosen, further debate arises over the appropriate type ofapproach. Similarly to the treatment decision of conservative vs. operative, scien-tific evidence is lacking for the superiority of one surgical technique over theother. Particularly for the frequent superior burst fracture (Fig. 3), a large varietyof surgical techniques are available. Finally, it depends on the surgical expertiseof the surgeon and their preference which technique is chosen. It is difficult tobase treatment recommendations on treatment outcome in the literature(Table 7).

Posterior Approach

Posterior Monosegmental Reduction and Stabilization

Posterior monosegmental

reduction and stabilization

is feasible in selected Type A

and B fractures

The group of Gotzen et al. [49, 59] was the first to publish their results aftermonosegmental reduction and stabilization (Case Study 2). In their initial report[49], 14 patients with unstable compression fractures Grade II were treated byposterior one-level internal fixation (9 patients had stabilization with plates andcerclage wire, 5 with internal fixator). The results were compared to a series of 11patients with equivalent fractures treated non-operatively. The authors concludethat posterior single level stabilization and fusion is a recommendable surgicalprocedure. In their second publication, Junge et al. [59] describe the technique,which always included a posterior allogenic bone grafting and to some extentalso transpedicular bone grafting. The 2-year follow-up of 39 patients demon-strated that 17 patients (43%) were completely free of pain and 17 patients wereonly sensitive to weather changes or had minor pain during great physical stress.


a b c

d e f

Case Study 2

This 39-year-old female fell from her bike and complained about severe back pain at the thoracolumbar junction. Onadmission, the patient was neurologically intact. Standard anteroposterior and lateral radiographs demonstrated anincomplete burst fracture of L1 (a, b). The sagittal CT reformation confirmed the diagnosis of a superior burst fracture (c).The axial CT scan showed a minor dislocation of the dorsoapical vertebral fragment without neural compromise andintact pedicles (d). Based on this fracture type non-operative as well as operative treatment was discussed. The patientopted for surgery and preferred the posterior over the anterior approach. The spine was instrumented monosegmentallywith the lower screw aiming towards the intact anterior vertebral cortex. A posterolateral fusion was added with autolo-gous bone graft from the iliac crest. Follow-up radiographs (e, f ) demonstrated an anatomic reduction of the fracture.The patient was fully mobile on the first postoperative day and remained symptomfree during a 5 years follow-up. (Cour-tesy University Hospital Balgrist).

However, five patients (13%) had pain even during slight physical stress or atrest. Importantly, no implant fatigue failure was noted although five minor com-plications occurred.

One-level posterior

instrumentation is indicated

only in incomplete burst

fractures with intact

pedicles

Wawro et al. [115] also published a small series of 14 patients that were stabi-lized over a single segment. In addition, they characterized the fracture type inwhich single-segment stabilization is possible and described differences in theoperation technique compared with multisegmental internal fixation. For exam-ple, the pedicle screws occasionally needed to be inserted extremely close to theendplates if the remaining part of the vertebral body had been destroyed and couldtherefore not provide stability. Contraindications to a monosegmental posteriorstabilization are broken pedicles and complete burst fractures of the body. Inaccordance with our concept, only incomplete burst fractures with intact pedicles


and inferior endplate (i.e., Type A1 and A3.1) should be considered for posteriormonosegmental reduction and stabilization. Probably the pathophysiologicallymost sound indication for a monosegmental dorsal stabilization is a Type B frac-ture with only ligamentous posterior injury combined with a Type A1 or A3.1fracture of the vertebral body with intact endplates and intact pedicles, becausethe dorsal stabilization restores the tension band function of the ruptured liga-ments.

In a similar small series of 18 patients undergoing posterior monosegmentalstabilization, Defino et al. [29] report a clinical and radiological follow-up after2–12 years (mean 6.6±3 years) to demonstrate that posterior monosegmentalfixation is an adequate and satisfactory procedure in specific types of thoraco-lumbar spine fractures. Clinical evaluation revealed low residual pain rates and ahigh level of patient satisfaction with the final result. Functional evaluationshowed that 95.5% of the patients returned to work on a full-time basis and pre-sented with a low disability index (Oswestry Disability Index =10.33%). Radio-graphic evaluation demonstrated increased kyphosis in the fixed vertebral seg-ment during the late postoperative period, accompanied by a reduced height ofthe intervertebral disc. There was no implant failure, and no signs of pseudoar-throsis were observed in any patient.

Posterior Bisegmental Reduction and Stabilization

Posterior two-level reduction

and fracture stabilization

remains the gold standard

for the vast majority

of thoracolumbar fractures

The bisegmental, two-level posterior approach (short segmental stabilization) isthe “working horse” of the posterior techniques that allows a secure fixation ofthe pedicle screws in the intact vertebra one level above and below the fracture(Fig. 8). With this construct, a good reduction and stable fixation is reliablyachieved.

Fredrickson et al. [45] studied the mechanisms of ligamentotaxis to reduce theintracanal fragment of a burst fracture. Examination of anatomic data providedby microtome section indicated that the fibers that actually reduce the intracanalfragment originate in the anulus of the superior vertebra in the midportion of theendplate and insert into the lateral margins of the intracanal fragment. Investiga-tions using MRI confirmed that these obliquely directed fibers account for theindirect reduction of the fragment. Further studies demonstrate that the poste-rior longitudinal ligament provided only a minor contribution in the reductionof the fracture in comparison to the attachments of the posterior portion of theanulus fibrosus.

Harrington et al. [51] studied the biomechanics of indirect reduction of boneretropulsed into the spinal canal in vertebral fracture and made several clinicallyrelevant observations. It was not possible to produce an anteriorly directed forcein the posterior longitudinal ligament at less than 35% canal occlusion, partlybecause the posterior longitudinal ligament stands away from the midbody of thevertebra. Regardless of the relative sagittal plane angulation of the vertebrae, dis-traction was the governing factor in generating force in the posterior longitudi-nal ligament. Because positioning the vertebrae in lordosis before applying dis-traction significantly slackens the posterior longitudinal ligament, it is suggestedthat distraction be applied before angular positioning of the vertebrae is per-formed. However, this procedure risks overdistraction with deleterious resultsfor the spinal cord.

A comminuted anterior

column demands anterior

load sharing support

Depending on the comminution of the fractured vertebral body, additionalanterior load sharing support is needed. McLain et al. [85] reported early failureof short-segment pedicle instrumentation for thoracolumbar fractures. Out of 19patients with unstable thoracolumbar fractures, 10 patients had early failure offixation: progressive kyphosis, osseous collapse, vertebral translation, screw


a b

c d

Figure 8. Surgical technique of two-level fracture reduction and stabilization

The technique demonstrates the use of the Fracture Module of Universal Spine System (Synthes) but the general princi-ples similarly apply to other fracture systems. a Schanz screws are inserted in the pedicles of the vertebral bodies superiorand inferior to the fracture. b Screw clamps connected with the rods are mounted and fixed (arrow). c The fracture can bereduced by lordosing both screwdrivers. However, it is often better to first tighten the two lower screws and reduce thefracture simultaneously by lordosing the cranial screw bilaterally with the help of the screwdriver. d If this reductionmaneuver does not suffice to restore vertebral height, a temporary C-clamp can be mounted and the fracture distractedafter loosening the upper screws. Care must be taken not to overdistract the fracture because of the inherent neurologi-cal risks. Finally, the Schanz screws are cut with a special screwcutter (not shown). Dependent on canal clearance andanterior vertebral column restoration, an additional anterior approach can be added (preferably in a second stage)

breakage or loosening. These results indicate the need for an adequate anteriorcolumn support and an optimal anterior-posterior column load sharing environ-ment.

Transpedicular cancellous

bone grafting is insufficient

to stabilize the anterior

column

If no anterior stabilization is planned, a posterolateral fusion [78, 88] is man-datory. In addition, transpedicular bone grafting in the disrupted disc space hasbeen a treatment option [26, 78, 90]. However, transpedicular bone graftingcould not prevent kyphosis after dorsal removal on implants [1, 68, 108]. Knopet al. [68] studied 56 patients after implant removal and concluded that, because


of the disappointing results, they cannot recommend the additional transpedicu-lar cancellous bone grafting as an interbody fusion technique after posterior sta-bilization in cases of complete or incomplete burst injury to the vertebral body.Similarly, Alanay et al. [1] concluded that short-segment transpedicular instru-mentation of thoracolumbar burst fractures is associated with a high rate of fail-ure that cannot be decreased by additional transpedicular intracorporeal graf-ting.

Posterior Reduction and Multisegmental Stabilization

Fracture dislocations usually

require multilevel spinal

stabilization

Multilevel stabilization is indicated for the very unstable thoracolumbar luxationfractures (Type C lesions) which usually cannot be accurately reduced and stabi-lized with a short two-level construct. Usually, fixation of two to three segmentsabove and below the injury is recommended for a stable fixation. Unstable frac-tures of the thoracic spine that need to be stabilized are often combined with asignificant thorax trauma or a polytrauma. In these patients, an early posteriorstabilization with additional bone grafting allows for (1) a stable fixation of thespine with restoration of the dorsal tension band function, (2) the possibility ofearly and orthosis-free mobilization in the intensive care unit or later in a centerof rehabilitation, and finally (3) bony fusion.

Anterior Approach

Rationale for the anterior

approach is that the spine

should be treated where

the injury has occurred

From the biomechanical point of view, it is obvious that the damaged spine has tobe treated according to the injury mechanism and the site of injury. In a flexioninjury (e.g., Chance fracture) with fracture of the pedicles and the vertebral body,stabilization can be performed by a dorsal approach and restores the tensionband function until bony healing has occurred. Similarly, the biomechanics ofthe anterior column has to be considered in the case of a burst fracture. About80% of the axial load of an intact spine is supported by the anterior column.When the anterior column is substantially injured, the anterior support is dra-matically reduced to about 10%, leaving 90% of the load to be resisted by theimplant and the posterior elements. These general biomechanical considerationssupport the use of an anterior load sharing support (e.g., by a tricortical bonegraft or a cage).

The primary indications for the anterior approach are:

) insufficient spinal decompression) insufficient anterior column restoration

Spinal canal compromise in patients presenting with neurological deficits whichcannot adequately be resolved by a dorsal approach alone requires anteriordecompression. An additional indication is a vertebral body fracture with sub-stantial comminution and dislocation which cannot be adequately restored by aposterior approach alone [50].

Type A fractures can be

treated by an anterior

approach alone

However, Type A fractures can be treated by an anterior approach alone.Kaneda et al. [60] reported a study on 150 consecutive patients who had a burstfracture of the thoracolumbar spine and associated neurological deficits. Thepatients were managed with a single-stage anterior spinal decompression, strut-grafting, and anterior spinal instrumentation. At a mean of 8 years (range5–12 years) after the operation, radiographs showed successful fusion of theinjured spinal segment in 140 patients (93%). Ten patients had a pseudarthrosis,and all were managed successfully with posterior spinal instrumentation and aposterolateral arthrodesis. Despite breakage of the Kaneda device in ninepatients, removal of the implant was not necessary in any patient. None of the


patients had iatrogenic neurological deficits. Subsequent to anterior decompres-sion, the neurological function of 142 (95%) of the 150 patients improved by atleast one Frankel grade. Fifty-six (72%) of the 78 patients who had preoperativeparalysis or dysfunction of the bladder recovered completely. One hundred andtwenty-five (96%) of the 130 patients who were employed before the injuryreturned to work after the operation, and 112 (86%) of them returned to theirprevious job without restrictions. The authors concluded that anterior decom-pression, strut-grafting, and fixation with the Kaneda device in patients who hada burst fracture of the thoracolumbar spine and associated neurological deficitsyielded good radiographic and functional results.

Wood et al. [122] conducted a prospective randomized study to evaluate dif-ferences in radiographic, clinical, or functional outcomes when individuals withstable burst fractures of the thoracolumbar junction (T10–L2) without neurolog-ical deficit are treated with either a posterior fusion with instrumentation oranterior reconstruction, fusion, and instrumentation. Of 43 enrolled patients,38 completed a minimum 2-year follow-up (average: 43 months; range:24–108 months). Eighteen patients received a posterior spine fusion and 20 ananterior approach. There were 17 “complications” including instrumentationremoval for pain in 18 patients treated posteriorly, but only 3 minor complica-tions in 3 patients treated anteriorly. Patient-related functional outcomes weresimilar for the two groups. The authors concluded that although patient out-comes are similar, anterior fusion and instrumentation for thoracolumbar burstfractures may present fewer complications or additional surgeries. Hence, usingminimally invasive techniques (see below) the collateral damage can signifi-cantly be reduced, which increases the indications for the anterior approach instable thoracolumbar fractures.

Sasso et al. [103] retrospectively analyzed 40 patients with unstable thoraco-lumbar injuries that were operated on between 1992 and 1998. The study wasconducted to evaluate the efficacy of stand-alone anterior decompression andreconstruction of unstable three-column thoracolumbar injuries, utilizing cur-rent-generation anterior spinal instrumentation. According to the AO classifica-tion, there were 24 (60%) Type B1.2, 10 (25%) Type B2.3, 5 (12.5%) Type C1.3,and 1 (2.5%) Type C2.1 injuries. One early construct failure due to technicalerror is reported. Thirty-seven of the remaining patients (95%) went on to

Selected Type B and C

fractures can be treated

with an anterior approach

alone when using rigid

angle-stable anterior

fixation

apparently stable arthrodesis. The authors conclude that current types of ante-rior spinal instrumentation and reconstruction techniques can allow some typesof unstable three-column thoracolumbar injuries to be treated in an anteriorstand-alone fashion. This allows direct anterior decompression of neural ele-ments, improvement in segmental angulation, and acceptable fusion rates with-out the need for supplemental posterior instrumentation.

Minimally Invasive Approach

Conventional surgical approaches for the treatment of thoracic and thoraco-lumbar fractures require extensive exposure and often lead to significant post-operative pain and morbidity. In order to reduce the collateral damage created

Access technology has

contributed to minimizing

collateral damage by the

anterior approach

by the large surgical access, lesser and minimally invasive methods have beendeveloped (Case Study 3). The use of a retractor system such as SynFrameallows the anterior spine to be accessed in an open but minimally invasive way.In an analysis of the first 65 patients, Kossmann et al. [72] reported no intra- orpostoperative complications related to this minimally invasive procedure. Inaddition, no intercostal neuralgia, no post-thoracotomy pain syndromes, nosuperficial or deep wound infections and no deep venous thromboses oc-curred.


a b c d

e f g h

Case Study 3

This 48-year-old female fell from a horse and presented with an incomplete burst fracture of L2 (Type A3.1) withoutneurological deficits (ASIA E). The MRI scan (a, b) was performed to evaluate the integrity of the dorsal elements. Thecoronal view (a) shows the T1 sequence and demonstrates a cranial fracture of L2 and a rupture of the disc L1/L2. TheSTIR sequence (b), which is very sensitive to edema, confirms the fracture of the vertebral body but does not show anyevidence of a posterior injury. This allows the distinction between a Type A injury and an unstable Type B injury andhelped us to choose the operative approach. We performed a monosegmental anterior stabilization with an expand-able cage (Stryker) and an angular stable implant (MACS), which was especially designed for the thoracoscopic tech-nique (c, d). After a small diaphragmatic split, one of the first steps is the positioning of a K-wire just above the endplateof L2 (c); in this figure, the retractor (left), the suctioning device (middle) and the aiming device for the K-wire (right) canbe distinguished. The polyaxial screws are inserted under fluoroscopic control, the ruptured disc and the cranial part ofthe fractured vertebral body are removed, and the cage is inserted (d). The postoperative control radiographs (e–g)demonstrate a correct positioning of the screws in the anteroposterior view (e) and lateral view (f ); in addition, the localbone transplant on the right side of the cage is seen in e. The conventional X-rays (g, h) demonstrate a physiologic align-ment and a correct positioning of the implants.

Minimally invasive anterior

access technologies offer

perioperative advantages

Thoracoscopic spinal surgery is another technique that reduces the morbidity ofextensive surgical approaches while it still achieves the primary goals of spinaldecompression, reconstruction, and stabilization. Since the development of spe-cially designed instruments and implants, the “pure” thoracoscopic operationtechnique has become possible and feasible. Through the transdiaphragmaticapproach it was also possible to open up the thoracolumbar junction, includingthe retroperitoneal segments of the spine, to the endoscopic technique. In anearly series, Bühren et al. [19] analyzed 38 patients. The authors conclude that,compared to the open method, minimally invasive surgery had the benefit ofreducing postoperative pain, shortening hospitalization, leading to early recov-ery of function and reducing the morbidity of the operative approach. Thesefindings have been confirmed in later reports [8, 9, 62]. The rate of severe compli-cations was low (1.3%), with one case each of aortic injury, splenic contusion,neurological deterioration, cerebrospinal fluid leak, and severe wound infection[62]. Overall, the complication rate was not increased when compared to the


open technique; however, there were clear advantages in terms of the reducedaccess morbidity.

Importantly, the endoscopic technique is also effective for anterior spinalcanal decompression. Beisse et al. [8] published a series of 30 patients with thora-columbar canal compromise that underwent endoscopic anterior spinal canaldecompression and report that 25% of patients with complete paraplegia and65% of those with incomplete neurological deficit improved neurologically.

The following factors have gradually opened up the entire spectrum of ante-rior spine surgery to endoscopic techniques [9]:

) a standardized operating technique) instruments and implants specially developed for the endoscopic procedure,

i.e.:) angle-stable plate and screw implants and) endoscopically implantable vertebral body replacements

Combined Anterior-Posterior Approach

Studies on posterior stabilization of thoracolumbar fractures demonstrated thatfractures with comminution of the anterior column often lead to early failure[85]. Therefore, in addition to the posterior two-level repositioning and stabili-zation, several techniques were introduced to stabilize the anterior column: iliacanterior crest [41], possibly in an inlay technique [71] or with vertebral bodyreplacements in different materials, shapes, sizes, and configurations (i.e., non-expandable vs. expandable cages). In our institution, we prefer to adhere to atwo-staged procedure that includes (Case Introduction):

) Stage 1: posterior fracture reduction and usually a two-level stabilization (w/o decompression depending on neural compromise)) Stage 2: delayed anterior surgery depending on the patients’ condition

Many peers recommend

a combined posterior/

anterior approach

for unstable fractures

It is evident that, although posterior reduction and stabilization provides effec-tive restoration of the sagittal alignment, the reduction capability of the intraca-nal bone fragments is distinctly limited [50, 107, 123]. The anterior reconstruc-tion method permits effective decompression of the spinal canal and offers supe-rior mechanical stability compared with the indirect decompression and stabili-zation of posterior instrumentation.

Treatment Guidelines

Most treatment recommen-

dations are not based

on scientific evidence

The conflicting results and the diversity of studies presented in this chapter indi-cate that there is no gold standard for the vast majority of fractures and treatmentdecisions are almost always lacking scientific evidence. Treatment options areoften based on the experience and the tradition of the institute and the treatingphysicians. Importantly, the patient and the treating team must be aware of theattainable results, the time course of the treatment, the pitfalls, and the complica-tion of the respective method, be it conservative or operative. Under these limita-

Critically evaluate anecdotal

treatment recommen-

dations before adaptation

tions, we have summarized some general guidelines (Fig. 9). However, we want toemphasize that these general recommendations may not apply to the individualcase and confounding variables have to be considered, e.g., general condition,injury pattern, polytrauma, age, associated diseases, etc.

Type A1 fractures are usually treated conservatively. However, if kyphosisbecomes relevant (more than 20°–25°) an operative correction of the kyphosishas to be considered. In this case, we advocate an early correction, i.e., when thefracture is not consolidated and still can be reduced to avoid more complex anddifficult correction surgery in a later stage. Also Type A2 fractures can be treated


Figure 9. General treatment guidelines1 Corpectomy, interbody fusion with strut graft/cage, anterior instrumentation2 Two-level instrumentation, reduction, posterolateral fusion (optional with one-level fusion and posterior implant

removal after 10 – 12 months to liberate the uninjured segment)3 One-level stabilization and fusion possible in cases of monosegmental lesions (incomplete burst fractures, anterior disc

disruption)4 Additional anterior approach (corpectomy w/o decompression, interbody fusion with strut graft/cage) is indicated in

cases of persistent neural compression (incomplete canal clearance) or comminuted anterior column or to enhancefusion in discoligamentous injuries

5 One-level stabilization and fusion possible in cases of discoligamentous injuries or concomitant incomplete burst frac-tures

6 Multilevel stabilization often required (two or three levels above/below the injury)

Pincer fractures are prone

to non-union and are better

treated surgically

conservatively with the exception of A2.3 type fractures, the so-called “pincer”type. In this fracture type, both discs are usually ruptured and pushed into thefractured vertebral body. This injury pattern often leads to non-union andresults in painful instability. From a pathophysiological and biomechanical view,an anterior approach makes most sense in these A2.3 fractures, because thepathology is treated where the pathology is located. Probably the most contro-versy exists in A3 type fractures particularly the incomplete burst fracture

Type A3.1 fractures are the

most controversial ones

regarding treatment

recommendations

(A3.1). In this fracture type, the accepted treatments range from bracing to com-bined anterior/posterior approach all with acceptable results (Case Studies 2, 3).The treatment options depend on the comminution of the vertebral body, thedegree of kyphosis, and the presence or absence of neurology. If one decides tostabilize A3 fractures, the goal of neural decompression, sagittal alignment, andanterior support will dictate the operative approach. In an emergency situation,a primarily posterior approach will allow to reduce and stabilize the fracture withan internal fixator with or without laminectomy to decompress neural structure(Case Introduction). At a later stage, the surgeon can decide if an additional ante-rior approach is needed, based on the persistence of neurological compressionand the comminution of the anterior column. A CT scan after the postoperative


approach is often helpful for decision making. Alternatively, an anteriorapproach only with corpectomy, interbody fusion with strut graft/cage, andanterior instrumentation will provide an appropriate stabilization (see CaseStudy 3).

The paradigm of a primarily posterior approach with or without an additionalanterior operation is also true for Type B and Type C fractures. One exception isthe purely osseous “Chance” fracture, because fractured bones heal better andfaster than ligamentous injuries. In this case, a thoracolumbar cast fixation thatprevents flexion/distraction movements of the injured segment is applied for6–8 weeks. Alternatively, one might also prefer to treat Chance fractures with anoperative stabilization and restore the ruptured tension band with a posteriorbisegmental stabilization without posterolateral fusion. Removal of the hardwareis then usually performed after 4 months. In B-type fractures, posterior stabiliza-tion is usually performed with a two-level instrumentation, reduction, and pos-terolateral fusion or optionally with a one-level fusion and posterior implant

The indication for an addi-

tional anterior approach

depends on neurological

compromise and anterior

column comminution

removal after 10–12 months to liberate the uninjured segment. Alternatively,two-level stabilization and fusion is possible in Type B cases with discoligamen-tous injuries or concomitant complete burst fractures. The decision whether anadditional anterior support is necessary or not depends on the persistence ofneural compression (incomplete canal clearance) or the comminution of theanterior column or the need to enhance arthrodeses by adding an interbody

Type C injuries are very

unstable and commonly

require multisegmental

fixation

fusion. In Type C injuries, multilevel stabilization is often required (two or threelevels above/below the injury) for reduction and stabilization. Additional ante-rior surgery again depends on canal clearance and anterior column reconstruc-tion.

Outcome of Operative Versus Non-operative Treatment

Despite many theoretical advantages of operative spinal fracture treatment, thereis a lack of scientific evidence which supports the benefits of surgery (Table 9).Many studies were not able to prove a substantial difference in functional out-come between the operative and non-operative treatment, regardless of the neu-rological injury [16, 17, 20, 73, 87, 92, 105, 116, 121]. Chow et al. [23] retrospec-tively reviewed 24 neurologically healthy patients (mean follow-up of 34 months)with unstable thoracolumbar burst fractures (T11–L2) managed with either cast-ing or bracing and early ambulation. Clinical follow-up examination was per-formed by the use of a questionnaire in which the patients were asked to rate theirpain, ability to work, ability to perform in recreational activities, and their over-all satisfaction with treatment. Kyphotic deformity could be corrected withhyperextension casting but tended to recur during the course of mobilization andhealing, as hypothesized by Magnus [82] and confirmed by other studies [96,111]. No correlation was found between kyphosis and clinical outcome. At finalfollow-up evaluation, 79% had little or no pain; 75% had returned to work; 75%stated that they had few or no restrictions in their ability to work; and 67% statedthat they had few or no restrictions in their ability to participate in recreational

Favorable outcome has

been reported with conser-

vative as well as operative

treatment when applying

the correct technique

activities. Only one patient (4%) reported being dissatisfied with the initial non-operative treatment of his spine fracture. The authors conclude that non-opera-tive management of thoracolumbar burst fractures with hyperextension castingor bracing is a safe and effective method of treatment in selected patients.

In the series of Daniaux et al. [27], 85% of patients with a thoracolumbar frac-ture were treated conservatively. In 40%, a functional treatment was possible;these were patients with stable impaction and split fractures as well as burst frac-tures that were considered to be stable and that had a kyphotic deformity of lessthan 10° for T12–L2 and 15° for T11, respectively. In 45%, a repositioning and


Table 9. Operative vs. non-operative treatment



Type oftreatment


Follow-up(months)

Outcome Conclusion

BurkeandMurray(1976)[17]

115(140)

retro-spec-tive

flexion/rota-tion (80)

compressionfractures(27)

pure liga-mentousinjuries (3)

hyperexten-sion (2)

other (3)

89 non-opera-tive (posturalreduction)

26 operative(posteriorstabilization± laminec-tomy)

62 % N/A conservative:secondary spinal fusionn = 3severe chronic pain: 2

neurological improve-ment 35 %

operative:severe chronic pain n = 8Neurological improve-ment 38 %

the indication for earlysurgery might be stillfurther restricted.

Recht-ineet al.(1999)[93]

235 chartreviewforcompli-cations

unstablethoracolum-bar fractures

117 operative118 non-opera-tive 6 weeksbed rest)

N/A comparable rates ofdecubitus, deepvenous thrombosis,pulmonary emboli,and mortalitybetween both groups

8 % deep wound infec-tions after operativetreatment

shorter hospital stayafter operative treat-ment

both treatment modali-ties are viable alter-natives

Shenet al.(2001)[105]

80 pro-spec-tive

single-levelburst frac-tures T11–L2, no frac-ture disloca-tions or ped-icle fractures

47 non-opera-tive:using a hyper-

extensionbrace

33 operative:posterior fixa-tion

none 288 less pain in the surgicalgroup after 3 andmonths. Complica-tions after surgery:1 superficial infectionand 2 broken screws

hospital charges were4 times higher in theoperative group

posterior fixation pro-vides partial kyphosiscorrection and earlierpain relief. Functionaloutcome at 2 years issimilar

Woodet al.(2003)[121]

47 pro-spec-tive,ran-domi-zed

single thora-columbarburstfractures(T10–L2)

24 operative:posterior or

anteriorinstru-mentedfusion

23 non-opera-tive:

body cast ororthosis

none 44 no difference betweengroups was found interms of pain, and returnto work. Non-operativelytreated patientsreported less disability

no long-term advan-tage for operative treat-ment of burst fracturescompared with non-operative treatment

retention in a cast according to Böhler’s principles was performed. A reposition-ing was possible in 90%; however, only 50% could be maintained over the treat-ment period, 20% returned to the initial kyphotic level and 5% had a worseresult.

Reinhold et al. [95] reviewed 43 patients 16.3 years after thoracolumbar frac-ture and non-operative therapy. On average, patients showed a radiologicincrease in the kyphosis angle of 5.2° compared to the time of injury. No differ-ence was noted between early functional therapy and treatment with closedreduction and immobilization by cast. Results of validated psychometric ques-tionnaires such as SF-36 and VAS showed the characteristic pattern of a popula-tion with chronic back pain. The authors conclude that a radiologic increase inthe traumatic kyphotic deformity in patients with a non-operative treatmentprotocol has to be expected and that measurable negative physical and sociallong-term consequences can be anticipated after sustaining a Type A fracture ofthoracolumbar vertebral bodies. However, no correlation between radiologicand functional results was observed.


In an earlier report, Weinstein et al. [116] also addressed the long-term results of42 patients with non-operative treatment for fractures of the thoracolumbarspine. Average time from injury to follow-up was 20.2 years. At follow-up, theaverage back pain score was 3.5, with 0 being no pain at all and 10 being verysevere pain. No patient required narcotic medication for pain control. Eighty-eight percent of patients were able to work at their usual level of activity. Follow-up radiographs revealed an average kyphosis angle of 26.4° in flexion and 16.8° inextension. The degree of kyphosis did not correlate with pain or function at fol-low-up.

Burke et al. [17] reported in his retrospective study that 3 of 89 patients withconservative therapy required a secondary spinal fusion for suspected instabilityafter a period of conservative treatment. Frankel [44] found that 2 of 394 conser-vatively treated patients required surgery because of instability.

Braakman et al. [16] prospectively studied 70 consecutive patients with inju-ries of the thoracic and lumbar spine with a neurological deficit. The authorscould not establish a difference in neurological recovery between those patientswho were managed conservatively and those in whom a surgical decompressionand stabilization procedure was performed. Surgical stabilizing procedures,however, resulted in immediate stabilization of the spine, diminished pain, facili-tated nursing care and allowed more rapid mobilization and earlier active reha-bilitation.

Shen at al. [104] studied 38 patients after functional treatment with a follow-up of 4.1 years. Four patients had moderate pain, 2 had moderate to severe pain,and 29 (76%) were able to work at the same level. The authors conclude thatactivity restriction and bracing may be important for pain control but probablydo not change the long-term result. The same authors [105] also conducted a pro-spective trial with 80 patients to compare the results of non-operative treatment(n=47) versus short-segment posterior fixation using pedicle screws; follow-upwas 2 years. They found that posterior fixation provides partial kyphosis correc-tion and earlier pain relief, but the functional outcome at 2 years is similar.

Wood et al. [121] published a prospective, randomized study comparing oper-ative (posterior or anterior arthrodesis and instrumentation) and non-operativetreatment (application of a body cast or orthosis) of stable thoracolumbar burstfractures in 47 patients without neurological deficit. After treatment, patientsindicated the degree of pain with use of the visual analog scale and they com-pleted the Roland and Morris Disability Questionnaire, the Oswestry Back-PainQuestionnaire, and the Short Form-36 (SF-36) Health Survey. No significant dif-ference was found between the two groups with respect to return to work. Thepreinjury scores were similar for both groups; however, at the time of the finalfollow-up (on average after 44 months), those who were treated non-operativelyreported less disability. The authors conclude that operative treatment of patientswith a stable thoracolumbar burst fracture and normal findings on the neurolog-ical examination provided no major long-term advantage compared with non-operative treatment.

The superiority of surgical

fracture treatment

is not well supported

in the literature

Rechtine et al. [93] reviewed the medical charts of 235 patients with thoraco-lumbar fractures to evaluate a difference in the occurrence of complications afterconservative (118 patients) or operative treatment (117 patients). There was nosignificant difference in the occurrence of decubitus, deep venous thromboses,pulmonary emboli, or mortality between the two groups. Deep wound infectionsoccurred in 8% of the operative cases. However, the length of stay was 24 dayslonger in the non-operative group. The authors conclude that the selection oftreatment method remains a matter of controversy.


Complications

The reported complication

rate in the literature

varies largely

A surgery-related complication is a relevant shortcoming of any operative proce-dure with potentially devastating consequences, especially in spine surgery (seeChapter 39 ). The reported complication rate in the literature is largely variableand critically dependent on the pathology and type of surgery [7, 8, 19, 25, 34, 35,38, 39, 42, 62, 68, 70, 83, 102, 110, 115].

One of the largest series which considered complications in the surgical treat-ment of spinal fractures is the multicenter study of the Spine Study Group of theGerman Trauma Association (DGU). Knop et al. [69] reviewed sources of errorand specific complications [67, 65, 66]. A total of 682 patients were operated onfor acute traumatic injuries of the thoracolumbar spine. In 101 cases (15%) atleast one complication occurred intra- or postoperatively. In 41 patients (6%) arevision was performed, and in 60 patients (9%) complications without opera-tive revision were observed. Typical errors and possible complications duringoperations were related to different steps of the operation:

) positioning and closed reduction of fractures) approach) decompression of the spinal canal) instrumentation and stabilization) intervertebral fusion

Postoperative neurological

complications are rare

In addition, there are general surgical complications, which are not specific tospinal operations.

) Complications specific to the procedure that were revised included (n=40):deep infection 15 (2.2%), hematoma/wound healing disorder 12 (1.8%),instability or segmental malalignment 5 (0.7%), misplacement of screw/implant 4 (0.6%), persisting liquor fistula 2 (0.3%), sewn-in drain 1 (0.1%),arterial embolism of femoral artery 1 (0.1%).) Complications specific to the procedure that were (n= 29) not revised

included: intraoperative bleeding 10 (1.5%), iatrogenic pedicle fracture 5(0.7%), misplacement of screw/implant 3 (0.4%), instability or consecutivemalalignment 2 (0.3%), infection/healing disorder iliac crest 2 (0.3%), notspecified 2 (0.3%), iatrogenic rip fracture, approach related 1 (0.1%), iatro-genic lesion of pleura/peritoneum 1 (0.1%), narrowing of spinal canal withbone graft 1 (0.1%), fracture of iliac crest after graft harvesting 1 (0.1%),persisting liquor fistula 1 (0.1%).) Neurological complications (n= 13), revised and non-revised included:

peripheral lesion of nerve roots (0.7%), remittent neurologic deficit 4(0.6%), neurologic deterioration (Frankel/ASIA E to D) 2 (0.3%), neurologicdeterioration (Frankel/ASIA D to A) 1 (0.1%), paresthesia without neurolog-ical deficit 1 (0.1%).


Recapitulation

Epidemiology. About 60 % of thoracic and lumbarspine fractures are located at the transition T11–L2,30 % in the thoracic spine and 10 % in the lowerlumbar spine. Spinal cord injury occurs in about10 – 30 % of traumatic spinal fractures.

Pathogenesis. The most relevant forces that pro-duce structural damage to the spine are axial com-pression, flexion/distraction, hyperextension, rota-tion, and shear. Axial load may result in a burst frac-ture; the posterior elements are usually intact. Inflexion/distraction injuries, the posterior ligamen-tous and osseous elements fail in tension; a wedgecompression fracture of the vertebral body is oftenassociated. Hyperextension may result in ruptureof the anterior ligament and the disc as well as incompression injuries of the posterior elements, i.e.,fracture of the facets, the laminae, or the spinousprocesses. Rotational injuries combine compres-sive forces and flexion/distraction mechanisms andare highly unstable injuries. Shear forces producesevere ligamentous disruption and usually result incomplete spinal cord injury.

Clinical presentation. In the case of a polytrauma,about 30 % of the patients have a spinal injury. Theneurological examination has to include the“search for a sacral sparing” which determines thecompleteness of the deficit and the prognosis.About one-third of all spinal injuries have concomi-tant injuries; the most frequent are: head injuries,chest injuries and long bone injuries. The historyshould include the type of trauma (high vs. low en-ergy injuries) and the time course of a possible neu-rological deficit. The initial focus of the physical ex-amination is on the assessment of vital functionsand neurological deficits. Because the spinal cordusually terminates at the level of L1, injuries to thethoracolumbar junction may result in various neu-rological symptoms: e.g., complete/incompleteparaplegia (distal spinal cord), malfunction of thevegetative system (conus medullaris), or caudaequina syndrome.

Diagnostic work-up. Static imaging studies are“snapshots in time” and do not reveal the real de-gree of spinal canal compromise that may havehappened during the injury. A posterior cortical dis-ruption seen in the lateral view or an interpedicularwidening seen in the anteroposterior view sug-gests a burst fracture that should be further ana-

lyzed by CT scan. CT is the imaging study of choiceto demonstrate bony destruction. MRI is recom-mended to identify a possible cord lesion or a cordcompression in patients with neurological deficits.MRI can be helpful in determining the integrity of theposterior ligamentous structures and thereby in dif-ferentiating between a Type A and a Type B lesion.

Non-operative treatment. Management of thora-columbar and sacral spinal fractures remains a con-troversial area in modern spinal surgery. The litera-ture demonstrates a wide range of conflicting re-sults and recommendations. Unfortunately, thevast majority of clinical studies can be criticized be-cause of their retrospective design, heteroge-neous patient populations and treatment strate-gies, limited follow-up, and poorly defined out-come measures.The main advantage of non-operative treatmentof thoracolumbar fracture is the avoidance of sur-gery-related complications. According to Böhler,the time of immobilization in a cast is usually3 –5 months depending on the fracture type. Im-portantly, skillful physical therapy is paramount toachieve good results. Because thoracolumbar frac-tures are bound to return to the initial deformity,functional bracing without repositioning is an alter-native to Böhler’s concept of repositioning and sta-bilization with a cast if the initial deformity is ac-ceptable. Many studies were not able to prove asubstantial difference in functional outcome be-tween the operative and non-operative treatment,regardless of the neurological injury.

Operative treatment. There is a general trend to-wards operative treatment of unstable fracturesmostly because surgical stabilizing procedures re-sult in early mobilization, diminished pain, facilitat-ed nursing care, earlier return to work, and avoid-ance of late neurological complications. In experi-mental animal models, persistent compression ofthe spinal cord is potentially reversible from a sec-ondary injury by early decompression. Most investi-gators recommend a surgical decompression inthe setting of major neurological deficit, progres-sive neurological loss, and substantial compromiseof the spinal canal. Currently, there are no goldstandards regarding the role and timing of de-compression in acute spinal cord injury. Posteriorbisegmental reduction and stabilization is the“working horse” of the posterior approach tech-nique that allows for fracture reduction and stable


fixation. Depending on the persistence of spinalcanal compromise or comminution of the fracturedvertebral body, an additional anterior approach isneeded. Transpedicular cancellous bone graftingfor interbody fusion after posterior stabilization isnot recommended in complete or incomplete burstfractures. Only incomplete Type A burst fractureswith intact pedicles and a lower endplate should beconsidered for posterior monosegmental reduc-tion and stabilization. Compared to the openmethod, minimally invasive surgery reduces post-operative pain, shortens hospitalization, leads toearly recovery of function and reduces morbidity of

the operative approach. A combined posterior andanterior approach is used to reduce and stabilizeseverely comminuted vertebral body fractures andto decompress the spinal canal. In Type C lesionsoften multisegmental instrumentation is neededto reliably stabilize the spine.

Complications. The reported complication rate inthe literature varies largely and ranges from 3.6 % to10 %. Postoperative neurological complicationsrange from 0.1 % to 0.7 %. Only honest and accurateassessment of complications will lead to scientificand clinical progress.

Key Articles

Böhler L (1951) Die Technik der Knochenbruchbehandlung. Maudrich, ViennaLorenz Böhler was one of the first to advocate a conservative treatment with fracturereduction and retention in a cast.

Roaf R (1960) A study of the mechanics of spinal injuries. J Bone Joint Surg Br42B:810 – 23

In this article Roaf studies the biomechanics of spinal injuries and describes the results ofstudies of spinal units when subjected to forces of different magnitude and direction, i.e.,compression, flexion, extension, lateral flexion, rotation, and horizontal shear.

Denis F (1983) The three column spine and its significance in the classification of acutethoraco-lumbar spinal injuries. Spine 8:817 – 31

This article is a presentation of the concept of the three-column spine. The conceptevolved from a retrospective review of 412 thoracolumbar spine injuries and observa-tions on spinal instability. The posterior column consists of what Holdsworth describedas the posterior ligamentous complex. The middle column includes the posterior longitu-dinal ligament, posterior anulus fibrosus, and posterior wall of the vertebral body. Theanterior column consists of the anterior vertebral body, anterior anulus fibrosus, andanterior longitudinal ligament.

Dick W (1987) The “fixateur interne” as a versatile implant for spine surgery. Spine12:882 –900

This article introduced a new angle-stable fixation device which first allowed a short seg-mental reduction and fixation of fractures.

Magerl F, Aebi M, Gertzbein SD, Harms J, Nazarian S (1994) A comprehensive classifica-tion of thoracic and lumbar injuries. Eur Spine J 3:184 – 201

This article describes a classification of thoracic and lumbar injuries. As a result of morethan a decade of consideration of the subject matter and a review of 1445 consecutive tho-racolumbar injuries, a comprehensive classification of thoracic and lumbar injuries isproposed. The classification is primarily based on pathomorphological criteria. Threemechanisms classify the injury pattern according to the AO classification: axial compres-sion (Type A), flexion distraction (Type B) and rotational/shear injuries (Type C).

Kaneda K, Taneichi H, Abumi K, Hashimoto T, Satoh S, Fujiya M (1997) Anterior decom-pression and stabilization with the Kaneda device for thoracolumbar burst fracturesassociated with neurological deficits. J Bone Joint Surg Am 79:69 – 83

One hundred and fifty consecutive patients who had a burst fracture of the thoracolum-bar spine and associated neurological deficits were managed with a single-stage anteriorspinal decompression, strut-grafting, and Kaneda spinal instrumentation. The authorsconclude that anterior decompression, strut-grafting, and fixation with the Kaneda


device in patients who had a burst fracture of the thoracolumbar spine and associatedneurological deficits yielded good radiographic and functional results. This article estab-lished the single stage anterior approach for this fracture type.

Knop C, Blauth M, Bühren V, Hax PM, Kinzl L, Mutschler W, Pommer A, Ulrich C, Wag-ner S, Weckbach A, Wentzensen A, Wörsdörfer O (1999) Surgical treatment of injuries ofthe thoracolumbar transition. 1: Epidemiology. Unfallchirurg 102:924 – 35

Knop C, Blauth M, Bühren V, Hax PM, Kinzl L, Mutschler W, Pommer A, Ulrich C, Wag-ner S, Weckbach A, Wentzensen A, Wörsdörfer O (2000) Surgical treatment of injuries ofthe thoracolumbar transition. 2: Operation and roentgenologic findings. Unfallchirurg103:1032 – 47

Knop C, Blauth M, Bühren V, Arand M, Egbers HJ, Hax PM, Nothwang J, Oestern HJ,Pizanis A, Roth R, Weckbach A, Wentzensen A (2001) Surgical treatment of injuries ofthe thoracolumbar transition – 3: Follow-up examination. Results of a prospective mul-ti-center study by the “Spinal” Study Group of the German Society of Trauma Surgery.Unfallchirurg 104:583 – 600

These three reports summarize the experience based on 682 patients included in a pro-spective multicenter study by the “Spinal” Study Group of the German Society of TraumaSurgery. All treatment methods under study were appropriate for achieving comparableclinical and functional outcome. The internal fixator was found superior in restoration ofthe spinal alignment. Best radiological outcomes were achieved by combined stabiliza-tion. Merely by direct reconstruction of the anterior column the postoperative re-kypho-sing is prevented and a gain in segmental angle is achieved. However, this benefit was notreflected in the clinical outcome.

Fehlings MG, Perrin RG (2005) The role and timing of early decompression for cervicalspinal cord injury: Update with a review of recent clinical evidence. Injury S-B13–S-B26

Evidence-based recommendations regarding spinal cord decompression in patients withacute spinal cord injury.

Beisse R (2006) Endoscopic surgery on the thoracolumbar junction of the spine. EurSpine J 15:687 – 704

This article summarizes the technique and results based on a large patient group from aGerman trauma center: A now standardized operating technique, instruments andimplants specially developed for the endoscopic procedure, from angle stable plate andscrew implants to endoscopically implantable vertebral body replacements, have gradu-ally opened up the entire spectrum of anterior spine surgery to endoscopic techniques.

References

1. Alanay A, Acaroglu E, Yazici M, Oznur A, Surat A (2001) Short-segment pedicle instrumenta-tion of thoracolumbar burst fractures: does transpedicular intracorporeal grafting preventearly failure? Spine 26:213– 7

2. Anderson PA, Henley MB, Rivara FP, Maier RV (1991) Flexion distraction and chance injuriesto the thoracolumbar spine. J Orthop Trauma 5:153–60

3. Anderson PA, Rivara FP, Maier RV, Drake C (1991) The epidemiology of seatbelt-associatedinjuries. J Trauma 31:60–7

4. Anderson PA, Bohlman HH (1992) Anterior decompression and arthrodesis of the cervicalspine: long-term motor improvement. Part II – Improvement in complete traumatic quadri-plegia. J Bone Joint Surg Am 74:683– 92

5. Anderson S, Biros MH, Reardon RF (1996) Delayed diagnosis of thoracolumbar fractures inmultiple-trauma patients. Acad Emerg Med 3:832–9

6. Bagley LJ (2006) Imaging of spinal trauma. Radiol Clin North Am 44:1–12, vii7. Been HD, Bouma GJ (1999) Comparison of two types of surgery for thoraco-lumbar burst

fractures: combined anterior and posterior stabilisation vs. posterior instrumentation only.Acta Neurochir (Wien) 141:349– 57

8. Beisse R, Muckley T, Schmidt MH, Hauschild M, Buhren V (2005) Surgical technique andresults of endoscopic anterior spinal canal decompression. J Neurosurg Spine 2:128–36

9. Beisse R (2006) Endoscopic surgery on the thoracolumbar junction of the spine. Eur Spine J15:687–704


10. Bensch FV, Kiuru MJ, Koivikko MP, Koskinen SK (2004) Spine fractures in falling accidents:analysis of multidetector CT findings. Eur Radiol 14:618– 24

11. Bensch FV, Koivikko MP, Kiuru MJ, Koskinen SK (2006) The incidence and distribution ofburst fractures. Emerg Radiol 12:124– 9

12. Benson DR (1988) Unstable thoracolumbar fractures, with emphasis on the burst fracture.Clin Orthop Relat Res 14– 29

13. Blauth M, Knop C, Bastian L (1998) Wirbelsäule. In: Tscherne H, Blauth M (eds) TscherneUnfallchirurgie, vol 3. Springer, Berlin Heidelberg New York, pp 241– 381

14. Bohlman HH, Anderson PA (1992) Anterior decompression and arthrodesis of the cervicalspine: long-term motor improvement. Part I – Improvement in incomplete traumatic quad-riparesis. J Bone Joint Surg Am 74:671– 82

15. Bohlman HH, Kirkpatrick JS, Delamarter RB, Leventhal M (1994) Anterior decompressionfor late pain and paralysis after fractures of the thoracolumbar spine. Clin Orthop 24–9

16. Braakman R, Fontijne WP, Zeegers R, Steenbeek JR, Tanghe HL (1991) Neurological deficitin injuries of the thoracic and lumbar spine. A consecutive series of 70 patients. Acta Neuro-chir (Wien) 111:11–7

17. Burke DC, Murray DD (1976) The management of thoracic and thoraco-lumbar injuries ofthe spine with neurological involvement. J Bone Joint Surg Br 58:72–8

18. Böhler L (1951) Die Technik der Knochenbruchbehandlung. Maudrich Verlag, Vienna19. Bühren V, Beisse R, Potulski M (1997) [Minimally invasive ventral spondylodesis in injuries

to the thoracic and lumbar spine]. Chirurg 68:1076–8420. Cantor JB, Lebwohl NH, Garvey T, Eismont FJ (1993) Nonoperative management of stable

thoracolumbar burst fractures with early ambulation and bracing. Spine 18:971–621. Carl AL, Tromanhauser SG, Roger DJ (1992) Pedicle screw instrumentation for thoracolum-

bar burst fractures and fracture-dislocations. Spine 17:S317–2422. Chance G (1948) Note on a type of flexion fracture of the spine. Br J Radiol 21:452–323. Chow GH, Nelson BJ, Gebhard JS, Brugman JL, Brown CW, Donaldson DH (1996) Func-

tional outcome of thoracolumbar burst fractures managed with hyperextension casting orbracing and early mobilization. Spine 21:2170– 5

24. Dai L-Y, Yao W-F, Cui Y-M, Zhou Q (2004) Thoracolumbar fractures in patients with multi-ple injuries: diagnosis and treatment – a review of 147 cases. J Trauma 56:348– 55

25. Daniaux H (1986) Transpedicular repositioning and spongioplasty in fractures of the verte-bral bodies of the lower thoracic and lumbar spine. Unfallchirurg 89:197– 213

26. Daniaux H, Seykora P, Genelin A, Lang T, Kathrein A (1991) Application of posterior platingand modifications in thoracolumbar spine injuries. Indication, techniques, and results.Spine 16:S125– 33

27. Daniaux H, Wagner M, Kathrein A, Lang T (1999) [Fractures of the thoraco-lumbar junc-tion. Conservative management]. Orthopade 28:682–91

28. Defino HL, Rodriguez-Fuentes AE (1998) Treatment of fractures of the thoracolumbar spineby combined anteroposterior fixation using the Harms method. Eur Spine J 7:187–94

29. Defino HL, Scarparo P (2005) Fractures of thoracolumbar spine: monosegmental fixation.Injury 36 Suppl 2:B90– 7

30. Denis F (1983) The three column spine and its significance in the classification of acute tho-racolumbar spinal injuries. Spine 8:817– 31

31. Denis F, Armstrong GW, Searls K, Matta L (1984) Acute thoracolumbar burst fractures in theabsence of neurologic deficit. A comparison between operative and nonoperative treat-ment. Clin Orthop Relat Res 142–9

32. Denis F, Burkus JK (1992) Shear fracture-dislocations of the thoracic and lumbar spine asso-ciated with forceful hyperextension (lumberjack paraplegia). Spine 17:156–61

33. DeWald RL (1984) Burst fractures of the thoracic and lumbar spine. Clin Orthop Relat Res150– 61

34. Dick W (1987) The “fixateur interne” as a versatile implant for spine surgery. Spine 12:882– 900

35. Dickson JH, Harrington PR, Erwin WD (1978) Results of reduction and stabilization of theseverely fractured thoracic and lumbar spine. J Bone Joint Surg Am 60:799– 805

36. el-Khoury GY, Whitten CG (1993) Trauma to the upper thoracic spine: anatomy, biome-chanics, and unique imaging features. AJR Am J Roentgenol 160:95–102

37. Evans L (1988) Risk of fatality from physical trauma versus sex and age. J Trauma 28:368–7838. Eysel P, Meinig G, Sanner F (1991) Comparative study of various dorsal stabilization proce-

dures in recent fractures of the thoracic spine. Unfallchirurgie 17:264–7339. Faciszewski T, Winter RB, Lonstein JE, Denis F, Johnson L (1995) The surgical and medical

perioperative complications of anterior spinal fusion surgery in the thoracic and lumbarspine in adults. A review of 1223 procedures. Spine 20:1592–9

40. Fehlings MG, Perrin RG (2005) The role and timing of early decompression for cervical spi-nal cord injury: Update with a review of recent clinical evidence. Injury S-B13–S-B26

41. Feil J, Wörsdörfer O (1992) [Ventral stabilization in the area of the thoracic and lumbarspine]. Chirurg 63:856– 65


42. Feil J, Wörsdörfer O (1992) Complications in surgical management of spinal injuries. Lan-genbecks Arch Chir Suppl Kongressbd 304–10

43. Floman Y, Fast A, Pollack D, Yosipovitch Z, Robin GC (1986) The simultaneous applicationof an interspinous compressive wire and Harrington distraction rods in the treatment offracture-dislocation of the thoracic and lumbar spine. Clin Orthop Relat Res 207–15

44. Frankel HL, Hancock DO, Hyslop G, Melzak J, Michaelis LS, Ungar GH, Vernon JD, Walsh JJ(1969) The value of postural reduction in the initial management of closed injuries of thespine with paraplegia and tetraplegia. I. Paraplegia 7:179– 92

45. Fredrickson BE, Edwards WT, Rauschning W, Bayley JC, Yuan HA (1992) Vertebral burstfractures: an experimental, morphologic, and radiographic study. Spine 17:1012– 21

46. Gertzbein SD (1992) Fractures of the thoracic and lumbar spine. Williams & Wilkins, Balti-more

47. Gertzbein SD (1992) Scoliosis Research Society. Multicenter spine fracture study. Spine17:528–40

48. Gopalakrishnan KC, el Masri WS (1986) Fractures of the sternum associated with spinalinjury. J Bone Joint Surg Br 68:178– 81

49. Gotzen L, Puplat D, Junge A (1992) Indications, technique and results of monosegmentaldorsal spondylodesis in wedge compression fractures (grade II) of the thoracolumbar spine.Unfallchirurg 95:445–54

50. Haas N, Blauth M, Tscherne H (1991) Anterior plating in thoracolumbar spine injuries. Indi-cation, technique, and results. Spine 16:S100– 11

51. Harrington RM, Budorick T, Hoyt J, Anderson PA, Tencer AF (1993) Biomechanics of indi-rect reduction of bone retropulsed into the spinal canal in vertebral fracture. Spine18:692–9

52. Hauser CJ, Visvikis G, Hinrichs C, Eber CD, Cho K, Lavery RF, Livingston DH (2003) Pro-spective validation of computed tomographic screening of the thoracolumbar spine intrauma. J Trauma 55:228–34; discussion 34–5

53. Henderson RL, Reid DC, Saboe LA (1991) Multiple noncontiguous spine fractures. Spine16:128–31

54. Holdsworth F (1963) Fractures, dislocations, and fracture-dislocations of the spine. J BoneJoint Surg Am 45:6– 20

55. Holdsworth F (1970) Fractures, dislocations, and fracture-dislocations of the spine. J BoneJoint Surg Am 52:1534–51

56. Hu R, Mustard CA, Burns C (1996) Epidemiology of incident spinal fracture in a completepopulation. Spine 21:492– 9

57. Inaba K, Munera F, McKenney M, Schulman C, de Moya M, Rivas L, Pearce A, Cohn S (2006)Visceral torso computed tomography for clearance of the thoracolumbar spine in trauma: areview of the literature. J Trauma 60:915–20

58. Jahna H, Wittich H (1985) Konservative Methoden in der Frakturbehandlung. Urban &Fischer, Vienna, pp 121–38

59. Junge A, Gotzen L, von Garrel T, Ziring E, Giannadakis K (1997) [Monosegmental internalfixator instrumentation and fusion in treatment of fractures of the thoracolumbar spine.Indications, technique and results]. Unfallchirurg 100:880–7

60. Kaneda K, Taneichi H, Abumi K, Hashimoto T, Satoh S, Fujiya M (1997) Anterior decom-pression and stabilization with the Kaneda device for thoracolumbar burst fractures associ-ated with neurological deficits. J Bone Joint Surg Am 79:69– 83

61. Kelly RP, Whitesides TE (1968) Treatment of lumbodorsal fracture-dislocations. Ann Surg167:705– 17

62. Khoo LT, Beisse R, Potulski M (2002) Thoracoscopic-assisted treatment of thoracic andlumbar fractures: a series of 371 consecutive cases. Neurosurgery 51:104–17

63. Kim DH, Silber JS, Albert TJ (2003) Osteoporotic vertebral compression fractures. InstrCourse Lect 52:541–50

64. King AG (1987) Burst compression fractures of the thoracolumbar spine. Pathologic anat-omy and surgical management. Orthopedics 10:1711–9

65. Knop C, Blauth M, Bühren V, Hax PM, Kinzl L, Mutschler W, Pommer A, Ulrich C, WagnerS, Weckbach A, Wentzensen A, Wörsdörfer O (1999) Surgical treatment of injuries of thethoracolumbar transition. 1: Epidemiology. Unfallchirurg 102:924– 35

66. Knop C, Blauth M, Bühren V, Hax PM, Kinzl L, Mutschler W, Pommer A, Ulrich C, Wagner S,Weckbach A, Wentzensen A, Wörsdörfer O (2000) Surgical treatment of injuries of the thora-columbar transition. 2: Operation and roentgenologic findings. Unfallchirurg 103:1032 –47

67. Knop C, Blauth M, Bühren V, Arand M, Egbers HJ, Hax PM, Nothwang J, Oestern HJ, PizanisA, Roth R, Weckbach A, Wentzensen A (2001) Surgical treatment of injuries of the thoraco-lumbar transition – 3: Follow-up examination. Results of a prospective multi-center studyby the “Spinal” Study Group of the German Society of Trauma Surgery. Unfallchirurg104:583– 600

68. Knop C, Fabian HF, Bastian L, Blauth M (2001) Late results of thoracolumbar fractures afterposterior instrumentation and transpedicular bone grafting. Spine 26:88– 99


69. Knop C, Bastian L, Lange U, Oeser M, Zdichavsky M, Blauth M (2002) Complications in sur-gical treatment of thoracolumbar injuries. Eur Spine J 11:214– 26

70. Knop C, Fabian HF, Bastian L, Rosenthal H, Lange U, Zdichavsky M, Blauth M (2002) Fate ofthe transpedicular intervertebral bone graft after posterior stabilisation of thoracolumbarfractures. Eur Spine J 11:251–7

71. Kossmann T, Ertel W, Platz A, Trentz O (1999) [Combined surgery for fractures of the tho-raco-lumbar junction using the inlay-span method]. Orthopade 28:432– 40

72. Kossmann T, Jacobi D, Trentz O (2001) The use of a retractor system (SynFrame) for open,minimal invasive reconstruction of the anterior column of the thoracic and lumbar spine.Eur Spine J 10:396– 402

73. Kraemer WJ, Schemitsch EH, Lever J, McBroom RJ, McKee MD, Waddell JP (1996) Func-tional outcome of thoracolumbar burst fractures without neurological deficit. J OrthopTrauma 10:541– 4

74. Krueger MA, Green DA, Hoyt D, Garfin SR (1996) Overlooked spine injuries associated withlumbar transverse process fractures. Clin Orthop 191– 5

75. La Rosa G, Conti A, Cardali S, Cacciola F, Tomasello F (2004) Does early decompressionimprove neurological outcome of spinal cord injured patients? Appraisal of the literatureusing a meta-analytical approach. Spinal Cord 42:503– 12

76. Larson SJ, Holst RA, Hemmy DC, Sances A (1976) Lateral extracavitary approach to trau-matic lesions of the thoracic and lumbar spine. J Neurosurg 45:628–37

77. Leidner B, Adiels M, Aspelin P, Gullstrand P, Wallen S (1998) Standardized CT examinationof the multitraumatized patient. Eur Radiol 8:1630– 8

78. Lindsey RW, Dick W (1991) The fixateur interne in the reduction and stabilization of thora-columbar spine fractures in patients with neurologic deficit. Spine 16:S140–5

79. Louis R (1977) Unstable fractures of the spine. III. Instability. A. Theories concerning insta-bility. Rev Chir Orthop Reparatrice Appar Mot 63:423–5

80. Magerl F, Aebi M, Gertzbein SD, Harms J, Nazarian S (1994) A comprehensive classificationof thoracic and lumbar injuries. Eur Spine J 3:184–201

81. Magerl F, Engelhardt P (1994) Brust- und Lendenwirbelsäule – Verlaufsformen. In: Witt AN,Rettig H, Schlegel KF (eds) Orthopädie in Praxis und Klinik, Spezielle Orthopädie (Wirbel-säule – Thorax – Becken). Thieme, Stuttgart New York, pp 3.82– 3.132

82. Magnus G (1930) Die Begutachtung und Behandlung des Wirbelbruchs. Arch OrthopUnfallchir 29:277

83. Mayer H, Schaaf D, Kudernatsch M (1992) Use of internal fixator in injuries of the thoracicand lumbar spine. Chirurg 63:944– 9

84. Maynard FM, Jr, Bracken MB, Creasey G, Ditunno JF, Jr, Donovan WH, Ducker TB, GarberSL, Marino RJ, Stover SL, Tator CH, Waters RL, Wilberger JE, Young W (1997) InternationalStandards for Neurological and Functional Classification of Spinal Cord Injury. AmericanSpinal Injury Association. Spinal Cord 35:266– 74

85. McLain RF, Sparling E, Benson DR (1993) Early failure of short-segment pedicle instrumen-tation for thoracolumbar fractures. A preliminary report. J Bone Joint Surg Am 75:162– 7

86. Meyer PR, Heim S (1989) Fractures of the thoracic spine T1–T10. In: Meyer PR (ed) Surgeryof spine trauma. Churchill Livingstone, Edinburgh, pp 525– 72

87. Mumford J, Weinstein JN, Spratt KF, Goel VK (1993) Thoracolumbar burst fractures. Theclinical efficacy and outcome of nonoperative management. Spine 18:955– 70

88. Müller U, Berlemann U, Sledge J, Schwarzenbach O (1999) Treatment of thoracolumbarburst fractures without neurologic deficit by indirect reduction and posterior instrumenta-tion: bisegmental stabilization with monosegmental fusion. Eur Spine J 8:284–9

89. Nicoll EA (1949) Fractures of the dorso-lumbar spine. J Bone Joint Surg Br 31:376–9490. Olerud S, Karlstrom G, Sjostrom L (1988) Transpedicular fixation of thoracolumbar verte-

bral fractures. Clin Orthop Relat Res 227:44–5191. Place HM, Donaldson DH, Brown CW, Stringer EA (1994) Stabilization of thoracic spine

fractures resulting in complete paraplegia. A long-term retrospective analysis. Spine19:1726– 30

92. Rechtine GR (1999) Nonsurgical treatment of thoracic and lumbar fractures. Instr CourseLect 48:413– 6

93. Rechtine GR, 2nd, Cahill D, Chrin AM (1999) Treatment of thoracolumbar trauma: compar-ison of complications of operative versus nonoperative treatment. J Spinal Disord 12:406– 9

94. Reid DC, Hu R, Davis LA, Saboe LA (1988) The nonoperative treatment of burst fractures ofthe thoracolumbar junction. J Trauma 28:1188–94

95. Reinhold M, Knop C, Lange U, Bastian L, Blauth M (2003) Non-operative treatment of tho-racolumbar spinal fractures. Long-term clinical results over 16 years. Unfallchirurg 106:566– 76

96. Resch H, Rabl M, Klampfer H, Ritter E, Povacz P (2000) Surgical vs. conservative treatmentof fractures of the thoracolumbar transition. Unfallchirurg 103:281–8

97. Richards PJ (2005) Cervical spine clearance: a review. Injury 36:248– 6998. Roaf R (1960) A study of the mechanics of spinal injuries. J Bone Joint Surg Br 42B:810– 23


99. Roy-Camille R, Saillant G (1984) Spinal injuries without neurologic complications. IntOrthop 8:155–62

100. Saboe LA, Reid DC, Davis LA, Warren SA, Grace MG (1991) Spine trauma and associatedinjuries. J Trauma 31:43– 8

101. Samuels LE, Kerstein MD (1993) ’Routine’ radiologic evaluation of the thoracolumbarspine in blunt trauma patients: a reappraisal. J Trauma 34:85– 9

102. Sasso RC, Cotler HB (1993) Posterior instrumentation and fusion for unstable fracturesand fracture-dislocations of the thoracic and lumbar spine. A comparative study of threefixation devices in 70 patients. Spine 18:450–60

103. Sasso RC, Best NM, Reilly TM, McGuire RA (2005) Anterior-only stabilization of three-col-umn thoracolumbar injuries. J Spinal Disord Tech 18 Suppl:S7–14

104. Shen WJ, Shen YS (1999) Nonsurgical treatment of three-column thoracolumbar junctionburst fractures without neurologic deficit. Spine 24:412– 5

105. Shen WJ, Liu TJ, Shen YS (2001) Nonoperative treatment versus posterior fixation for tho-racolumbar junction burst fractures without neurologic deficit. Spine 26:1038– 45

106. Sheridan R, Peralta R, Rhea J, Ptak T, Novelline R (2003) Reformatted visceral protocolhelical computed tomographic scanning allows conventional radiographs of the thoracicand lumbar spine to be eliminated in the evaluation of blunt trauma patients. J Trauma55:665– 9

107. Shono Y, McAfee PC, Cunningham BW (1994) Experimental study of thoracolumbar burstfractures. A radiographic and biomechanical analysis of anterior and posterior instru-mentation systems. Spine 19:1711– 22

108. Speth MJ, Oner FC, Kadic MA, de Klerk LW, Verbout AJ (1995) Recurrent kyphosis afterposterior stabilization of thoracolumbar fractures. 24 cases treated with a Dick internalfixator followed for 1.5–4 years. Acta Orthop Scand 66:406–10

109. Spitz J, Becker C, Tittel K, Weigand H (1992) [Clinical relevance of whole body skeletalscintigraphy in multiple injury and polytrauma patients]. Unfallchirurgie 18:133–47

110. Spivak JM, Neuwirth MG, Giordano CP, Bloom N (1994) The perioperative course of com-bined anterior and posterior spinal fusion. Spine 19:520– 5

111. Steindl A, Schuh G (1992) Late results after lumbar vertebrae fracture with Lorenz Böhlerconservative treatment. Unfallchirurg 95:439–44

112. Transfeldt EE, White D, Bradford DS, Roche B (1990) Delayed anterior decompression inpatients with spinal cord and cauda equina injuries of the thoracolumbar spine. Spine15:953– 7

113. 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 spinalcord injury. Spine 22:2609– 13

114. Vaccaro AR, Kim DH, Brodke DS, Harris M, Chapman JR, Schildhauer T, Routt ML, SassoRC (2004) Diagnosis and management of thoracolumbar spine fractures. Instr Course Lect53:359– 73

115. Wawro W, Konrad L, Aebi M (1994) Single segment internal fixator device in treatment ofthoracolumbar vertebral fractures. Unfallchirurg 97:114– 20

116. Weinstein JN, Collalto P, Lehmann TR (1988) Thoracolumbar “burst” fractures treatedconservatively: a long-term follow-up. Spine 13:33–8

117. Weitzman G (1971) Treatment of stable thoracolumbar spine compression fractures byearly ambulation. Clin Orthop 76:116– 22

118. White AA, 3rd, Panjabi MM (1978) The basic kinematics of the human spine. A review ofpast and current knowledge. Spine 3:12–20

119. Whitesides TE (1977) Traumatic kyphosis of the thoracolumbar spine. Clin Orthop 78–92120. Woltmann A, Bühren V (2004) Emergency room management of the multiply injured

patient with spine injuries. A systematic review of the literature. Unfallchirurg 107:911–9121. Wood K, Butterman G, Mehbod A, Garvey T, Jhanjee R, Sechriest V (2003) Operative com-

pared with nonoperative treatment of a thoracolumbar burst fracture without neurologi-cal deficit. A prospective, randomized study. J Bone Joint Surg Am 85-A:773–81

122. Wood KB, Bohn D, Mehbod A (2005) Anterior versus posterior treatment of stable thora-columbar burst fractures without neurologic deficit: a prospective, randomized study. JSpinal Disord Tech 18 Suppl:S15– 23

123. Young B, Brooks WH, Tibbs PA (1981) Anterior decompression and fusion for thoracolum-bar fractures with neurological deficits. Acta Neurochir (Wien) 57:287–98


33Primary Tumors of the Spine

Bruno Fuchs, Norbert Boos

Core Messages

✔ Primary spine tumors are relatively rare✔ Cancer is a genetic disease✔ The acquired capabilities of cancer are: self-suf-

ficiency to growth signals, insensitivity to anti-growth signals, tissue invasion and metastasis,limitless replicative potential, sustained angio-genesis, evading apoptosis

✔ Spine tumors are classified based on the histol-ogy

✔ Pain, spinal deformity, and neurologic deficitsfrequently are presenting symptoms

✔ Age and location are important parameters forestablishing a differential diagnosis

✔ CT and MRI are essential for systemic and surgi-cal staging

✔ Biopsy is required to establish the tissue diagnosis

✔ The biopsy has to be placed so that it does notcompromise subsequent surgical resection

✔ Do not rely completely on the result of thebiopsy – the final histology may be different

✔ The “wait and see” approach is very rarely indi-cated

✔ Conservative treatment is only indicated forbenign tumors and in asymptomatic patients

✔ Malignant tumors in general are treated surgi-cally

✔ In sensitive tumors, chemo- and radiotherapy areconsidered as an adjuvant treatment

✔ The goal of surgery is to remove the primarytumor in its entirety followed by stable recon-struction of the spine

Epidemiology

Primary spinal tumors are

rare

Approximately 2000 new cases of bone cancer and 6000 new cases of soft tissuetumor are diagnosed in the United States each year [30]. Of these, only about 5%involve the spine. The incidence of primary spinal tumors has been estimated at2.5–8.5 per 100000 people per year [15]. Tumors of the lymphoid system, e.g.,

Plasmocytomas are tumors

of the lymphoreticular

system

plasmocytoma, are generally considered in the discussion of spine tumorsalthough they are tumors of the lymphoreticular system. Some bone tumorshave a special predilection for the vertebral column (e.g., osteoblastoma), whileothers occur exclusively in the spine (e.g., chordoma). There are two importantclinical features to be considered when evaluating the potential of malignancy ofa spine lesion, i.e.:

) age) location

In children younger than 6 years of age, most spinal tumors are malignant, e.g.:

) neuroblastoma) astrocytoma) sarcoma (less commonly)

However, benign spinal tumors outnumber malignant tumors by a ratio of 2 :1among children of all ages.

Tumors and Inflammation Section 951

a b

c

d e

Case Introduction

A 20-year-old girl presented with severe intermittent dorsal pain with occasional radiation into the ribcage. The patientwas unsuccessfully treated with physiotherapy. The pain got progressively worse particularly during the night; she wasthen referred for further evaluation. Standard radiographs of the thoracic spine were unremarkable although it wasnoted that she had a significant shift to the left side (a). The patient noticed a decrease of symptoms when she tookNSAIDs. An MRI scan demonstrated increased signal intensity in the posterior elements of T7 on the left side (b, c). Thebone scan showed increased uptake in that region (d). A CT scan showed the typical features of an osteoidosteoma witha hypodense lesion with a nidus (e). The lamina was exposed for an excision biopsy. However, since the nidus was clearlyvisible it was decided to remove it by curettage. The bed of the nidus was cleaned with a high-speed air drill. The patient’ssymptoms completely disappeared after the operation and she remained painfree during follow-up.

In adults older than 35 years, most spinal tumors are:

) metastatic adenocarcinoma) multiple myeloma) osteosarcoma

Spinal tumors exhibit

a specific anatomic

predilection

Spinal tumors demonstrate a specific anatomic predilection. Osseous tumors ofthe anterior vertebral body are most likely metastatic lesions, multiple myeloma,histiocytosis, chordoma, and hemangioma. The most common osseous spinaltumors involving the posterior elements are:

) aneurysmal bone cysts) osteoblastoma) osteoid osteoma

952 Section Tumors and Inflammation

Age and tumor location

help to classify tumor lesion

Malignant osseous tumors occur much more commonly in the anterior than theposterior spinal elements.

Tumor Biology

Molecular Tumor Biology

Recent advances in basic research of musculoskeletal tumors revealed that thesheer complexity of the molecular process of carcinogenesis may be conceptu-ally reduced to a small number of molecular, biochemical, and cellular traitsthat are shared by most if not all types of human cancer. Hanahan and Wein-berg [25] described the hallmarks of cancer which represent a fundamentalconcept that governs the development of malignant transformation. It ishypothesized that a developing cancer may represent the interplay betweenthese fundamental concepts. The acquired capabilities of malignant tumors areshown in Fig. 1.

Whenever a cell divides, the telomeres (i.e., ends of chromosomes) shortenuntil a point of no return and the cell then dies. Cancer cells can switch on a pro-tein component of telomerase that allows them to maintain their telomeres andto divide indefinitely. The normal cell has a built-in cellular program to die orundergo apoptosis, respectively. For a cancer cell to become immortal, it needs toescape apoptosis. A malignant cell needs to have the capacity to mimic extracel-lular growth signals, for example by activating mutations, in order for the tumorto grow. Malignant tumors need to produce their own blood supply if they are togrow beyond a certain size. The nature of the angiogenic switch is still unclear,but endothelial cells must be recruited, grow, divide, and invade the tumor toform blood vessels. A further capacity of a malignant cell is to acquire the poten-

Figure 1. The hallmarks of cancer

According to Hanahan and Weinberg, most if not all cancers have acquired the same set of functional capabilities duringtheir development, although through various mechanistic strategies. (Redrawn from Hanahan et al. [25] with permissionfrom Elsevier).

Primary Tumors of the Spine Chapter 33 953

tial to break away from the original tumor mass, resist anoikis (apoptosis that isinduced by inadequate or inappropriate cell-matrix interactions) and crawlthrough the extracellular matrix into blood or lymphatic vessels in order to recurand survive in a distant organ.

The hallmarks represent

a concept of carcinogenesis

The hallmarks of cancer help us to understand the complexity of such a dis-ease in terms of a relatively small number of underlying molecular principles.Obviously, these hallmarks only represent a working model. An emerging para-digm is that this set of principles has a specific mechanism for each tumor typeso that each tumor bears its own molecular circuitry that needs to be character-ized individually.

Pathways of Metastasis

More than a hundred years ago, Sir Stephen Paget first launched the “seed andsoil” hypothesis, asking the question: “What is it that decides what an organ shallsuffer in case of disseminated cancer?” His answer is basically still valid today:“The microenvironment of each organ (the soil) influences the survival andgrowth of tumor cells (the seed).”

Figure 2. The metastatic cascade

The schematic drawing exemplifies the main steps in the formation of a metastasis. (Redrawn from Fidler [18] with per-mission from Macmillan Publishers Ltd.).


The process of metastatic spread of a primary tumor can be described in the fol-lowing steps (Fig. 2):

) local tumor proliferation) angiogenesis) migration and invasion) intravasation) adhesion) extravasation) migration and invasion) metastatic growth in target organ

Stem cells appear to play

a key role in metastasis

In the metastatic process, the primary tumor proliferates locally until it reachesa size when nutrition cannot be provided by diffusion alone. Neovascularizationor angiogenesis is therefore present at an early stage in a tumor. The tumor cellthen detaches from the neighboring cells and invades the surrounding normaltissue. It seeks access to the blood and/or lymphatic system (intravasation),where it gets distributed in the body until it adheres in the capillaries of the targetorgan. The metastatic tumor cell then crawls through the vessel wall (extravasa-tion) and invades the tissue of the target organ, where finally it may grow into themetastatic nodule. It is not yet entirely understood how these processes are gov-erned. Originally, it was assumed that metastasis is the clonal expansion of a pri-

Figure 3. Evolution of the cancerous bone cell

Oncogenic mutations may occur in bone stem cells (red) and can cause the transformation to a bone cancer stem cell,generating “poor-prognosis” tumors (orange). Mutations which occur in differentiated progenitor cells (yellow) may forma non-metastatic “good-prognosis” bone carcinoma (pink). Under the influence of stromal fibroblasts, only the popula-tion of bone cancer stem cells has the ability to metastasize. There might be variant cancer stem cells that differ in theirtissue selectivity for metastasis, expressing an additional tissue-specific profile (e.g., green liver, purple lung). (Redrawnand adapted to bone from Weigelt et al. [42] with permission from Macmillan Publishers Ltd.).


mary tumor cell. Microarray analyses revealed that for several cancers, theexpression profile of a primary tumor is indifferent to its metastatic site, thus incontrast to the clonal expansion theory. The current theory implies that stemcells may play an important role. The current model of metastasis synthesizes theclonal expansion theory, the expression profiles and stem cells. Oncogenic muta-tions in stem cells cause transformation, thereby generating “poor-prognosis”tumors. However, mutations occurring in differentiated progenitor cells mightform a non-metastatic good-prognosis tumor that does not metastasize. In themetastatic poor-prognosis tumors, under the influence of stromal fibroblasts,only the populations of stem cells have the ability to metastasize (Fig. 3). Theremight be variant stem cells that differ in their tissue selectivity for metastasis,expressing an additional tissue-specific profile. At the site of metastasis, the dis-seminated cancer stem cells would again induce a similar stromal response as inthe primary tumor.

Histology and Biology of Spinal Tumors

Spine tumors are classified according to their histology. Based on the age of thepatient, the anatomic location of the lesion, supplemented by modern imaging,and tumor histology, the biological behavior of the tumor can be determined(Table 1).

Table 1. Primary benign spinal tumors

Lesion Age Location Histology Imaging

Osteoidoste-oma

second decade posterior elements (75 %) vascularized connec-tive tissue, nidus sur-rounded by reactivecortical bone

radiolucent nidus with sur-rounding sclerosis, rarelyextended to vertebral body,epidural or paraspinalspaces

Osteoblasto-ma

Second andthird decades

posterior elements; equallydistributed in the cervical,thoracic, and lumbar seg-ments

osteoid-producingneoplasms

expansile destructive lesionpartially calcified; commonextension to vertebral body

Osteo-chondroma

third decade exclusively posterior ele-ments; predilection for spi-nous processes of cervicalspine

cartilage cap withnormal bone compo-nent

continuity of the lesionwith marrow and cortex ofthe underlying bone

Hemangio-ma

any age; peakfourth decade

vertebral body vascular spaces linedby endothelial cells

vertical parallel densitieslower thoracic-upper lumbarregions

spotted appearance on CThigh signal on T1W andT2W images; involvementof posterior elements

Aneurysmalbone cyst

young patients posterior osseous elements60 %

cystic spaces contain-ing blood products

lytic expansile lesion withfluid-filled levels

<20 years vertebral body 40 % involvement of contiguousvertebraethoracic, lumbar

Langerhanscell histiocy-tosis

first, seconddecades

vertebral body sheets of Langerhanscells, lymphocytes,and eosinophils

lytic lesion of the vertebralbody leading to collapserarely posterior elements,

thoracic, rarely lumbar, cervi-cal


Clinical Presentation

History

A complete history, detailed general assessment and physical examination areessential for evaluating patients with spinal tumors. Patients with spinal tumorsusually present with:

) pain) spinal deformity) neurologic deficit

Pain is the cardinal symptomBack pain is the most common symptom (Case Introduction) [16]. Pain in spinaltumors usually is:

) persistent) unrelated to activity) worsening during rest and at night

Night pain is a warning

signal

Persistent, non-mechanical back pain must be distinguished from common backpain, which is often the opposite. Night pain is an important differential symp-tom of certain skeletal neoplasms such as osteoid osteoma and osteoblastoma.

Pathological fracture of vertebral bodies can occur and can cause severe acutepain similar to that seen in traumatic vertebral compression fractures. Spinalnerve root and cord compression from a pathological fracture or invasion of neo-plasm results in local pain, radicular pain along the affected nerve roots or mye-lopathy [24]. Symptoms of spinal instability and neurologic compromise arisewith increasing vertebral destruction and tumor expansion [14, 19].

Malignant lesions with metastases usually cause associated systemic symp-toms. Systemic symptoms usually are present in malignant lesions, especially intumors such as:

) lymphoma) myeloma) Ewing’s sarcoma) tumors with metastasis

With the progression of the disease, patients can present with:

) weight loss) fever) fatigue) general deterioration

However, these symptoms often appear late during the disease.

Physical Findings

A palpable mass is rarely

the initial finding

Although spinal tumors seldom present with obvious physical findings, a localpalpable mass may be present in some instances. Sacral tumors like chordoma,after growth of an anterior mass, may cause bowel or bladder symptoms and maybe palpable on rectal examination [16]. Benign tumors such as osteoid osteomaare often associated with scoliosis and typically present with paraspinal musclespasm and stiffness. Structurally, there is absence of a lumbar or thoracic humpas in adolescent idiopathic scoliosis. The necessity for a thorough neurologicexamination is self-evident but it usually reveals only findings in late tumorstages.


Diagnostic Work-up

Imaging Studies

The evaluation of spinal tumors includes plain radiographs, bone scans, com-puted tomography (CT), magnetic resonance imaging (MRI), angiography, aswell as single photon emission computed tomography (SPECT) bone scanning[22] and positron emission tomography (PET) scans.

Standard Radiographs

Standard radiography

is the imaging modality

of first choice

Standard radiographs are still the first imaging modality used to explore thespine when a tumor is suspected and they may demonstrate the tumor lesion.Neoplasms in the vertebrae can present as:

) osteolytic (Fig. 4a, b)) osteoblastic/sclerotic (Fig. 4c, d)) mixed

a b

c d

Figure 4. Radiogra-phic findings

a Osteolytic lesion in thevertebral body of C3.b This lesion was primar-ily overlooked and pro-gressed to a severedestruction of the verte-bral body of C3 withkyphotic deformity(histology: chordoma).c, d AP and lateral radio-graphs show a dense,sclerotic bone lesion withextension in the paraspi-nal muscles (arrowheads)on the right side (histol-ogy: osteosarcoma).


Malignant neoplasm usually

preserves the intervertebral

disc

Benign tumors such as osteoid osteoma and osteoblastoma frequently are seen assclerotic lesions in the posterior elements of the spine, with a central lytic areasurrounded by reactive bone [39]. Lytic destruction of pedicles with the winkingowl sign (see Chapter 34 , Case Study 2) seen on an anteroposterior view is themost classic early sign of vertebral involvement by malignant lesions, although

Lytic processes become

visible on radiographs not

before 30 – 50 % of the bone

is destroyed

the vertebral body typically is affected first. Before changes can be recognizedradiographically, 30–50% of a vertebral body must be destroyed. In contrast,slight lysis of the pedicle can be seen early on the AP radiographs [26]. It is diffi-cult to differentiate pathological compression fracture secondary to tumor fromcompression fractures of osteoporosis (Case Study 1). This differential diagnosisis always prompted when osteoporotic spine fractures are diagnosed. The inter-vertebral disc is usually preserved in patients with neoplasm. This helps in differ-entiating tumors from pyogenic infection where the disc is frequently destroyedalong with the adjacent vertebral body [6]. Sometimes, a soft tissue shadow canbe seen on the radiographs extending from a vertebral body lesion through theouter cortex.

Magnetic Resonance Imaging

MRI should be used to fully define the extent and nature of the lesion [7] and isrecommended for investigating the suspected lesion in terms of:

) spinal level) extent of suspected lesions) vertebral bone marrow infiltration) infiltration of the paraspinal soft-tissues (muscles, vessels)) infiltration of the nerve roots, thecal sac, and spinal cord

Generally, MRI is a very sensitive imaging modality for detecting alterations ofthe bone marrow, but it does not allow a type specific diagnosis. The only excep-

High signal in T1W and T2W

images indicates an

hemangioma

tion may be a benign cavernous hemangioma. This lesion is unique in that itshows increased signal intensity relative to the bone marrow on T1W and T2Wimages, allowing a diagnosis with a very high probability (Fig. 5). MRI features ofother tumors are not characteristic and MRI can at best narrow the differentialdiagnosis (Fig. 6, Tables 1, 2). Contrast enhancement is useful to detect a strongvascular uptake which can prompt an angiography. It is particularly useful forassessing the response to chemotherapy. Diffusion weighted MRI may poten-tially be capable of detecting and quantifying the amount of tumor necrosis afterneoadjuvant therapy, but it is premature to finally conclude on this possibility[32].

Computed Tomography

In general, CT is more reliable in demonstrating the cortical outlines of boneand calcification in comparison to MRI. It can better show the extent of the

CT can better show the

extent of bony destruction

tumor destruction (Fig. 7). Occasionally, CT allows the direct demonstrationof the tumor, e.g., in case of an osteoidosteoma (Case Introduction). In termsof tumor biopsies, CT allows accurate assessment of proper needle placementduring needle biopsies. However, in general, CT is not as sensitive as MRI inthe detection of both metastatic disease and primary malignant bone tumors[1, 2, 13].


a b c

d e f

Case Study 1

A 72-year-old male presented with acute onset of thoracolumbar back pain after an unusual movement. The pain wasworse on motion and the patient could not be mobilized. An initial lateral radiograph demonstrated compression frac-tures at L1 and L2 (a). Non-operative treatment failed and the patient was referred for a vertebroplasty. An MRI investiga-tion was done showing fresh compression fractures at L1 and L2 and older endplate fractures of L4 and L5. Note the bonemarrow changes which are hypointense on the T1W image (b) and the hyperintense signal intensity on the T2W image(c). The signal intensity increase is better visible on the STIR sequence (d). The patient underwent a biportal vertebropla-sty of L1 and L2, which instantaneously resolved the patient’s symptoms (e, f ). The patient was sent for a formal assess-ment of the putative osteoporosis during which a multiple myeloma was diagnosed. In retrospect, the assessmentshould have been done prior to the treatment by vertebroplasty although it would not have changed the indication fora vertebroplasty.


a b c

d e f

Case Study 2

A 16-year-old female underwent an i.v. pyelogram for a diagnostic assessment of recurrent urinary tract infections. Theradiologist noticed a disappearance of the regular structure of the L3 pedicle on the left side (winking owl sign) (a). Areferral and further diagnostic work-up were prompted. The MRI scan showed a large cyst without significant septal par-titions on the T2W sagittal (b) and T2W axial (c) scans. No soft tissue infiltration was seen. The CT scan confirmed the diag-nosis of a large cyst (d). The biopsy ruled out malignancy although a confirmation of the suspected aneurysmatic bonecyst was not reliably possible on the material submitted. Because of the benign lesion, an intralesional resection of thetransverse process and a curettage of the superior articular process and the pedicle was done. The medial border to thethecal sac was covered with Gelfoam and the defect was filled with autologous cancellous bone. At one year follow-upthe patient is symptom free and the CT scan shows a nice remodeling of the pedicle (e, f ).

Radionuclide Studies

A technetium-99m (99mTc) bone scan is widely used in the initial diagnosis andfollow-up of bone tumors. Technetium scans are sensitive to any area ofincreased osteoid reaction to destructive processes in bones (Case Introduction).They can detect lesions as small as 2 mm, and as little as a 5–15% alteration in

A bone scan is the screening

method of choice for

investigating extraspinal

tumor manifestation

local bone turnover. They can identify changes in osteolytic or osteoblastic dis-ease 2–18 months sooner than radiographs [22, 31]. Total body scans can showmost of the (also remote) skeletal lesions, and therefore are used as a screeningtest to determine whether a lesion is solitary or multifocal in expression and localextent. Plasmocytoma is particular in that it may be purely lytic, and therefore anordinary scan may be negative. In these patients, 99mTc-sestamibi has beenproven to very useful with a specificity of 96% and sensitivity of 92%. As an alter-native, MRI may be regarded as today’s standard.


a b

Figure 5. MRI findings of a benign hemangioma

Typical spotted bright signal intensity changes within the vertebral body of L1 on a T1W and b T2W image suggestinga benign hemangioma.

a b

c

Figure 6. MRI findings in primary spinal tumors

a Expansive lesion with a pseudocapsule with compression of the spinal cord and the retropharyngeal space. Note theskip lesion at the level of C7 (arrow, same patient as in Fig. 4a, b). Extension of a hypointense mass into the foramen L5and the adjacent facet joint L4/5 on a T2W axial (b) and T1W sagittal image (c) (same patient as in Fig. 4c, d).


Table 2. Primary malignant spinal tumors

Lesion Age Location Histology Imaging

Osteosarcoma Fourth decade Vertebral body Osteoid within sarco-matous tissue

Osteosclerotic and osteolyticareas with soft tissue compo-nent; common extension toposterior elements

Lumbosacral region

Chondro-sarcoma

Fifth decade Predilection for vertebralbody

Hyaline cartilagewith increased cellu-larity within myxoidmatrix

Bone destruction with charac-teristic punctuate calcifica-tionsThoracic region

Malignantfibrous histi-ocytoma

Second toeighth decades

Vertebral body Mixture of histio-cytes, fibroblasts andprimitive mesenchy-mal cells

Lytic lesion with low signal onT1W and high signal on T2Wimages

Giant celltumor

Third decade Vertebral body Osteoclastic giantcells intermixed withspindle cells

Osteolytic geographic areawith soft tissue componentSacrum

Plasmo-cytoma

>40 years old Vertebral body Sheets of plasmacells on a delicatereticular stroma

Radiolucent areas or reduc-tion in bone densityThoracic and lumbar spineHypointense on T1W andhyperintense on T2W images

Ewing’ssarcoma

Second tothird decades

Vertebral body, lumbosa-cral spine

Sheets of small roundblue cells

Lytic lesion, associated softtissue mass

Chordoma Middle-agedpatients

Exclusively affects vertebralbody; most often sacrum,rarely mobile spine

Lobulated mass withmucinous containingcells

Destructive midline expansilelesion with associated soft tis-sue mass; extension into adja-cent vertebra

a b

Figure 7. Computer tomography findings of primary spinal tumors

a Axial CT scan showing an extensive infiltration and destruction of the posterior wall (histology: plasmocytoma). b Axialscan indicating increased bone density in the lamina (histology: osteoblastoma).

Spinal Angiography

Spinal angiography has only rare indications for spinal lesions, usually when richvascular structures such as aneurysmal bone cysts and hemangiosarcoma arepresent. Angiography is capable of showing the vascularity of all feeding anddraining vessels and can be used for selective embolization of hypervascularlesions to reduce intraoperative blood loss [35].


Biopsy

One of the most important principles of tumor surgery is that of including thebiopsy track with an adequate margin of healthy tissue which can be excised at

The biopsy type and track

must be carefully

considered

definitive resection. This is sometimes impossible in the spine if an approach vio-lating the anatomic planes is used. Poorly planned biopsies increase the localrecurrence risk by tumor dissemination along fascial planes and the biopsy tract.There are three different types of biopsies:

) needle) open incisional) excisional

For tumors limited to the posterior elements, an excisional biopsy is both diag-nostic and therapeutic. Most needle biopsies are performed under fluoroscopicor CT control [23]. In experienced hands, the accuracy rate ranges from 80% to90%, but it is non-diagnostic in 25% of patients [34]. CT guidance offers a greatmargin of safety for surrounding blood vessels and viscera, but complications

Place the biopsy track so

that it can be excised

at definitive surgery

include pain, bleeding, and pneumothorax. If open incisional biopsy is planned,several fundamental principles should be considered. The incision has to beplanned such that it can be excised at definitive surgery. Bone windows should besmall and carefully planned so that pathological fractures do not result. They arepacked with bone wax and Gelfoam, hydroxyapatite or cement, depending on thesurgeon’s preference. Postoperative hematomas need to be avoided because theycarry the potential of disseminating tumor cells along fascial planes.

Acceptable biopsy techniques for malignant tumors of the spine depend on theanatomic extent and location of the tumor. In the cervical spine, posterior tumorswith or without extraosseous soft tissue involvement are easily sampled by needleusing CT guidance. However, because of the predominance of benign lesions in theposterior elements and when confined to the osseous elements, excisional biopsytechniques may be preferred. Anteriorly, in the craniocervical region, transpharyn-geal stereotactic needle biopsy is an alternative to open biopsy using the approachesfor resection of tumors in this region. Tumors of the anterior thoracic spine aresampled via posterior percutaneous CT-directed needle biopsy. An open biopsy canbe performed through a posterolateral approach by costotransversectomy, withcareful consideration of biopsy placement. In the lower thoracic and lumbar spine,CT-guided biopsy techniques can be used; for anteriorly located lesions, transpedi-cular biopsy placement is possible, but later necessitates resection of the involvedpedicle and soft tissue track if the lesion turns out to be malignant.

Laboratory Investigations

A complete laboratory work-up should be ordered. For patients with multiplemyeloma and metastatic osteolytic lesions, serum calcium should be evaluatedand the possible hypercalcemia corrected. Anemia, hypoalbuminemia and elec-trolyte imbalances need to be corrected before considering surgery. There are notumor specific biochemical markers yet available for spine tumors.

Tumor Staging

A benign tumor is defined by its incapacity to metastasize, whereas a malignanttumor has the potential to metastasize. Boriani et al. [11] have suggested a surgi-cal staging system for the spine based on Enneking’s pioneering work [17] forlimb lesions (Fig. 8).


82

Figure 8. Staging of benign and malignant spinal tumors.

The staging considers the presence of a capsule (pseudocapsule), aggressiveness of the lesion, presence of skip lesions,extracompartmental growth, and metastases (for details see text). (Redrawn and modified from Boriani et al. [11], repro-duced with permission from Lippincott, Williams & Wilkins).

Benign Tumors

Benign tumors are staged into:

) latent lesion) active lesion) aggressive lesion


Stage 1

Stage 1 (S1, latent, inactive) lesions include asymptomatic lesions, bordered by atrue capsule. In these tumors, a well-defined margin around the circumferenceof the lesion is seen even on plain radiographs. These tumors usually do not grow

No treatment is required

for stage 1 lesions

or if they do then only very slowly. No treatment is required for S1 lesions, unlesspalliative surgery is needed for decompression or stabilization. Examples includehemangiomas of bone and osteochondroma.

Stage 2

Stage 2 (S2, active) lesions grow slowly and cause mild symptoms. There is a thincapsule around the tumor and a layer of reactive tissues, sometimes seen on

Intralesional resection

can be performed for

Stage 2 lesions

plain radiographs as an enlargement of the tumor outline and sometimes clearlydefined on MRI. Bone scans are often positive. An intralesional excision is per-formed with a low rate of recurrence. Examples include osteoid osteoma, aneu-rysmal bone cysts, and giant cell tumor of bone.

Stage 3

Stage 3 (S3, aggressive) lesions are represented by rapidly growing benigntumors. The capsule is very thin, incomplete, or absent. The tumor invades

Intralesional resection

is insufficient for

Stage 3 lesions

neighboring compartments and often has an associated wide, reactive, hypervas-cularized pseudocapsule, which sometimes is permeated by neoplastic digitati-ons. There are fuzzy limits on plain radiographs; bone scans are also positive. CTscans show the tumor extension, and MRI defines the pseudocapsule and its rela-tionship to adjacent neurologic structures. Intralesional curettage is often notenough and is associated with a high recurrence rate.

Malignant Tumors

Malignant tumors are divided into low grade tumors, high grade tumors, andtumor metastasis (independent of grade).

Stage I

Wide en bloc resection

is indicated in Stage 1

and 2 lesions

Stage I (low grade) malignant tumors are further subdivided with regard to thecontainment into:

) Stage IA, i.e., the tumor remains inside the vertebra, and) Stage IB, i.e., the tumor invades paravertebral compartments

No true capsule is associated with these lesions, but a thick pseudocapsule ofreactive tissue often is penetrated by small, microscopic islands of tumor.Because resection along the pseudocapsule may leave behind residual foci oftumor, wide en bloc excision is indicated if possible.

Stage II

Stage II (high grade) malignant tumors are accordingly defined as:

) Stage IIA, i.e., the tumor remains inside the vertebra, and) Stage IIB, i.e., the tumor invades paravertebral compartments

The neoplastic growth is so rapid that the host has no time to form a continuousreactive tissue layer. There is seeding with satellite tumor cells as well as skiplesions at some distance. These tumors show up on plain radiographs as radiolu-


cent and destructive lesions, often associated with pathological fractures. CT andMRI confirm the absence of a reactive tissue margin. Invasion of the epiduralspace is rapid particularly in Ewing’s sarcoma or lymphoma, and is characterizedby infiltrating tumor spread beyond the cortical border of the vertebra with noevident destruction. The resection should be wide or en bloc. The survivalbetween Stages 1 and 3 differs significantly, whereas there is no difference in sur-vival between patients with A or B lesions [3].

Stage III

In Stage III malignant tumors, metastasis represents the situation where thetumor has spread to a distant organ different from, and independent of, the histo-logical grade of the primary tumor.

Non-operative Treatment

The treatment of spine tumors is determined by the:

) biology) location) extent of the lesion

The wait and see approach

is rarely indicated

For these reasons, establishing the tissue diagnosis is of great importance. It isextremely dangerous to wait and see if the biopsy is not reliable and the imagingstudies not entirely conclusive.

Even if the imaging findings indicate a benign lesion such as a vertebral heman-gioma, the final histology may reveal a malignant lesion such as a solitary plasmo-cytoma [8]. For benign lesions, there are only rare indications for non-operativetreatment, such as hemangioma or Langerhans cell histiocytosis. For malignantlesions, non-surgical treatment generally is an adjunct to surgery and consists of:

) pain management) chemotherapy) radiotherapy

Non-steroidal Anti-inflammatory Drugs

Non-steroidal anti-inflammatory drugs (NSAIDs) are often used for mild pain.Opioid drugs are used for severe pain. Other options include epidural and intra-thecal administration of local anesthesia. Systemic steroids are used to controlpain and mitigate neurologic deficit in patients with spinal cord compression.Chemotherapy has been valuable for the treatment of selected primary tumorsand metastases such as osteosarcoma, Ewing’s sarcoma and multiple myeloma.Radiotherapy has been the mainstay for treating radiosensitive primary malig-nant tumors such as Ewing’s sarcoma as well as metastases [29].

Adjuvant Therapy

Radiotherapy is indicated

for radiosensitive lesions

The goal of radiotherapy is to maximally destroy the tumor while minimizing theeffects on normal tissue [10]. Radiotherapy may be the choice of initial treatmentfor radiosensitive lesions. With the advances in surgical technique and instru-mentation, initial surgical excision followed by radiation if indicated is preferred

Chemotherapy is indicated

particularly for osteosarcoma

and Ewing’s sarcoma

because of the risk of developing postirradiation sarcoma. Chemotherapy is usedparticularly for the most common primary bone tumors such as osteosarcomaand Ewing’s sarcoma. Its main effect is directed at reducing tumor volume andsurrounding edema.


Operative Treatment

General Principles

The indication for operative treatment of spine tumors has to be carefully consid-ered and treatment should be performed using a team approach. The biopsy pathhas to be carefully selected in order not to compromise further surgery. The type ofresection depends on the synthesis of a plethora of parameters such as the biologyof the tumor, the precise anatomic location, and the patient’s general condition.

Traditionally, the indications for open surgery included:

) spinal instability due to bony destruction) progressive neurologic deficit) radioresistant tumor that is growing) the need for open biopsy) intractable pain unresponsive to non-surgical treatment

The primary goal is wide or

en bloc resection and

spinal reconstruction

Advances in vertebral resection and stabilization and improved survival withvarious neoadjuvant therapies have expanded the indications for surgical inter-vention of primary spinal tumors. Today, the ultimate goal must be a “wide” andpreferably an en bloc resection of the primary tumor in combination with a spi-nal reconstruction which allows for early mobilization.

The surgical techniques are classified by the tissue planes and approach as:

) curettage) intralesional resection) en bloc resection

Curettage and intralesional resection describe a piecemeal removal of the tumor.En bloc resection indicates the attempt to remove the whole tumor in one piecetogether with a layer of normal tissue.

The resected pathological specimen is histologically analyzed, and furtherclassified into:

) intralesional) marginal) wide

The term “intralesional” is used when the tumor mass is violated; marginal isappropriate when the surgeon dissects along the pseudocapsule, the layer ofreactive tissue around the tumor; and “wide” is appropriate if surgical separationhas occurred outside the pseudocapsule, removing the tumor with a continuousshell of healthy tissue.

It is essential to distinguish the removal en bloc, i.e., the whole tumor in onepiece, from a simple intralesional procedure. Intralesional resection of malignanttumors may provide functional palliation and pain relief, but has a very highincidence of local recurrence [5]. When resecting a malignant spinal tumor, the

The widest possible margin

should be sought for the

excision of malignant spinal

tumors

widest possible surgical margin should be sought. The goal of surgery should becomplete extirpation of the tumor with stable reconstruction of the vertebral col-umn. Resections involving extensively contaminated surgical margins or debul-king should be avoided. An aggressive approach with adequate resection canenhance local control and prolong survival.

Surgical planning and

decision-making are

complex and require

a team approach

Surgical planning and decision-making are complex processes. To address thisdifficulty, the vertebral elements are divided into zones [11, 27], thereby predicat-ing the resectability of any particular lesion based on the zones involved [36, 43].In the transverse plane, the vertebra is divided into 12 radiating zones (num-bered 1–12 in clockwise order) and into five layers (A to E), starting from the


Figure 9. Surgical staging system

The transverse tumor extension is described with reference to 12 radiating zones and five concentric layers. (Redrawnand modified from Boriani et al. [11], reproduced with permission from Lippincott, Williams & Wilkins).

paravertebral osseous region to the dural involvement (Fig. 9). The longitudinalextent of the tumor is assessed by counting the spine segments involved. Compre-hensive imaging studies are needed preoperatively to assess and describe thetransverse and longitudinal expansion of a tumor, which allows appropriate sur-gical planning.

Surgical Techniques

The final tumor diagnosis

may be different than

expected

The surgical techniques of primary spinal tumors are very complex and demandexcellent surgical skills. Particularly for the en bloc resection of spinal tumors,the surgical strategy and reconstruction measure have to be decided on an indi-vidual basis because of a high variability of tumor location and extension. Thesurgeon should always consider that the final histological diagnosis may be dif-ferent than expected or diagnosed on the biopsy material. Even in that case thesurgeon should be capable of appropriately treating the case.

Consider referring primary

spine tumors to a larger

center

A detailed description of the surgical techniques is far beyond the scope of thischapter. We prefer to concentrate on general principles rather than on a “how todo” approach. The surgery for primary malignant tumors should be concen-trated in centers with sufficient case load and experience.

Intralesional Resection

This surgical technique is only used for benign tumors (Case Introduction) or fordebulking of inoperable primary or metastatic lesions. The surgical approach forany malignant tumor of the spine is determined by the:

) tumor location) extent of the tumor


The approach should be planned in such a manner as to provide the opportunityto excise the lesion completely as well as to stabilize the spine mechanically.Often, a combination of anterior and posterior approaches is used [12, 38]. Ingeneral, lesions involving the posterior elements of the spine with or without softtissue extension are approached posteriorly for both resection and reconstruc-tion (Case Study 2). If the lesion extends into the soft tissue, an appropriate softtissue resection is required. In case of a typical osteoidosteoma, the lesion can becuretted and the bed of the tumor should be excised using a high-speed airdrill(Case Introduction).

If a malignant tumor involves the anterior vertebral body with or without softtissue extension, but not the pedicle of the vertebral body or posterior elements,then an anterior approach is indicated. If a malignant lesion involves both ante-rior and posterior elements, an en bloc resection with a wide or even marginalresection is usually impossible unless the patient is willing to become paraplegic.The resection is usually accomplished by a combination of anterior and posteriorapproaches with intralesional contamination at the level of the pedicle when it istransected at the time of removal of the posterior elements [41]. In the thoracicand lumbar spine, some lesions involving both anterior and posterior elementsare amenable to marginal resection through a posterolateral approach, therebysacrificing a nerve root at the level of resection and one level above. The selectedsurgical approaches are chosen depending on the anatomic locations.

En Bloc Resection and Reconstruction of the Spine

There are three major methods of performing en bloc resections in the thoraco-lumbar spine:

) vertebrectomy) sagittal resection) resection of the posterior arch

The term “vertebrectomy,” also termed “spondylectomy,” is used to describeremoval of the entire tumor in one piece together with portions of the posteriorelements [37, 41, 43]. This approach is indicated if:

) tumor is confined to zones 4–8 or 5–9) tumor is centrally located in the vertebral body) at least one pedicle is free from tumor

The procedure can be performed in one or two stages. The posterior approachinvolves excision of the posterior elements, which allows the section of the anulusfibrosus and the posterior longitudinal ligament, careful hemostasis of the epidu-ral venous plexus and posterior stabilization. The anterior approach, either by atranspleural thoracotomy, retroperitoneal, or thoracoabdominal approaches,allows the ligature of segmental vessels, proximal and distal discectomies, the enbloc removal of the vertebral body and anterior reconstruction [20, 38]. A bilat-eral approach for vertebrectomy has the main advantage of dissecting the tumoroff the anterior soft-tissues under direct vision, thereby achieving a better margin.

When the tumor predominately involves the posterior spinal elements on oneside (e.g., chondrosarcoma), an en bloc resection is feasible even in the presence ofextensive soft tissue extension. In such cases, posterior serial pedicle and sagittalvertebral osteotomies in conjunction with rib resection are necessary (Case Study 3).

For tumors of the sacrum in particular, the surgical approach depends on thebiology of the tumor as well as the anatomic location. The general principle is toremove the entire tumor mass in toto [4, 9, 28, 33]. It has been shown that forlesions below S3, a posterior approach only is sufficient whereas for lesions above


a b

c

d e

f g

Case Study 3

A 50-year-old male presented with a painful parasagittal mass at the midthoracic spine. A diagnostic assessmentincluded MRI, thoracoabdominal CT, bone scan and laboratory investigations. The T1W (a) and T2W MR (b) imagesshowed a large polylobulated mass with varying signal intensity and a not clearly visible capsule. The tumor appearedto originate from the posterior part of the T7 pedicle (not shown). The soft tissue infiltration suggested a malignant


h

i

j k

Case Study 3 (Cont.)

tumor. The axial T2Wscans (c) demonstratedextension to the ribcage.A biopsy revealed the his-tological diagnosis of aGrade II chondrosarcoma.No metastases were dis-covered. An en bloc resec-tion was planned. Thelines indicate the level ofosteotomies of the lami-nae, pedicles and ribs.The skin with the biop-sy channel was excised(d). Prior to tumor resec-tion, the spine was instru-mented with pediclescrews at T3–T12 on theright side and at T3, T4,T11 and T12 on the leftside. Tumor resection wasperformed along the indi-cated lines. The en blocresection was done withserial contralateral lami-notomies at T5–T10 (e),ipsilateral pedicle osteo-tomies at T5–T9, and ribosteotomies at T5–T10.An en bloc resection ofthe tumor was achievedwith wide margins (f, g).Particularly the osteoto-mies at the level of thepedicles (arrows) and ribs(arrowheads) were tumorfree. The resected pleurawas covered with an arti-ficial membrane (asterisk)and the dura with Gel-foam sponges (arrow-heads). The spine wasstabilized at T3–T12 andfusion was carried out onthe right side (h). Thedefect was covered withan ipsilateral latissimusdorsi flap (i). Three yearsafter surgery, the patientis functioning wellalthough he had initialproblems with the mobil-ity of the left shoulder(unstable scapula). Thefollow-up radiographsshow the stabilization ofthe spine at T3–T12 (j, k).Regular follow-up imag-ing studies (MRI, and tho-racoabdominal CT scan)demonstrate a tumor-freecourse so far.


S3 a combined anterior and posterior approach is preferred [21]. The possibledisadvantages of a posterior only approach include hemorrhage and laceration ofpelvic viscera including ureters. The combined approach allows exposure of theentire pelvic contents and safe ligation of the internal iliac vessels, which assistsin reducing bleeding during mobilization of the specimen from posteriorly. It hasbeen shown that the combined approach reduces the local recurrence rate inpatients with chordomas, and does not compromise the harvest and use of a ped-icled transpelvic rectus flap for posterior wound closure [21].

Adjuvant Treatment and Local Recurrences

The local recurrence is

directly related to the

surgical margin

There are few large studies dealing with malignant primary bone tumors of thespine. Talac et al. [40] showed that local recurrence is directly related to the surgi-cal margin obtained during surgery, with a fivefold increase comparing marginaland intralesional resections over wide resections. Because primary bone tumorsare rare overall, in primary spine tumors in particular there are no randomizedstudies available which have assessed the outcome of combined treatment regi-mens. Basically, patients are treated, e.g., by chemotherapy according to the biol-ogy of the tumor independent of the location, including spinal locations. Thereare no large series which have assessed the effect of adjuvant treatment on theoutcome of patients with primary malignant spine tumors. In a recent series,with the small numbers available, no conclusion could be drawn with respect toadjuvant treatment except for the fact that over 90% of patients who had localrecurrences died from their disease.

Recapitulation

Epidemiology. Primary spine tumors are relativelyrare. The incidence is estimated at 2.5 – 8.5 per100 000 individuals per year. When evaluating thepotential of malignancy of a spine lesion, age of thepatient and location of the lesion are the most im-portant parameters.

Tumor biology. Cancer is a molecular disease. Can-cer development is determined by the five hall-marks of cancer: unlimited replicative potential,avoidance of apoptosis, self-sufficient proliferation,angiogenesis and metastasis. Metastasis is thestepwise progression which includes proliferation,migration, invasion, intra- and extravasation, andlocal growth in the target organ.

Classification. Spine tumors are classified based onthe histological diagnosis. Together with the ageof the patient and the location of the lesion, the bi-ology can be predicted, and treatment is per-formed accordingly.

Clinical presentation. Patients with spinal tumorspresent with pain, spinal deformity and neurologicdeficit. Back pain is the most common symptom. It

is persistent and usually not related to activity, andoften aggravates during the night. Patients withspinal tumors rarely present with a palpable mass.Spinal instability and neurologic compromise mayarise from a lesion in the vertebral body and de-pend on the level and location.

Diagnostic work-up. This includes laboratory inves-tigations, imaging studies, and tumor staging witha biopsy from the lesion. Imaging studies includestandard radiographs in two planes, CT and MRI aswell as a bone scan. Tumor staging defines the sys-temic extent of the disease, which allows the prog-nosis to be determined, as well as the local extent,which is mandatory for surgical planning andshould be done in accordance with the surgeonperforming the tumor resection. The biopsy needsto be planned such that it does not compromisesubsequent surgical resection. Serum calcium hasto be evaluated, and anemia, hypoalbuminemiaand electrolyte imbalances need to be assessedand corrected prior to surgery.

Treatment. Non-operative treatment is only indi-cated for benign lesions and if the patient is asymp-


tomatic. If surgery cannot be performed for malig-nant tumors, pain management is very important,and radiotherapy as well as chemotherapy needs tobe taken into consideration. Surgical treatment canbe performed as curettage, intralesional or en blocremoval of the tumor. Histologically, en bloc

removal is classified into wide, marginal or intrale-sional resection. The goal of surgery is the com-plete extirpation of the tumor with stable recon-struction of the vertebral column. The surgicalapproach and technique is determined by the leveland anatomic extent of the tumor lesion.

Key Articles

Hanahan D, Weinberg RA (2000) The hallmarks of cancer. Cell 100:57 – 70

Landmark paper on modern principles of carcinogenesis. This article describes the nec-essary key steps which a cell of a given tissue has to fulfill to become cancerous.

Sundaresan N, Boriani S, Rothman A, Holtzman R (2004) Tumours of the spine. J Neu-rooncology 69:273 – 290

This article provides a detailed overview of primary benign and malignant as well as met-astatic bone tumors.

Fisher CG, Keynan O, Boyd MC, Dvorak MF (2005) The surgical management of primarytumors of the spine. Spine 30:1899 – 1908

This article underlines the importance of the surgical principles in the treatment of pri-mary tumors of the spine.

Talac R, Yaszemki MJ, Currier BL, Fuchs B, Dekutoski MB, Kim CW, Sim FH (2002) Rela-tionship between surgical margins and local recurrence in sarcomas of the spine. ClinOrthop Rel Res 397:127 – 132

This article comprises one of the largest and most recent series on the outcome of surgicaltreatment of primary bone sarcomas of the spine. It exemplifies the importance of obtain-ing a wide surgical margin.

Fuchs B, Dickey ID, Yaszemski MJ, Inwards CY, Sim FH (2005) Operative management ofsacral chordoma. J Bone Joint Surg [Am] 87:2211 – 16

This article includes the largest series on surgically treated chordomas of the sacrum. Itshows that for lesions above the S3 level, a combined anterior-posterior approach is pre-ferred over a posterior approach alone.

Garg S, Dormans JP (2005) Tumors and tumor-like conditions of the spine in children.J Am Acad Orthop Surg 6:372 – 81

This article provides a comprehensive overview on tumors and tumor-like conditions inchildren. It highlights the differential diagnosis of back pain in children and adolescentsand illustrates diagnostic and therapeutic options.

References

1. Algra PR, Bloem JL, Tissing H, Falke TH, Arndt JW, Verboom LJ (1991) Detection of vertebralmetastases: comparison between MR imaging and bone scintigraphy. Radiographics11:219–32

2. Avrahami E, Tadmor R, Dally O, Hadar H (1989) Early MR demonstration of spinal metasta-ses in patients with normal radiographs and CT and radionuclide bone scans. J ComputAssist Tomogr 13:598– 602

3. Bacci G, Savini R, Calderoni P, Gnudi S, Minutillo A, Picci P (1982) Solitary plasmacytoma ofthe vertebral column. A report of 15 cases. Tumori 68:271– 5

4. Bailey CS, Fisher CG, Boyd MC, Dvorak MF (2006) En bloc marginal excision of a multilevelcervical chordoma. Case report. J Neurosurg Spine 4:409–14

5. Bilsky MH, Boland PJ, Panageas KS, Woodruff JM, Brennan MF, Healey JH (2001) Intralesio-nal resection of primary and metastatic sarcoma involving the spine: outcome analysis of 59patients. Neurosurgery 49:1277–86; discussion 1286– 7

6. Black P (1979) Spinal metastasis: current status and recommended guidelines for manage-ment. Neurosurgery 5:726– 46


7. Body JJ (1992) Metastatic bone disease: clinical and therapeutic aspects. Bone 13 Suppl1:S57– 62

8. Boos N, Goytan M, Fraser R, Aebi M (1997) Solitary plasma-cell myeloma of the spine in anadolescent. Case report of an unusual presentation. J Bone Joint Surg Br 79:812– 4

9. Boriani S, Bandiera S, Biagini R, Bacchini P, Boriani L, Cappuccio M, Chevalley F, Gasbar-rini A, Picci P, Weinstein JN (2006) Chordoma of the mobile spine: fifty years of experience.Spine 31:493–503

10. Boriani S, De Iure F, Bandiera S, Campanacci L, Biagini R, Di Fiore M, Bandello L, Picci P,Bacchini P (2000) Chondrosarcoma of the mobile spine: report on 22 cases. Spine 25:804–12

11. Boriani S, Weinstein JN, Biagini R (1997) Primary bone tumors of the spine. Terminologyand surgical staging. Spine 22:1036– 44

12. Bruder E, Zanetti M, Boos N, von Hochstetter AR (1999) Chondromyxoid fibroma of twothoracic vertebrae. Skeletal Radiol 28:286–9

13. Chin CT (2002) Spine imaging. Semin Neurol 22:205–2014. Constans JP, de Divitiis E, Donzelli R, Spaziante R, Meder JF, Haye C (1983) Spinal metasta-

ses with neurological manifestations. Review of 600 cases. J Neurosurg 59:111–815. Dreghorn CR, Newman RJ, Hardy GJ, Dickson RA (1990) Primary tumors of the axial skele-

ton. Experience of the Leeds Regional Bone Tumor Registry. Spine 15:137–4016. Enneking W (1983) Spine. New York: Churchill Livingstone, 1983: 303– 35417. Enneking WF, Spanier SS, Goodman MA (1980) A system for the surgical staging of muscu-

loskeletal sarcoma. Clin Orthop Relat Res:106–2018. Fidler IJ (2003) The pathogenesis of cancer metastasis: the ’seed and soil’ hypothesis revis-

ited. Nat Rev Cancer 3:453–819. Fielding JW, Pyle RN, Jr, Fietti VG, Jr (1979) Anterior cervical vertebral body resection and

bone-grafting for benign and malignant tumors. A survey under the auspices of the Cervi-cal Spine Research Society. J Bone Joint Surg Am 61:251–3

20. Fourney DR, Abi-Said D, Rhines LD, Walsh GL, Lang FF, McCutcheon IE, Gokaslan ZL(2001) Simultaneous anterior-posterior approach to the thoracic and lumbar spine for theradical resection of tumors followed by reconstruction and stabilization. J Neurosurg94:232–44

21. Fuchs B, Dickey ID, Yaszemski MJ, Inwards CY, Sim FH (2005) Operative management ofsacral chordoma. J Bone Joint Surg Am 87:2211– 6

22. Gates GF (1998) SPECT bone scanning of the spine. Semin Nucl Med 28:78–9423. Ghelman B, Lospinuso MF, Levine DB, O’Leary PF, Burke SW (1991) Percutaneous com-

puted-tomography-guided biopsy of the thoracic and lumbar spine. Spine 16:736– 924. Griffin JB (1978) Benign osteoblastoma of the thoracic spine. Case report with fifteen-year

follow-up. J Bone Joint Surg Am 60:833–525. Hanahan D, Weinberg RA (2000) The hallmarks of cancer. Cell 100:57– 7026. Harrington KD (1986) Metastatic disease of the spine. J Bone Joint Surg Am 68:1110– 527. Hart RA, Boriani S, Biagini R, Currier B, Weinstein JN (1997) A system for surgical staging

and management of spine tumors. A clinical outcome study of giant cell tumors of the spine.Spine 22:1773–82; discussion 1783

28. Heary RF, Vaccaro AR, Benevenia J, Cotler JM (1998) “En-bloc” vertebrectomy in the mobilelumbar spine. Surg Neurol 50:548–56

29. Heidecke V, Rainov NG, Burkert W (2003) Results and outcome of neurosurgical treatmentfor extradural metastases in the cervical spine. Acta Neurochir (Wien) 145:873–80; discus-sion 880– 1

30. Jemal A, Murray T, Ward E, Samuels A, Tiwari RC, Ghafoor A, Feuer EJ, Thun MJ (2005)Cancer statistics, 2005. CA Cancer J Clin 55:10–30

31. Joo KG, Parthasarathy KL, Bakshi SP, Rosner D (1979) Bone scintigrams: their clinical use-fulness in patients with breast carcinoma. Oncology 36:94–8

32. Lang P, Johnston JO, Arenal-Romero F, Gooding CA (1998) Advances in MR imaging ofpediatric musculoskeletal neoplasms. Magn Reson Imaging Clin N Am 6:579– 604

33. Min K, Espinosa N, Bode B, Exner GU (2005) Total sacrectomy and reconstruction withstructural allografts for neurofibrosarcoma of the sacrum. A case report. J Bone Joint SurgAm 87:864–9

34. Simmons ED, Zheng Y (2006) Vertebral tumors: surgical versus nonsurgical treatment. ClinOrthop Relat Res 443:233– 47

35. Sundaresan N (1986) Chordomas. Clin Orthop Relat Res:135–4236. Sundaresan N, Boriani S, Rothman A, Holtzman R (2004) Tumors of the osseous spine. J

Neurooncol 69:273– 9037. Sundaresan N, DiGiacinto GV, Krol G, Hughes JE (1989) Spondylectomy for malignant

tumors of the spine. J Clin Oncol 7:1485–9138. Sundaresan N, Steinberger AA, Moore F, Sachdev VP, Krol G, Hough L, Kelliher K (1996)

Indications and results of combined anterior-posterior approaches for spine tumor surgery.J Neurosurg 85:438–46

39. Sweriduk ST, DeLuca SA (1987) The sclerotic pedicle. Am Fam Physician 35:161–2


40. Talac R, Yaszemski MJ, Currier BL, Fuchs B, Dekutoski MB, Kim CW, Sim FH (2002) Rela-tionship between surgical margins and local recurrence in sarcomas of the spine. ClinOrthop Relat Res:127–32

41. Tomita K, Kawahara N, Baba H, Tsuchiya H, Fujita T, Toribatake Y (1997) Total en bloc spon-dylectomy. A new surgical technique for primary malignant vertebral tumors. Spine22:324–33

42. Weigelt B, Peterse JL, van’t Veer LJ (2005) Breast cancer metastasis: markers and models. NatRev Cancer 5:591– 602

43. Yao KC, Boriani S, Gokaslan ZL, Sundaresan N (2003) En bloc spondylectomy for spinalmetastases: a review of techniques. Neurosurg Focus 15:E6


XIII Contents - bücher.de · Acute Low Back Pain Without Radicular Symptoms,WithoutTrauma ........

Documents

Transcript of XIII Contents - bücher.de · Acute Low Back Pain Without Radicular Symptoms,WithoutTrauma ........