Surgical Anatomy & Techniques to the Spine [2 ed.] 9781455709892

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Surgical Anatomy & Techniques to the Spine

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Surgical Anatomy & Techniques to the Spine SECOND EDITION

Daniel H. Kim, MD Director Reconstructive Spinal and Peripheral Nerve Surgery Mischer Neuroscience Institute Professor Vivian L. Smith Department of Neurosurgery University of Texas Health Science Center at Houston Houston, Texas

1600 John F. Kennedy Blvd. Ste 1800 Philadelphia, PA 19103-2899

SURGICAL ANATOMY & TECHNIQUES TO THE SPINE Copyright © 2006, 2013 by Saunders, an imprint of Elsevier Inc.

ISBN: 978-1-4557-0989-2

No part of this publication may be reproduced or transmitted in any form or by any means, electronic or mechanical, including photocopying, recording, or any information storage and retrieval system, without permission in writing from the publisher. Details on how to seek permission, further information about the Publisher’s permissions policies and our arrangements with organizations such as the Copyright Clearance Center and the Copyright Licensing Agency, can be found at our website: www.elsevier.com/permissions. This book and the individual contributions contained in it are protected under copyright by the Publisher (other than as may be noted herein).

Notices Knowledge and best practice in this field are constantly changing. As new research and experience broaden our understanding, changes in research methods, professional practices, or medical treatment may become necessary. Practitioners and researchers must always rely on their own experience and knowledge in evaluating and using any information, methods, compounds, or experiments described herein. In using such information or methods they should be mindful of their own safety and the safety of others, including parties for whom they have a professional responsibility. With respect to any drug or pharmaceutical products identified, readers are advised to check the most current information provided (i) on procedures featured or (ii) by the manufacturer of each product to be administered, to verify the recommended dose or formula, the method and duration of administration, and contraindications. It is the responsibility of practitioners, relying on their own experience and knowledge of their patients, to make diagnoses, to determine dosages and the best treatment for each individual patient, and to take all appropriate safety precautions. To the fullest extent of the law, neither the Publisher nor the authors, contributors, or editors, assume any liability for any injury and/or damage to persons or property as a matter of products liability, negligence or otherwise, or from any use or operation of any methods, products, instructions, or ideas contained in the material herein.

Content Strategist: Charlotta Kryhl Managing Editor: Kathryn DeFrancesco Publishing Services Manager: Patricia Tannian Project Manager: Carrie Stetz Design Direction: Steven Stave

Printed in China Last digit is the print number:  9  8  7  6  5  4  3  2  1

Associate Editors Dosang Cho, MD, PhD

Associate Professor Department of Neurosurgery Ewha Womens University Medical Center Seoul, Korea

Curtis A. Dickman, MD

Director, Spinal Research Associate Chief, Spine Section Division of Neurological Surgery Barrow Neurological Institute Phoenix, Arizona Clinical Assistant Professor Division of Neurosurgery University of Arizona College of Medicine Tucson, Arizona

Ilsup Kim, MD

Assistant Professor Department of Neurosurgery St. Vincent’s Hospital The Catholic University of Korea Suwon, Korea

Sangkook Lee, MD

Clinical Professor Department of Neurosurgery Guri Hospital Hanyang University Medical Center Guri, Gyeonggi-do, Korea

Alexander R. Vaccaro, MD, PhD Professor of Orthopaedic Surgery Thomas Jefferson University The Rothman Institute Philadelphia, Pennsylvania

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To my wife Anslie, my daughters Elise and Rebecca, and Sarah. Daniel H. Kim

To my wife Seunglim, my daughters Rachel and Jai, and my whole family. Dosang Cho

To my wife Celeste; my children Alexander, Rachel, and Jacob; and my entire family. Thank you for enriching my life, for teaching me, and for your love. Curtis A. Dickman

To my father Daejo, my mother Insun, my wife Okran, and my son Justin. Ilsup Kim

To my wife Kyongran Choi, my children Taehui and Taerin, and my entire family. I appreciate my mentors, Dr. Sehoon Kim and Dr. Daniel H. Kim, for supporting me and giving me a great opportunity. I always have the greatest respect and honor for you. Sangkook Lee

To my wife Lauren, and children Alex and Juliana. Without their love and support my continued dedication to education and writing would not be possible. Alexander R. Vaccaro

Acknowledgments I would like to acknowledge medical editor Michelle Ong and medical illustrators Mijin Jung and Sangwon Yeo, whose combined hard work, long hours, and dedicated resolve made this book possible. Daniel H. Kim

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Preface The fundamentals of spine surgery revolve around a thorough understanding of anatomy and surgical technique. With new instrumentation and minimally invasive techniques, spinal surgery has become complex in the twentyfirst century. From occipital cervical fusions to sacroiliac fixation, the spine surgeon of today is confronted with an extensive array of surgical options. The rapid pace of technological change in this field has left many spine surgeons and colleagues struggling to keep up. The increasing variety of options for surgical treatments of spinal injury and disease renders the decision-making process regarding the use of any particular approach, procedure, or technology more and more difficult. In addition to instrumentation, minimally invasive spinal techniques are becoming common. With smaller and smaller incisions, spine surgeons find themselves working with a smaller aperture and, subsequently, a limited view. Without exposure of the adjacent anatomic structures, these techniques can create a challenge. This challenge occurs not only with decompressions, but also with percutaneous instrumentation placement. This instrumentation and these techniques are being used for an increasing patient base. Spinal instrumentation

is used not only for trauma and degenerative disease, but also, with new techniques, increasingly in cases of tumor and infection. In light of the myriad advancements, the topic of occipital cervical fusion is addressed, including cervical plating techniques along with atlantoaxial fixation devices. In addition, a review of fusions of the cervicothoracic and thoracolumbar regions is provided, as these transition zones have led to a new level of complexity. Last, longer fusion constructs have led to sacroiliac fixation. Whether confronted with new instrumentation or minimally invasive techniques, the spine surgeon has to rely on the fundamentals of anatomy and technique. Thus, these essential items are reviewed to provide the spine surgeon with an armamentarium to approach increasingly complex issues facing medicine today. Max C. Lee, MD Clinical Instructor Department of Neurosurgery Stanford University Medical Center Stanford, California

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Contributors Daniel Aghion, MD

Resident, Department of Neurosurgery, Brown University, Rhode Island Hospital and Hasbro Children’s Hospital, Providence, Rhode Island Surgical Approaches to the Craniovertebral Junction in Rheumatoid Arthritis

Henry Ahn, MD

Scientist, Keenan Research Centre of the Li Ka Shing Knowledge Institute of St. Michael’s Hospital; Assistant Professor, Division of Orthopaedic Surgery; Assistant Professor, University of Toronto Spine Program, University of Toronto, Toronto, ON, Canada Surgical Approach to Posttraumatic Thoracic Kyphosis

Jaren D. Ament, MD

Resident, Department of Neurological Surgery, University of California–Davis School of Medicine, Sacramento, California Cervical Microforaminotomy and Decompressive Laminectomy

Anubhav G. Amin, MD

Resident, Department of Neurosurgery, New York Medical College, Valhalla, New York Posterior Approaches to the Craniovertebral Junction: Lateral Transcondylar Approach

Howard S. An, MD

Professor of Orthopedic Surgery, Rush University Medical Center, Chicago, Illinois Cervical Laminoplasty

Frank Attenello, MD

Resident, Department of Neurological Surgery, Keck School of Medicine, University of Southern California, Los Angeles, California Lumbar Microdiskectomy: Midline Open and FarLateral Techniques

Ioannis Avramis, MD

Orthopedic Surgeon, Minimally Invasive Spine Institute, Dallas, Texas Iliac Fixation

Neil Badlani, MD

Orthopedic Surgeon/Spine Surgeon, The Orthopedic Sports Clinic, Houston, Texas Cervical Laminoplasty

Rahul Basho, MD

Riverside County Regional Medical Center, Los Angeles, California Surgical Approaches to Cervical Kyphosis and Deformity x

Monique J. Boomsaad, MD

Resident, Department of Neurosurgery, University of Michigan, Ann Arbor, Michigan Surgical Decompression and Stabilization Techniques in Thoracic Trauma

Darrel S. Brodke, MD

Professor and Vice Chairman, Department of Orthopedics, Director of the University Spine Center, University of Utah School of Medicine, Salt Lake City, Utah Anterior Transthoracic Approaches to the Thoracic Spine

Colin C. Buchanan, MD

Department of Neurosurgery, David Geffen School of Medicine, University of California–Los Angeles, Los Angeles, California Transmaxillary and Transmandibular Approaches to the Clivus and Upper Cervical Spine

Kevin S. Cahill, MD, PhD, MPH

Department of Neurological Surgery, University of Miami Miller School of Medicine, Miami, Florida Anterior Lumbar Interbody Fusion

Thomas D. Cha, MD, MBA

Instructor, Orthopaedic Surgery, Harvard Medical School; Orthopaedic Spine Surgeon, Massachusetts General Hospital, Boston, Massachusetts Lumbar Facet Screw Fixation Techniques

Fady T. Charbel, MD

Department of Neurosurgery, College of Medicine, University of Illinois at Chicago, Chicago, Illinois Vascular Lesions of the Spinal Cord

Samuel K. Cho, MD

Assistant Professor, Adult and Pediatric Spinal Surgery, Leni & Peter W. May Department of Orthopaedics, Mount Sinai School of Medicine and Hospital, New York, New York Surgical Anatomy and Biomechanics in the Cervicothoracic Junction and Thoracic Spine

Gun Choi, MD, PhD

President, Medical Affairs, Wooridul Spine Hospital; Chief, Endoscopic Spinal Treatment Center; Invited Assistant Professor, College of Medicine, Hanyang University, Seoul, Korea Percutaneous Endoscopic Diskectomy

Contributors

Haroon F. Choudhri, MD

Associate Professor, Department of Neurosurgery, Chief, Section of Adult Neurosurgery, Director, Neurosurgery Spine Service at Georgia Health Sciences University, Augusta, Georgia Anterior Cervical Instrumentation Techniques

Omar Choudhri, MD

Resident, Department of Neurosurgery, Stanford University, Stanford, California Cervical Corpectomy, Fusion, and Vertebral Restoration Techniques

John S. Claff, MD

Department of Orthopaedic Surgery, Massachusetts General Hospital, Boston, Massachusetts Lumbar Facet Screw Fixation Techniques

Nader S. Dahdaleh, MD

Department of Neurosurgery, University of Iowa, Iowa City, Iowa Surgical Stabilization Techniques for Thoracolumbar Fractures

Andrew Dailey, MD

Department of Neurosurgery, University of Utah, Salt Lake City, Utah Ossification of the Posterior Longitudinal Ligament

Curtis A. Dickman, MD

Director, Spinal Research and Associate Chief, Spine Section, Division of Neurological Surgery, Barrow Neurological Institute, Phoenix, Arizona; Clinical Assistant Professor, Division of Neurosurgery, University of Arizona College of Medicine, Tucson, Arizona C1–C2 Trauma Injuries and Stabilization Techniques Bone Graft Harvesting Techniques

Dzung Dinh, MD, MBA

Professor of Neurosurgery, University of Illinois College of Medicine, Peoria, Illinois Surgical Anatomy and Biomechanics of the Craniovertebral Junction

Mark S. Eskander, MD

Orthopaedic Surgeon, Christiana Spine Center, Christiana Health Care System, Newark, Delaware Spondylolisthesis Reduction

Kyle M. Fargen, MD

Resident, Department of Neurosurgery, University of Florida College of Medicine, Gainesville, Florida Transoral Approach to the Craniocervical Junction and Upper Cervical Spine Approaches to the Craniocervical Junction: Posterior and Lateral Approaches

Farrokh R. Farrokhi, MD

Department of Neurosurgery, University of Washington, Seattle, Washington Ossification of the Posterior Longitudinal Ligament

Iman Feiz-Erfan, MD

Department of Neurosurgery, St. Joseph’s Hospital and Medical Center, Phoenix, Arizona C1–C2 Trauma Injuries and Stabilization Techniques

Michael Finn, MD

Assistant Professor, Department of Neurosurgery, University of Colorado School of Medicine, Aurora, Colorado Dural Tears

Todd B. Francis, MD

Department of Neurosurgery, Cleveland Clinic, Cleveland, Ohio Transpedicular Screw Fixation: Open and Percutaneous Techniques

Anthony K. Frempong-Boadu, MD

Associate Professor, Director of Neuro Residency Training Program, Director, Division of Spinal Surgery, Department of Neurosurgery, New York University Langone Medical Center, New York, New York Posterior Approaches to the Cervicothoracic Junction: Transpedicular, Costotransversectomy, Lateral Extracavitary, and Parascapular Extrapleural Approaches

Jared Fridley, MD

Resident, Department of Neurosurgery, Baylor College of Medicine, Houston, Texas Surgical Decompression and Stabilization for Lumbar Lesions: Osteomyelitis and Tumors

Aruna Ganju, MD

Department of Neurological Surgery, Northwestern University Feinberg School of Medicine, Chicago, Illinois Facet Dislocation Injuries and Surgical Management Surgical Anatomy and Operative Techniques of Lumbar Stenosis

Maurice Goins, MD

Surgeon, Resurgens PC Orthopaedics, Morrow, Georgia Ankylosing Spondylitis: Posterior Approaches (Osteotomy) to the Cervical and Lumbar Spine in the Management of a Fixed Sagittal Plane Deformity

Andrew Grossbach, MD

Department of Neurosurgery, University of Iowa, Iowa City, Iowa Surgical Stabilization Techniques for Thoracolumbar Fractures

Munish Gupta, MD

Professor, Co-Director of Spine Center, Chief of Orthopaedic Spinal Disorders Service, University of California–Davis, Sacramento, California Sacral Screw Fixation and Plating Techniques Iliac Fixation Anterior and Posterior Treatment for Thoracolumbar and Lumbar Scoliosis

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Contributors

Sachin Gupta, MD

University of California–Davis, Sacramento, California Anterior and Posterior Treatment for Thoracolumbar and Lumbar Scoliosis

Yoon Ha, MD, PhD

Department of Neurosurgery, Severance Hospital, College of Medicine, Yonsei University, Seoul, Korea Posterior Cervical Stabilization Techniques: Cervical Pedicle Screw Fixation, Lateral Mass Screw Fixation, and Wiring

Jeffrey S. Henn, MD

Assistant Professor, Department of Neurosurgery, University of Florida, Gainesville, Florida Bone Graft Harvesting Techniques

Sarah Henry, MPH

Professional Research Assistant, Department of Orthopaedics, University of Colorado, Denver, Colorado Dural Tears

Joshua P. Herzog, MD

Department of Orthopaedic Surgery, Massachusetts General Hospital, Boston, Massachusetts Lumbar Facet Screw Fixation Techniques

Alan Hilibrand, MD

Professor of Orthopaedic Surgery and Neurosurgery, Rothman Institute and Jefferson Medical College, Philadelphia, Pennsylvania Ankylosing Spondylitis: Posterior Approaches (Osteotomy) to the Cervical and Lumbar Spine in the Management of a Fixed Sagittal Plane Deformity

Jayme R. Hiratzka, MD

Department of Orthopaedics, University of Utah School of Medicine, Salt Lake City, Utah Anterior Transthoracic Approaches to the Thoracic Spine

Patrick W. Hitchon, MD

Professor of Neurosurgery and Bioengineering, Director, Spine Fellowship, Department of Neurosurgery, University of Iowa, Iowa City, Iowa Surgical Stabilization Techniques for Thoracolumbar Fractures

Daniel J. Hoh, MD

Assistant Professor of Neurological Surgery, University of Florida Malcom Randall VA Medical Center; Joint Assistant Professor of Neuroscience, University of Florida, Gainesville, Florida Transoral Approach to the Craniocervical Junction and Upper Cervical Spine Approaches to the Craniocervical Junction: Posterior and Lateral Approaches

Patrick Hsieh, MD

Assistant Professor of Clinical Neurological Surgery, Keck School of Medicine, University of Southern California, Los Angeles, California Lumbar Microdiskectomy: Midline Open and FarLateral Techniques

Steven W. Hwang, MD

Division of Pediatric Neurosurgery, Floating Children’s Hospital, Department of Neurosurgery, Tufts University, Boston, Massachusetts Surgical Approaches to Craniovertebral Junction Congenital Malformations, Chiari Malformations, and Cranial Settling (Invagination) Anterior Release and Fusion Techniques for Scoliosis

Daniel S. Ikeda, MD

Department of Neurological Surgery, The James Comprehensive Cancer Center and The Wexner Medical Center at the Ohio State University, Columbus, Ohio Surgical Approaches to Thoracic Primary and Secondary Tumors

Sivakumar Jaikumar, MD

Assistant Professor, Section Chief of Spinal Neurosurgery, Department of Neurosurgery, University of North Carolina School of Medicine, Chapel Hill, North Carolina Surgical Approaches to Lumbar Fractures

Andrew Jea, MD

Assistant Professor, Neuro-Spine Program, Division of Pediatric Neurosurgery, Texas Children’s Hospital, Department of Neurosurgery, Baylor College of Medicine, Houston, Texas Surgical Approaches to Craniovertebral Junction Congenital Malformations, Chiari Malformations, and Cranial Settling (Invagination) Anterior Release and Fusion Techniques for Scoliosis

David H. Jho, MD, PhD

Neurosurgery Service, Massachusetts General Hospital and Harvard Medical School, Boston, Massachusetts Endoscopic Anterior Cervical Foraminotomy (Jho Procedure)

Diana H. Jho, MD

Department of Neuroendoscopy, Jho Institute for Minimally Invasive Neurosurgery, Allegheny General Hospital, Drexel University College of Medicine, Pittsburgh, Pennsylvania Endoscopic Anterior Cervical Foraminotomy (Jho Procedure)

Hae-Dong Jho, MD, PhD

Professor and Chairman, Department of Neuroendoscopy, Jho Institute for Minimally Invasive Neurosurgery, Allegheny General Hospital, Drexel University College of Medicine, Pittsburgh, Pennsylvania Endoscopic Anterior Cervical Foraminotomy (Jho Procedure)

Contributors

Sungsam Jung, MD, PhD

Department of Neurosurgery, Eulji University School of Medicine, Daejeon, Korea High Cervical Retropharyngeal Approach to the Craniocervical Junction

M. Yashar S. Kalani, MD

Resident, Division of Neurological Surgery, Barrow Neurological Institute, Phoenix, Arizona C1–C2 Trauma Injuries and Stabilization Techniques

Iain H. Kalfas, MD

Department of Neurosurgery, Cleveland Clinic, Cleveland, Ohio Transpedicular Screw Fixation: Open and Percutaneous Techniques

James D. Kang, MD

Vice Chairman, Department of Orthopaedic Surgery, Director of the Ferguson Laboratory for Spine Research, Professor of Orthopaedic and Neurological Surgery, UPMC Endowed Chair in Orthopaedic Spine Surgery, University of Pittsburgh and UPMC, Pittsburgh, Pennsylvania Spondylolisthesis Reduction

Sadashiv Karanth, MD

Resident, Department of Neurosurgery, University of Illinois College of Medicine, Peoria, Illinois Surgical Anatomy and Biomechanics of the Craniovertebral Junction

Abhishek Kashyap, MD

Assistant Professor, Central Institute of Orthopedics, VMMC and Safdarjang Hospital, New Delhi, India Percutaneous Endoscopic Diskectomy

Noojan Kazemi, MD

Senior Fellow, Department of Neurosurgery, University of Washington, Seattle, Washington Anterior and Posterior Cervicothoracic Junction Stabilization Techniques

Michael Kelly, MD

Assistant Professor, Orthopaedic Surgery, Washington University School of Medicine, St. Louis, Missouri Surgical Treatment of Adolescent Idiopathic Scoliosis: Lenke Curve Types 1 Through 6

Christopher Kepler, MD, MBA

Professor of Orthopaedic Surgery, Jefferson University Hospitals; Spine Surgeon, Rothman Institute and Jefferson Medical College, Philadelphia, Pennsylvania Ankylosing Spondylitis: Posterior Approaches (Osteotomy) to the Cervical and Lumbar Spine in the Management of a Fixed Sagittal Plane Deformity

Edward E. Kerr, MD

Resident, Department of Neurological Surgery, University of California, Davis Medical Center, Sacramento, California Surgical Technique for Resection of Intradural Tumors

Daniel H. Kim, MD

Director, Reconstructive Spinal and Peripheral Nerve Surgery, Mischer Neuroscience Institute; Professor, Vivian L. Smith Department of Neurosurgery, University of Texas Health Science Center, Houston, Texas Anterior Approaches to the Cervicothoracic Junction Thoracoscopic and Posterior Endoscopic Approaches to the Thoracic Spine Surgical Anatomy and Posterior Approach to the Thoracic and Thoracolumbar Spine Thoracoabdominal Approach to the Thoracolumbar Junction Posterior and Transforaminal Lumbar Interbody Fusion Surgical Resection of Sacral Tumors/Sacrectomy and Lumbopelvic Reconstruction

Ilsup Kim, MD

Assistant Professor, Department of Neurosurgery, St. Vincent’s Hospital, The Catholic University of Korea, Suwon, Korea Anterior Approaches to the Cervicothoracic Junction Thoracoscopic and Posterior Endoscopic Approaches to the Thoracic Spine Posterior and Transforaminal Lumbar Interbody Fusion Surgical Resection of Sacral Tumors/Sacrectomy and Lumbopelvic Reconstruction

Kee D. Kim, MD

Associate Professor, Chief, Spinal Neurosurgery, University of California–Davis School of Medicine, Sacramento, California Cervical Microforaminotomy and Decompressive Laminectomy Primary Malignant and Benign Tumors of the Spine Secondary Metastatic Tumors of the Spine Surgical Technique for Resection of Intradural Tumors

Yong-Chul Kim, MD

Professor, Department of Anesthesiology and Pain Medicine, Seoul National University College of Medicine; Director, Pain Management Center, Seoul National University Hospital, Seoul, Korea Vertebroplasty and Kyphoplasty

Matthew M. Kimball, MD

Resident, Department of Neurosurgery, University of Florida College of Medicine, Gainesville, Florida Transoral Approach to the Craniocervical Junction and Upper Cervical Spine Approaches to the Craniocervical Junction: Posterior and Lateral Approaches

Eric O. Klineberg, MD

Assistant Professor, Spine Fellowship Program Director, Assistant Residency Director, University of California– Davis, Sacramento, California Primary Malignant and Benign Tumors of the Spine

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Contributors

Brian Kwon, MD

Assistant Clinical Professor, Department of Orthopedic Surgery, Tufts University School of Medicine, New England Baptist Hospital, Boston, Massachusetts Posterior and Posterolateral Approaches to the Lumbar Spine

Heum Dai Kwon, MD

Ronald Lehman, MD

Department of Orthopaedics and Rehabilitation, Walter Reed National Military Medical Center, Division of Orthopaedics, Department of Surgery, Uniformed Services University of the Health Sciences, Bethesda, Maryland Surgical Treatment of Flat Back Deformity

Visiting Scholar, Department of Neurological Surgery, University of California–Davis School of Medicine, Sacramento, California Cervical Microforaminotomy and Decompressive Laminectomy

G. Michael Lemole Jr, MD

Matthew Lafleur, MD

Lawrence G. Lenke, MD

Orthopaedic Surgeon, North Oaks Health System, Hammond, Louisiana Axial Lumbar Interbody Fusion

Division of Neurological Surgery, Department of Surgery, University of Arizona Health Sciences Center, Tucson, Arizona Vascular Lesions of the Spinal Cord

Department of Neurological Surgery, Cedars Sinai Medical Center, Los Angeles, California Anterior Lumbar Interbody Fusion

The Jerome J. Gilden Endowed Professor, Orthopaedic Surgery; Chief, Orthopedic Spine Surgery; Co-Director, Adult/Pediatric Scoliosis and Reconstructive Spinal Surgery; Professor, Neurological Surgery, Washington University School of Medicine, St. Louis, Missouri Surgical Treatment of Adolescent Idiopathic Scoliosis: Lenke Curve Types 1 Through 6

Tien V. Le, MD

Michael Lim, MD

Carl Lauryssen, MD

Department of Neurosurgery and Brain Repair, University of South Florida, Tampa, Florida Surgical Anatomy and Biomechanics in the Mid and Lower Cervical Spine

John Y.K. Lee, MD

Assistant Professor of Neurosurgery, Attending Neurosurgeon, and Medical Director, Penn Gamma Knife, Pennsylvania Hospital, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania Endoscopic Approaches to the Craniovertebral Junction

Jun Ho Lee, MD

Assistant Professor of Neurosurgery and Oncology, Director of the Metastatic Brain Tumor Center, Director of Brain Tumor Immunotherapy, Johns Hopkins University School of Medicine, Baltimore, Maryland Posterior Approaches to the Craniovertebral Junction: Lateral Transcondylar Approach

John C. Liu, MD

Department of Neurological Surgery, Cedars Sinai Medical Center, Los Angeles, California Lateral Lumbar Interbody Fusion

Steven C. Ludwig, MD

Neurosurgeon, Wooridul Spine Hospital, Seoul, Korea Anterior and Posterior Endoscopic Approaches to the Cervical Spine

Associate Professor of Orthopaedics, Department of Orthopaedics, University of Maryland, Baltimore, Maryland Surgical Management of Sacral Fractures

Peter Lee, MD

Hani R. Malone, MD

Sang-Ho Lee, MD, PhD

Rex A.W. Marco, MD

Department of Neurological Surgery, Northwestern University Feinberg School of Medicine, Chicago, Illinois Surgical Anatomy and Operative Techniques of Lumbar Stenosis Founder and President, Wooridul Spine Hospital; President-Elect, International Musculoskeletal Laser Society (IMLAS) and Founding President of Asian Academy of Minimally Invasive Spinal Surgery, Seoul, Korea Percutaneous Endoscopic Diskectomy

William Lee, MD

Resident, Department of Neurosurgery, University of Illinois College of Medicine, Peoria, Illinois Surgical Anatomy and Biomechanics of the Craniovertebral Junction

Resident, Department of Neurosurgery, Columbia University Medical Center, New York, New York Thoracic Microdiskectomy: Lateral and Posterolateral Approaches Associate Professor of Surgery, Chief of Spine Surgery and Musculoskeletal Oncology, University of Texas Medical School; Clinical Assistant Professor, Department of Orthopaedic Surgery, Baylor College of Medicine; Adjunct Assistant Professor, Department of Bioengineering, Rice University, Houston, Texas Anterior Retroperitoneal Approach to the Lumbar Spine Surgical Management of Degenerative Lumbar Scoliosis

Contributors

Nikolay L. Martirosyan, MD

Division of Neurological Surgery, Department of Surgery, University of Arizona Health Sciences Center, Tucson, Arizona Vascular Lesions of the Spinal Cord

Tobias A. Mattei, MD

Fellow, Department of Neurosurgery, University of Illinois College of Medicine, Peoria, Illinois Surgical Anatomy and Biomechanics of the Craniovertebral Junction

Marcus D. Mazur, MD

Resident, Department of Neurosurgery, University of Utah School of Medicine, Salt Lake City, Utah Odontoid Fractures and Screw Fixation

Beck Deal McAllister, MD

Tri-Parish Orthopedic & Neurological Institute, Houma, Louisiana

Todd McCall, MD

Assistant Professor of Neurosurgery, University of Illinois College of Medicine, Peoria, Illinois Surgical Anatomy and Biomechanics of the Craniovertebral Junction

Ehud Mendel, MD

Department of Neurological Surgery, The James Comprehensive Cancer Center and The Wexner Medical Center at the Ohio State University, Columbus, Ohio Surgical Approaches to Thoracic Primary and Secondary Tumors

Ahmed Mohyeldin, MD

Jae Keun Oh, MD

Spine Center, Department of Neurosurgery, Hallym University Sacred Heart Hospital, Seoul, Korea Posterior Cervical Stabilization Techniques: Cervical Pedicle Screw Fixation, Lateral Mass Screw Fixation, and Wiring

Ibrahim Omeis, MD

Assistant Professor, Department of Neurosurgery, Baylor College of Medicine, Houston, Texas Surgical Decompression and Stabilization for Lumbar Lesions: Osteomyelitis and Tumors

Jennifer Orning, MD

Resident, Department of Neurosurgery, University of North Carolina School of Medicine, Chapel Hill, North Carolina Surgical Approaches to Lumbar Fractures

Adetokunbo Oyelese, MD, PhD

Assistant Professor, Department of Neurosurgery, Brown Unversity, Providence, Rhode Island Surgical Approaches to the Craniovertebral Junction in Rheumatoid Arthritis

Donato Pacione, MD

Department of Neurosurgery, New York University Langone Medical Center, New York, New York Posterior Approaches to the Cervicothoracic Junction: Transpedicular, Costotransversectomy, Lateral Extracavitary, and Parascapular Extrapleural Approaches

Ripu R. Panchal, DO

Department of Neurological Surgery, The James Comprehensive Cancer Center and The Wexner Medical Center at the Ohio State University, Columbus, Ohio Surgical Approaches to Thoracic Primary and Secondary Tumors

Assistant Professor, Department of Neurological Surgery, University of California, Davis Medical Center, Sacramento, California Primary Malignant and Benign Tumors of the Spine Secondary Metastatic Tumors of the Spine Surgical Technique for Resection of Intradural Tumors

Robert A. Morgan, MD

Paul Park, MD

Sergey Neckrysh, MD

Soo Young Park, MD

Alfred T. Ogden, MD

Akash J. Patel, MD

Assistant Professor of Orthopaedic Surgery, University of Minnesota; Orthopaedic Surgeon, Regions Hospital, St. Paul, Minnesota Surgical Management of Scheuermann Kyphosis Department of Neurosurgery, College of Medicine, University of Illinois at Chicago, Chicago, Illinois Vascular Lesions of the Spinal Cord Director, Minimally Invasive Spine Surgery Program, New York Presbyterian Hospital/Columbia University Medical Center, New York, New York Thoracic Microdiskectomy: Lateral and Posterolateral Approaches

Assistant Professor, Neurological Surgery, University of Michigan, Ann Arbor, Michigan Surgical Decompression and Stabilization Techniques in Thoracic Trauma President of Medical Affairs, Seoul Chungdam Wooridul Spine Hospital, Seoul, Korea Vertebroplasty and Kyphoplasty Neuro-Spine Program, Division of Pediatric Neurosurgery, Texas Children’s Hospital; Department of Neurosurgery, Baylor College of Medicine, Houston, Texas Surgical Approaches to Craniovertebral Junction Congenital Malformations, Chiari Malformations, and Cranial Settling (Invagination) Anterior Release and Fusion Techniques for Scoliosis

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Contributors

Vikas Patel, MD

Associate Professor of Orthopaedic Surgery, University of Colorado School of Medicine; Chief, Orthopaedic Spine Surgery, University of Colorado Hospital, Denver, Colorado Axial Lumbar Interbody Fusion Dural Tears

Noel Perin, MD

Professor and Director of Minimally Invasive Spine Surgery, Department of Neurosurgery, New York University Langone Medical Center, New York, New York Posterior Approaches to the Cervicothoracic Junction: Transpedicular, Costotransversectomy, Lateral Extracavitary, and Parascapular Extrapleural Approaches

Tiffany Grace Perry, MD

Spine Fellowship, Cleveland Clinic, Cleveland, Ohio Surgical Approaches to Lumbar Fractures

Elizabeth S. Robinson, BS

University of Colorado Denver Health Sciences, Denver, Colorado Dural Tears

Stephen I. Ryu, MD

Staff Neurosurgeon, Palo Alto Medical Foundation and Stanford University Medical Center; Consulting Professor of Electrical Engineering, Stanford University, Stanford, California Cervical Corpectomy, Fusion, and Vertebral Restoration Techniques

Faheem Sandhu, MD

Associate Professor, Department of Neurosurgery, Georgetown University, Washington, DC Craniovertebral Junction Instabilities and Surgical Fixation Techniques

Meic H. Schmidt, MD

General Orthopedic Surgery, Bay Area Bone & Joint Center, Sacramento, California Chapter 53

Chief, Division of Spine Surgery; Associate Professor of Neurosurgery; Director, Spinal Oncology Service, Huntsman Cancer Institute; Director, Neurosurgery Spine Fellowship, University of Utah, Salt Lake City, Utah Odontoid Fractures and Screw Fixation

Edwin Ramos, MD

Jonathan Sellin, MD

Nicholas Pirnia, MD

Department of Neurological Surgery, The James Comprehensive Cancer Center and The Wexner Medical Center at the Ohio State University, Columbus, Ohio Surgical Approaches to Thoracic Primary and Secondary Tumors

Wilson Z. Ray, MD

Department of Neurosurgery, University of Utah, Salt Lake City, Utah Ossification of the Posterior Longitudinal Ligament

Shaan M. Raza, MD

Neurosurgical Resident Physician, Baylor College of Medicine, Houston, Texas Surgical Anatomy, Approaches, and Biomechanics in the Lumbosacral Pelvic Junction

Basheer A. Shakir, MD

Resident, Department of Neurosurgery, Georgia Health Sciences University, Augusta, Georgia Anterior Cervical Instrumentation Techniques

Jai-Joon Shim, MD, PhD

The Orthopedic Institute of Wisconsin, Milwaukee, Wisconsin

Associate Professor, Department of Neurosurgery, Soonchunhyang University Cheonan Hospital, Chungcheongnam-do, Korea Surgical Anatomy and Posterior Approach to the Thoracic and Thoracolumbar Spine Thoracoabdominal Approach to the Thoracolumbar Junction Surgical Decompression and Stabilization for Lumbar Lesions: Osteomyelitis and Tumors

Jay Rhee, MD

Amit Sood, MD

Chief Resident, Department of Neurosurgery, Johns Hopkins Medical Institutions, Baltimore, Maryland Posterior Approaches to the Craniovertebral Junction: Lateral Transcondylar Approach

Brandon J. Rebholz, MD

Resident, Department of Neurosurgery, Georgetown University Hospital, Washington, DC Anterior Cervical Diskectomy and Fusion

Albert L. Rhoton Jr, MD

Professor and Chairman, Department of Neurological Surgery, University of Florida, Gainesville, Florida Transoral Approach to the Craniocervical Junction and Upper Cervical Spine Approaches to the Craniocervical Junction: Posterior and Lateral Approaches

Resident, Department of Orthopaedics, University of Medicine and Dentistry–New Jersey Medical School, Newark, New Jersey Bacterial, Fungal, and Tuberculosis Diskitis and Osteomyelitis of the Cervical, Thoracic, and Lumbar Spine

Contributors

Patrick A. Sugrue, MD

Department of Neurological Surgery, Northwestern University Feinberg School of Medicine, Chicago, Illinois Facet Dislocation Injuries and Surgical Management Lateral Lumbar Interbody Fusion

Peter Syre, MD

Resident, Department of Neurosurgery, University of Pennsylvania, Philadelphia, Pennsylvania Endoscopic Approaches to the Craniovertebral Junction

Gabriel Tender, MD

Associate Professor of Clinical Neurosurgery, Adjunct Professor, Family Nursing Department at Louisiana State University School of Medicine, New Orleans, Louisiana Surgical Management of Gunshot Wounds to the Spine

Khoi D. Than, MD

Resident, Department of Neurosurgery, University of Michigan, Ann Arbor, Michigan Surgical Decompression and Stabilization Techniques in Thoracic Trauma

Nicholas Theodore, MD

Division of Neurological Surgery, Department of Surgery, University of Arizona Health Sciences Center, Tucson, Arizona Vascular Lesions of the Spinal Cord

Trent L. Tredway, MD

Department of Neurological Surgery and Department of Orthopaedics and Sports Medicine, University of Washington, Seattle, Washington Anterior and Posterior Cervicothoracic Junction Stabilization Techniques

Juan S. Uribe, MD

Department of Neurosurgery and Brain Repair, University of South Florida, Tampa, Florida Surgical Anatomy and Biomechanics in the Mid and Lower Cervical Spine

Juan M. Valdivia-Valdivia, MD

Michael J. Vives, MD

Associate Professor, Department of Orthopaedics, University of Medicine and Dentistry–New Jersey Medical School, Newark, New Jersey Bacterial, Fungal, and Tuberculosis Diskitis and Osteomyelitis of the Cervical, Thoracic, and Lumbar Spine

Jean-Marc Voyadzis, MD

Assistant Professor, Department of Neurosurgery, Medical Director, CMH Neurosurgery Program, Georgetown University Hospital, Washington, DC Anterior Cervical Diskectomy and Fusion

Jeff Wang, MD

University of California–Los Angeles, Los Angeles, California Surgical Approaches to Cervical Kyphosis and Deformity

Michael Y. Wang, MD

Associate Professor, Departments of Neurological Surgery & Rehabilitation Medicine, University of Miami Miller School of Medicine, Miami, Florida Anterior Lumbar Interbody Fusion

Taylor Wilson, BS

New York University Langone Medical Center, New York, New York Posterior Approaches to the Cervicothoracic Junction: Transpedicular, Costotransversectomy, Lateral Extracavitary, and Parascapular Extrapleural Approaches

M. Neil Woodall, MD

Resident, Department of Neurosurgery, Georgia Health Sciences University, Augusta, Georgia Anterior Cervical Instrumentation Techniques

Robert J. Woodruff, MD

Physician, Black Hills Orthopedic and Spine Center, Rapid City, South Dakota Surgical Management of Degenerative Lumbar Scoliosis

Clinical Lecturer, Neurological Surgery, Department of Neurosurgery, University of Michigan, Ann Arbor, Michigan Surgical Decompression and Stabilization Techniques in Thoracic Trauma

Albert P. Wong, MD

Steven Viljoen, MD

Kirkham B. Wood, MD

Department of Neurosurgery, University of Iowa, Iowa City, Iowa Surgical Stabilization Techniques for Thoracolumbar Fractures

Department of Neurological Surgery, Northwestern University Feinberg School of Medicine, Chicago, Illinois Surgical Anatomy and Operative Techniques of Lumbar Stenosis Regions Hospital, St. Paul, Minnesota

Isaac Yang, MD

Department of Neurosurgery, David Geffen School of Medicine, University of California–Los Angeles, Los Angeles, California Transmaxillary and Transmandibular Approaches to the Clivus and Upper Cervical Spine

xvii

xviii

Contributors

Seong Yi, MD, PhD

Assistant Professor, Department of Neurosurgery, Yonsei University College of Medicine, Seoul, Korea Cervical Disk Arthroplasty Techniques

Do Heum Yoon, MD, PhD

Professor, Chief of Spinal Neurosurgery Section, Department of Neurosurgery, Yonsei University College of Medicine, Seoul, Korea Cervical Disk Arthroplasty Techniques Posterior Cervical Stabilization Techniques: Cervical Pedicle Screw Fixation, Lateral Mass Screw Fixation, and Wiring

Usman Zahir, MD

Spine Fellow, Department of Orthopaedics, University of Maryland, Baltimore, Maryland Surgical Management of Sacral Fractures

Contents SECTION A Craniovertebral Junction and Upper Cervical Spine,  1   1 Surgical Anatomy and Biomechanics of the Craniovertebral Junction,  2

DZUNG DINH, TODD MCCALL, TOBIAS A. MATTEI, SADASHIV KARANTH, AND WILLIAM LEE

  2 Transoral Approach to the Craniocervical Junction and Upper Cervical Spine,  17

MATTHEW M. KIMBALL, KYLE M. FARGEN, ALBERT L. RHOTON JR, AND DANIEL J. HOH

  3 Transmaxillary and Transmandibular

Approaches to the Clivus and Upper Cervical Spine,  30 COLIN C. BUCHANAN AND ISAAC YANG

  4 High Cervical Retropharyngeal Approach to the Craniocervical Junction,  38 SUNGSAM JUNG

  5 Approaches to the Craniocervical Junction: Posterior and Lateral Approaches,  47

KYLE M. FARGEN, MATTHEW M. KIMBALL, ALBERT L. RHOTON JR, AND DANIEL J. HOH

  6 Posterior and Far-Lateral Approaches to the Craniovertebral Junction: Lateral Transcondylar Approach,  54

ANUBHAV G. AMIN, SHAAN M. RAZA, AND MICHAEL LIM

  7 Endoscopic Approaches to the Craniovertebral Junction,  60

PETER SYRE AND JOHN Y.K. LEE

  8 Surgical Approaches to Craniovertebral

Junction Congenital Malformations, Chiari Malformations, and Cranial Settling (Invagination),  69 AKASH J. PATEL, STEVEN W. HWANG, AND ANDREW JEA

12 C1–C2 Trauma Injuries and Stabilization Techniques,  110

M. YASHAR S. KALANI, IMAN FEIZ-ERFAN, AND CURTIS A. DICKMAN

SECTION B Mid and Lower Cervical Spine,  119 13 Surgical Anatomy and Biomechanics in the Mid and Lower Cervical Spine,  120 TIEN V. LE AND JUAN S. URIBE

14 Anterior Cervical Diskectomy and Fusion,  131 JAY RHEE AND JEAN-MARC VOYADZIS

15 Endoscopic Anterior Cervical Foraminotomy (Jho Procedure),  139

HAE-DONG JHO, DIANA H. JHO, AND DAVID H. JHO

16 Anterior and Posterior Endoscopic Approaches to the Cervical Spine,  153 JUN HO LEE

17 Cervical Corpectomy, Fusion, and Vertebral Restoration Techniques,  162 OMAR CHOUDHRI AND STEPHEN I. RYU

18 Anterior Cervical Instrumentation Techniques,  182

BASHEER A. SHAKIR, M. NEIL WOODALL, AND HAROON F. CHOUDHRI

19 Cervical Disk Arthroplasty Techniques,  187 DO HEUM YOON AND SEONG YI

20 Cervical Microforaminotomy and Decompressive Laminectomy,  196

JARED D. AMENT, HEUM DAI KWON, AND KEE D. KIM

21 Cervical Laminoplasty,  203 NEIL BADLANI AND HOWARD AN

22 Posterior Cervical Stabilization

Junction in Rheumatoid Arthritis,  77

Techniques: Cervical Pedicle Screw Fixation, Lateral Mass Screw Fixation, and Wiring,  214

DANIEL AGHION AND ADETOKUNBO OYELESE

DO HEUM YOON, YOON HA, AND JAE KEUN OH

  9 Surgical Approaches to the Craniovertebral

10 Craniovertebral Junction Instabilities

and Surgical Fixation Techniques,  92 FAHEEM SANDHU

11 Odontoid Fractures and Screw Fixation,  103

MARCUS D. MAZUR AND MEIC H. SCHMIDT

23 Facet Dislocation Injuries and Surgical Management,  222

PATRICK A. SUGRUE AND ARUNA GANJU

24 Ossification of the Posterior Longitudinal Ligament,  232

WILSON Z. RAY, FARROKH R. FARROKHI, AND ANDREW DAILEY

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xx

Contents

SECTION C Cervicothoracic Junction and Thoracic Spine,  242

37 Anterior Retroperitoneal Approach

25 Surgical Anatomy and Biomechanics in

38 Posterior and Posterolateral Approaches to the

the Cervicothoracic Junction and Thoracic Spine,  243 SAMUEL K. CHO

26 Anterior Approaches to the Cervicothoracic Junction,  249

ILSUP KIM AND DANIEL H. KIM

27 Posterolateral Approaches to the Cervicothoracic Junction: Transpedicular, Costotransversectomy, Lateral Extracavitary, and Parascapular Extrapleural Approaches,  254 DONATO PACIONE, TAYLOR WILSON, NOEL PERIN, AND ANTHONY FREMPONG-BOADU

28 Anterolateral Transthoracic Approaches to the Thoracic Spine,  267

JAYME R. HIRATZKA AND DARREL S. BRODKE

29 Anterior and Posterior Cervicothoracic Junction Stabilization Techniques,  274 NOOJAN KAZEMI AND TRENT L. TREDWAY

30 Thoracic Microdiskectomy: Lateral and Posterolateral Approaches,  282 HANI R. MALONE AND ALFRED T. OGDEN

31 Thoracoscopic and Posterior Endoscopic Approaches to the Thoracic Spine,  294 ILSUP KIM AND DANIEL H. KIM

32 Surgical Decompression and Stabilization Techniques in Thoracic Trauma,  309

KHOI D. THAN, MONIQUE J. BOOMSAAD, JUAN M. VALDIVIA-VALDIVIA, AND PAUL PARK

33 Surgical Approaches to Thoracic Primary and Secondary Tumors,  315

DANIEL S. IKEDA, AHMED MOHYELDIN, EDWIN RAMOS, AND EHUD MENDEL

to the Lumbar Spine,  375 REX A.W. MARCO

Lumbar Spine,  382 BRIAN KWON

39 Surgical Approaches to Lumbar Fractures,  389 TIFFANY GRACE PERRY, JENNIFER ORNING, AND SIVAKUMAR JAIKUMAR

40 Surgical Decompression and Stabilization for Lumbar Lesions: Osteomyelitis and Tumors,  397

JARED FRIDLEY, JAI-JOON SHIM, AND IBRAHIM OMEIS

41 Lumbar Microdiskectomy: Midline Open and FarLateral Techniques,  404

FRANK ATTENELLO AND PATRICK HSIEH

42 Percutaneous and Endoscopic Diskectomy,  412 GUN CHOI, SANG-HO LEE, AND ABHISHEK KASHYAP

43 Surgical Anatomy and Operative Techniques of Lumbar Stenosis,  426

PETER LEE, ALBERT P. WONG, AND ARUNA GANJU

44 Transpedicular Screw Fixation: Open and Percutaneous Techniques,  432 IAIN H. KALFAS AND TODD B. FRANCIS

45 Posterior and Transforaminal Lumbar Interbody Fusion,  440

ILSUP KIM AND DANIEL H. KIM

46 Anterior Lumbar Interbody Fusion,  450 MICHAEL Y. WANG, KEVIN S. CAHILL, AND CARL LAURYSSEN

47 Lateral Lumbar Interbody Fusion,  459 PATRICK A. SUGRUE AND JOHN C. LIU

48 Spondylolisthesis Reduction,  470 MARK S. ESKANDER AND JAMES D. KANG

49 Lumbar Facet Screw Fixation Techniques,  477 JOHN S. CLAPP, JOSHUA P. HERZOG, AND THOMAS D. CHA

SECTION D Thoracolumbar and Lumbar Spines,  324 34 Surgical Anatomy and Posterior Approach to the Thoracic and Thoracolumbar Spine,  325 JAI-JOON SHIM AND DANIEL H. KIM

35 Thoracoabdominal Approach to the Thoracolumbar Junction,  344 JAI-JOON SHIM AND DANIEL H. KIM

36 Surgical Stabilization Techniques for Thoracolumbar Fractures,  365

NADER S. DAHDALEH, STEPHANUS VILJOEN, ANDREW J. GROSSBACH, AND PATRICK W. HITCHON

SECTION E Lumbar Sacral Pelvic Junction,  482 50 Surgical Anatomy, Approaches,

and Biomechanics in the Lumbosacral Pelvic Junction,  483 JONATHAN N. SELLIN

51 Surgical Management of Sacral Fractures,  497 USMAN ZAHIR AND STEVEN C. LUDWIG

52 Axial Lumbar Interbody Fusion,  506 MATT LAFLEUR AND VIKAS PATEL

Contents

53 Sacral Screw Fixation and Plating Techniques,  513

MUNISH GUPTA AND NICHOLAS PIRNIA

54 Iliac Fixation,  526 IOANNIS AVRAMIS AND MUNISH GUPTA

55 Surgical Resection of Sacral Tumors/Sacrectomy and Lumbopelvic Reconstruction,  532 ILSUP KIM AND DANIEL H. KIM

65 Secondary Metastatic Tumors of the Spine,  633 RIPUL R. PANCHAL AND KEE D. KIM

66 Surgical Technique for Resection of Intradural Tumors,  639

RIPUL R. PANCHAL, EDWARD E. KERR, AND KEE D. KIM

67 Vascular Lesions of the Spinal Cord,  646 NIKOLAY L. MARTIROSYAN, SERGEY NECKRYSH, FADY T. CHARBEL, NICHOLAS THEODORE, AND G. MICHAEL LEMOLE JR

SECTION F Spinal Deformity,  545

SECTION H Inflammatory Disease,  661

56 Surgical Approaches to Cervical Kyphosis and

68 Ankylosing Spondylitis: Posterior Approaches

Deformity,  546

RAHUL BASHO, BECK DEAL MCALLISTER, BRANDON J. REBHOLZ, AND JEFFREY WANG

57 Surgical Management of Scheuermann Kyphosis,  558

ROBERT A. MORGAN AND KIRKHAM B. WOOD

58 Surgical Approach to Posttraumatic Thoracic Kyphosis,  564 HENRY AHN

59 Anterior Release and Fusion Techniques for Scoliosis,  568

STEVEN W. HWANG, AKASH PATEL, AND ANDREW JEA

60 Anterior and Posterior Treatment for

Thoracolumbar and Lumbar Scoliosis,  578 SACHIN GUPTA AND MUNISH GUPTA

61 Surgical Treatment of Adolescent Idiopathic

Scoliosis: Lenke Curve Types 1 Through 6,  587 LAWRENCE G. LENKE AND MICHAEL P. KELLY

62 Surgical Treatment of Flat Back Deformity,  601 RONALD LEHMAN

63 Surgical Management of Degenerative Lumbar Scoliosis,  610

REX A.W. MARCO AND ROBERT J. WOODRUFF

SECTION G Spinal Tumors and Vascular Lesions,  621 64 Primary Malignant and Benign Tumors of the Spine,  622

RIPUL R. PANCHAL, ERIC O. KLINEBERG, AND KEE D. KIM

(Osteotomy) to the Cervical and Lumbar Spine in the Management of a Fixed Sagittal Plane Deformity,  662 ALAN HILIBRAND, MAURICE GOINS, AND CHRISTOPHER KEPLER

SECTION I Spinal Infection,  671 69 Bacterial, Fungal, and Tuberculosis Diskitis and Osteomyelitis of the Cervical, Thoracic, and Lumbar Spine,  672 MICHAEL J. VIVES AND AMIT SOOD

SECTION J Miscellaneous,  685 70 Surgical Management of Gunshot Wounds to the Spine,  686 GABRIEL TENDER

71 Vertebroplasty and Kyphoplasty,  694 SOO YOUNG PARK AND YONG-CHUL KIM

72 Bone Graft Harvesting Techniques,  704 JEFFREY S. HENN AND CURTIS A. DICKMAN

73 Dural Tears,  710 VIKAS PATEL, SARAH E. HENRY, ELIZABETH S. ROBINSON, AND MICHAEL FINN

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SECTION

A Craniovertebral Junction and Upper Cervical Spine

1

1

Surgical Anatomy and Biomechanics of the Craniovertebral Junction DZUNG DINH, TODD MCCALL, TOBIAS A. MATTEI, SADASHIV KARANTH, and WILLIAM LEE

Overview The anatomic relationship at the craniovertebral junction (CVJ) is quite complex. The foramen magnum, the atlas, and the axis together comprise the CVJ and provide the anatomic anchor that connects the cranium to the cervical spine below. The special bony configuration and articulation in this transitional zone are unique and have more built-in flexibility than any other region in the spine. The stability and complex movement of the CVJ region is dependent on highly intricate arrangements of ligamentous, membranous, and muscular structures. This chapter covers the developmental embryology of the CVJ, its anatomy, and the biomechanics unique to this region.

Embryology of the Craniovertebral Junction NORMAL DEVELOPMENTAL EMBRYOLOGY OF THE CRANIOVERTEBRAL JUNCTION The CVJ is a unique entity distinct in its form, function, and development from the remainder of the vertebral skeletal system. It comprises the occipital somites and the first three cervical somites (Fig. 1-1): the occipital somites are the first four somites; the first three cervical somites are numbered five through seven. Controversy is ongoing regarding the proper number of occipital somites in vertebrates, ranging from four to five according to various authors; for the purposes of our discussion, we will concede that the first four somites are included in this group. The first three occipital somites give rise to an axial perichordal sclerotome and a lateral sclerotome. The axial perichordal sclerotomes at these levels, however, do not undergo resegmentation and therefore never subdivide into loose cranial and dense caudal zones. Because of the absence of a dense zone, the intervertebral boundary zone (IBZ) fails to form, and they all eventually fuse into a single unit, which chondrifies to become the rostral basiocciput. The lateral sclerotomes of these occipital somites, like their vertebral counterparts, do in fact form dense and loose zones; the loose zones of the second and third sclerotomes ultimately develop into the upper and lower hypoglossal nerve roots and the corre2

sponding arteries, and the dense zones form the bony hypoglossal canal.1 The fourth occipital somite differs from the first three in that it does show resegmentation. The caudal dense zone is incorporated into the cranial loose half of the first cervical somite to form the transitional sclerotome called the proatlas. The cranial half of the axial sclerotome of the proatlas combines with the other three axial occipital sclerotomes to form the basion of the skull base, and the most caudal portion of the first cervical axial sclerotome, likely derived from the first cervical somite, forms the foundation for the apical segment of the odontoid. Late in resegmentation, a boundary zone between this apical predecessor of the odontoid and the basiocciput allows this tissue to be incorporated into the odontoid. This unique formation of a physical separation between the basiocciput and the odontoid distinguishes the transitional zone from other vertebral levels. Typically, the IBZ that forms at the caudal end of the dense zone forms intervertebral disks. But at this level, this unique physical separation allows the skull to become completely independent from the vertebral column, thus differentiating it from the development at all other somitic or sclerotomal levels. Finally, the dense zones of the lateral sclerotomes of the proatlas ultimately form the two occipital condyles (OCs) and complete the rim of the foramen magnum (FM).1 The first three cervical somites also deserve their distinction from the remainder of the vertebral column. Resegmentation occurs in the typical fashion as the caudal half of somite five and the cranial half of somite six form the first cervical sclerotome; likewise, the caudal half of somite six and the cranial half of somite seven thus form the second cervical sclerotome. The formation of dense and loose zones in the axial perichordal sclerotome also progresses in the usual fashion to form the basal segment of the odontoid, from the axial sclerotome of the first cervical sclerotome and the body of the axis from the axial sclerotome of the second cervical sclerotome. At this point in development, however, the first two cervical sclerotomes do not form true intervertebral disks; the IBZ soon develops into the upper and lower dental synchondroses, which ultimately allows for the fusion of the apical to basal odontoid and the basal odontoid to the body of the axis, respectively.1 The development of the vertebral column occurs in three stages: membranous, cartilaginous, and osseous. The somite

1  •  Surgical Anatomy and Biomechanics of the Craniovertebral Junction

Figure 1-1  Correlation between the embryologic origin and final product in the craniovertebral junction. The dotted line is the severance line, which demarcates the final separation of the skull from the cervical spine.

1 2

3

4 Figure 1-2  Centers of ossification of the atlas. This specimen has four synchondroses. 1, Anterior midline synchondrosis; 2, accessory synchondrosis; 3, neurocentral synchondrosis; and 4, posterior midline synchondrosis.

formation and the sclerotome segmentation occur in the membranous stage in the third week of gestation. At the fourth week, chondrification centers appear on each side of the vertebral body, notochord, and on each half of the neural arch. As these centers form and join, they squeeze the notochord cells into the disk space, where they eventually become the nucleus pulposus. However, at the occipital bone level, the notochord cells regress and do not give rise to any structure. At the seventh to eighth week of gestation, the ossification stage begins in the midthoracic region and progresses rostrally and caudally. This ossification process continues until early childhood.

DEVELOPMENTAL ANOMALIES OF THE CRANIOVERTEBRAL JUNCTION The atlas has three centers of ossification (Fig. 1-2). At birth, the anterior arch consists mainly of cartilage. A separate center appears at the end of the first year and progressively joins the two lateral masses between the sixth and eighth years. Occasionally, only two centers of ossification are present, one on each half and the anterior arch, formed by forward extension of the two lateral masses. The axis has six centers of ossification (Fig. 1-3). The upper and lower synchondroses separate the apical dental segment, the basal dental segment, and the body of the

Figure 1-3  Six ossification centers of the axis.

axis. These three components undergo chondrogenesis around 6 weeks of gestation but remain separated by the two synchondroses. The ossification of the synchondrosis occurs in three waves (Fig. 1-4). The first wave appears as a single ossification center within the axial body around 4 months of gestation. The second wave gives rise to two ossification centers on each side of the basal odontoid at 6 months of gestation; at birth these two centers begin to fuse, and thus begins the bony fusion of the dental process to the body of the axis, although this may not be completed even into the fifth or sixth year of life. Finally, the third wave of ossification occurs at 3 to 5 years of age, at which the tip of the odontoid undergoes bony fusion via the ossification of the upper synchondrosis; this may not be completed until adolescence. As one could presume, abnormalities in the various developmental phases of the CVJ can result in a variety of pathologic conditions, and in fact, embryology can be helpful in identifying some pathologic findings in the CVJ.1,2 Ossiculum terminale persistens is the term for an unfused apical dental segment, likely because of failure of the upper synchondrosis. There is little debate about this finding, and it is usually nonsyndromic. Less clear is the etiology of the more often seen os odontoideum. One theory speculates that os odontoideum is simply a nonunion of an odontoid fracture, whereas another proposes that it is in fact a developmental anomaly in which the basal odontoid fails to fuse

3

4

SECTION A  •  Craniovertebral Junction and Upper Cervical Spine Synchondroses 1st ossification center Paired 2nd ossification centers Ossifying lower synchondrosis

Cartilaginous axis (8 wk. embryo)

Paired 3rd ossification centers

(4 mo. fetus) (6 mo. fetus) (Birth) (3 yrs) Bony axis (adolescence)

Figure 1-4  The three developmental phases of C2 and the three waves of ossification. The primordial structures for the odontoid components is assembled during the membranous phase. Upper and lower dental synchondroses are shown as dense lines. The first wave of ossification at the fourth fetal month consists of bilateral centers for the neural arches and a single center for the centrum. Second wave at the sixth fetal month consists of bilateral ossification centers for the basal dental segment. At birth, the basal dental centers should have integrated in the midline and should have begun to fuse to the centrum. The third wave of C2 ossification occurs from 3 to 5 years at the apical dental segment, which does not become fused to the basal odontoid until the sixth to ninth year and is fully formed during adolescence.

with the body of the axis. Another abnormality of resegmentation is the extremely rare os avis, in which the apical dental segment is attached to the basiocciput and not to the main dental process. The odontoid is thus shortened but clearly fused to the axis. Os avis is often associated with neurologic deterioration caused by a posterior dislocation of C1 on C2.1

Surgical Anatomy of the Craniovertebral Junction BONY STRUCTURES OF THE CRANIOVERTEBRAL JUNCTION Foramen Magnum and Occipital Condyle The FM is the outlet for the transition of the cranium to the spinal column below. The FM is located in the occipital bone and is flanked anterolaterally by the OCs (Fig. 1-5). The most anterior midline point of the FM is the basion, and the most posterior point is the opisthion. Numerous morphometric anatomic studies have provided considerable understanding of the FM and surrounding areas to assist neurosurgeons with safe navigation through these complex and narrow surgical corridors. The FM is slightly oval shaped with a sagittal diameter of 34.7 ± 2.5 mm (range, 29.5 to 43.5 mm).3 The average transverse diameter of the FM is 27.9 mm (range, 23 to 32 mm).4 The FM is found to be ovoid in 46% to 58% of specimens and is asymmetric 10% of the time.4,5 Located anterolaterally from the FM are two OCs that articulate with the first cervical vertebra and provide the transition from the cranium above to the cervical spine below.

Occipital Condyle.  The OC that articulates with the atlas is an oval bone mass located on the anterior half of the FM; it converges mesially toward the basion at 30 ± 7.5 degrees and delineates the lateral limits of the CVJ (Fig. 1-6; see also Fig. 1-5).3 The OC protrudes into the FM in 57% of the skulls examined.5 In articulating with the trapezoidal lateral mass of the atlas below, the condylar external surface is convex downward, facing outward and sloping cephalocaudal in both sagittal and coronal views.6 The mean length of the OC is 23.6 ± 2.5 mm, mean width is 10.6 ± 1.4 mm, and mean height is 9.2 ± 1.4 mm.3 The intercondylar distance is 29.4 mm (range, 26.2 to 37.0 mm).6 Although the OC is most commonly oval in shape, known as type 1, other possible shapes include kidney, S, figureeight, triangle, ring, two-portioned, and deformed profiles.3 These morphometric parameters have significant clinical implications because the shape of the condyle may influence the extent of the condylectomy during surgical approaches to this region. Among the various profiles, the triangle, kidney-shaped, and deformed condylar types may require more extensive condylar resection to adequately expose the ventral lesions. In addition, the OC varies in length, and it can be classified as short (condylar length 26 mm, 14.1%).3,5 In all these morphometric analyses, it is well established that no correlation exists between condylar length and head circumference or FM diameter (basionopisthion distance). Posterior to the condyle is the condylar fossa, a bony depression located behind the condyle that is often perforated to form the condylar canal (see Fig. 1-6), through which the condylar emissary vein connects the vertebral venous plexus with the sigmoid sinus. A more important canal for the surgeon to be aware of when performing the

1  •  Surgical Anatomy and Biomechanics of the Craniovertebral Junction

Petro-occip. fiss. Pharyngeal tubercle Styloid process Stylomastoid for.

Jug. foramen Jug. process

Occip. condyle Mastoid process

Foramen magnum

Occip. condyle Cond. fossa

Ext. occip. crest Inf. nuchal line Ext. occip. protuberance

Figure 1-5  Foramen magnum (FM) anatomy with occipital condyles protruded into the FM.

VA

OC

OC Med CT

CF

CT CF

Figure 1-6  Axial computed tomography at the occipital condyle (OC). CT, cerebellar tonsil; Med, medulla; VA, vertebral arteries (thin arrows); CF, condylar foramen (thick arrows).

transcondylar approach is the hypoglossal canal (HC), which transmits the hypoglossal nerve anterolaterally, from intracranial to extracranial, at 45 degrees to the sagittal plane (Fig. 1-7, A). The average length of the HC is 12.6 mm (range, 11 to 15 mm).4 The intracranial orifice of the HC is situated about 10 mm (range, 4.2 to 15.8 mm) superior and posterior to the anterior tip of the OC.3 Most of the time, the intracranial origin of the HC is found in the middle third of the OC. The distance between the posterior margin of the OC and the intracranial HC orifice is critical because it indicates the maximum amount of condyle resectable without violating the HC. The average distance between the posterior OC and HC was found to be 12.2 mm4 in one study, although other studies have shown that this distance can be as short as 7.9 mm (average, 9.8 mm; range, 7.5 to 12.2 mm).5 This distance can be reliably measured with three-dimensional (3D) computed tomography (CT).5 The jugular foramen is located lateral and slightly superior to the anterior half of the condyles. It is bordered posteriorly by the jugular process and anteriorly by the jugular fossa. The jugular tubercle (JT) is situated anterosuperior to the OC and HC at the junction of the basilar and condylar

portions of the occipital bone.5 The mean anatomic length, width, and height of the JT were found to be 15.4, 9.6, and 7.7 mm, respectively. In a previous anatomic study, a “tall” JT (height >8.5 mm) was present in 23% of dry specimens, and a “flat” JT (height 140° = Platybasia

Koenigsberg angle Chamberlain line

McGregor line

Posterior margin of hard palate to inferior surface of basiocciput

McRae line Wackenheim clivus baseline

Basion to opisthion Inferior extension of posterior surface of clivus tangent

Clivus canal angle

Angle between Wackenheim clivus baseline and posterior vertebral body line

Cervicomedullary angle

Angles between tangents of upper spinal cord and medulla oblongata Distance between McGregor line and midpoint of inferior end plate of axis Distance between the center of the pedicle of the axis and transverse axis of the atlas Perpendicular distance between tip of the odontoid and the internal occipital protuberance–tuberculum sellae line Lines dividing lateral projection of odontoid/body of axis in three equal parts Three parallel lines: Inferior end plate of axis Tangential to inferior border of anterior arch of atlas Tangential to tip of the odontoid VAAI: Ratio of distance between first two lines and first and third lines

Redlund-Johnell criterion Ranawat criterion Klaus height index

Clark stations Kulkarni-Goel index; vertical atlantoaxial index (VAAI)

Obtuseness more than 140 degrees is suggestive of platybasia. Using the center of the pituitary fossa, similar angles have been described by McGregor and Poppel.36,37 Koenigsberg and colleagues37a have recently described similar angles formed by a line extending across the anterior cranial fossa to the tip to the dorsum sellae with a second connecting line drawn along the posterior margin of the clivus. Angles more than 124 degrees in children and more than 127 degrees in adults are suggestive of platybasia.38 Chamberlain and McGregor lines: A Chamberlain line is drawn from the posterior end of the hard palate to the most posterior margin of the FM, at the opisthion (see Fig. 1-14). Because the opisthion is not always visible, a modification was made by McGregor to draw a line, from the posterior margin of the hard palate to the lowest part of the basisquamous occiput, now called the McGregor line (see Fig. 1-14). In normal morphology, the tip of the odontoid process should be not more than 5 mm above the Chamberlain line and 7 mm above the McGregor line. The anterior arch of the atlas lies below both these lines. McRae line: The McRae line joins the basion and opisthion. The tip of the odontoid process normally lies below this line (see Fig. 1-14). Wackenheim clivus baseline: This line is otherwise known as the basilar line. It is the inferior extension of line drawn

Adults: >124° = Platybasia Children: >127° = Platybasia Tip of the odontoid should not be more than 5 mm above this line and anterior. Arch of atlas typically lies below this line. Tip of the odontoid should not be more than 7 mm above. Anterior arch of atlas typically lies below this line. Tip of the odontoid should not be above this line. The odontoid falls in front or tangent to it, and the clival baseline may intersect the posterior third of the odontoid. Range: 150° maximum in flexion and 180° maximum in extension 34 mm in males and >29 mm in females Normal: >15 mm in males and >13 mm in females 0.8 Mild: 0.61-0.70 Moderate: 0.41-0.60 Severe: SPO PSO > SPO PSO > SPO SPO > PSO SPO > PSO SPO > PSO SPO > PSO

the PSO, large surfaces of bone are approximated, thus creating a more robust area for successful fusion compared with the SPO. The deformity best suited for PSO is a sharp, angular deformity or one with significant positive sagittal imbalance (> 12 cm).33 Although clear advantages are evident, the procedure is lengthy and technically demanding, and it is associated with significant blood loss. Anterior subluxation of the vertebrae is possible during closure of the osteotomy and requires careful monitoring during final deformity correction.33 The PSO should also be avoided when an anterior pseudarthrosis or preexisting anterior instrumentation is present.13

Surgical Technique23,32,39 1. Patient positioning and surgical approach is identical to that of an SPO. 2. Two levels above and below the intended osteotomy site are exposed. However, in patients with poor bone stock, or if a level cannot be instrumented with pedicle screws, additional levels may require exposure. 3. Subperiosteal dissection is used to expose all of the posterior elements or fusion mass at the intended osteotomy site. The correct level should be confirmed fluoroscopically prior to bone resection. 4. Aside from the osteotomy site, the exposed levels are then prepared and instrumented bilaterally with pedicle screws. Correct placement is confirmed using intraoperative fluoroscopy and pedicle screw stimulation. 5. The spinous processes at the osteotomy level and the process on the level above are resected with a rongeur. 6. Wide laminectomy is next performed from the midline out laterally to the facets. The ligamentum flavum is also resected laterally, toward the facet joints. If a fusion mass is present, it is thinned with a burr or a combination of curettes and rongeurs and is carefully resected away from the midline to expose the spinal canal. 7. The epidural space is now accessible, nerve roots are identified, and the epidural space is decompressed centrally. 8. All posterior elements are then resected to completely isolate the pedicles at the osteotomy level. 9. The lateral aspect of the pedicle is removed along with the transverse processes. Care must be taken to avoid the segmental artery and exiting nerve root. 10. The pedicle bases are curetted into the main vertebral body, and care is taken not to disrupt the medial pedicle wall, which protects the neural elements and dura.

11. Increasingly larger curved and angled curettes and various rongeurs are used to enter the vertebral body, through the base of the right and left pedicles, and carve out a hollow space within the vertebral body. The cavity is made progressively larger, until the anterior vertebral body wall is reached, and the left and right sides communicate. Alternatively, bone removal is stopped at the anterior one third of the body, and the remaining bone is fractured upon closure of the osteotomy. Attention must be paid to ensure the anterior vertebral body cortex is not violated in order for it to act as a hinge and prevent anterior translation. The cavity is tapered into a wedge-shaped “V” in the sagittal plane with the apex toward the anterior vertebral body. 12. Significant bleeding may occur at this stage secondary to the raw cancellous bone surfaces. Hemostasis is achieved using a combination thrombin-soaked Gelfoam, FloSeal, and packing. 13. The posterior vertebral wall, now a thin cortical shell, is resected next, along with the medial pedicle bases with reverse-angled curettes and rongeurs. A dural retractor is used to medially retract the thecal sac. Straight osteotomes are used, directed anteriorly along the cranial and caudal margins of the posterior wall osteotomy, to ensure the osteotomy margins are parallel to each other. Enough wall must be resected to allow for effective closure of the osteotomy. 14. The lateral body walls are next carefully dissected free of soft tissue using a small Cobb elevator. The lateral walls are then resected with a pituitary rongeur, and care is taken to ensure that resection is equal on both sides to allow symmetric osteotomy closure. The depth of lateral wall resection can be monitored using fluoroscopy. 15. Once it has been determined that an adequate amount of bone has been removed, osteotomy closure proceeds after placement of contoured rods via symmetric compression and cantilever bending of the cranial and caudal pedicle screws and gradual extension of the hips. The dura and exiting nerve roots must be closely monitored to ensure they are not impinged during closure. 16. Deformity correction is assessed by visual inspection and intraoperative fluoroscopy.12,41

ANTERIOR SURGERY Frequently, posterior vertebral osteotomy is insufficient in isolation to correct flat back deformity and maintain the reduction. In these scenarios, anterior releases and/or fusion and strut grafting supplement posterior procedures. Situations in which anterior procedures are needed include, but are not limited to, cases with multiple anterior pseudarthroses, circumferential fusions along several segments, and cases with scarring of the ALL or anterior disk that prevents complete closure of an SPO.13,33 In 2005, Cho and colleagues12 published a series in which 39% of patients who underwent a PSO had additional anterior surgery, and 87% of patients undergoing an SPO had a concomitant anterior procedure. Furthermore, Kostuik and colleagues21 presented their series, in which 86% of patients had decreased pain; in addition, a 29% improvement of lumbar

607

608

SECTION F  •  Spinal Deformity

lordosis was appreciated in patients treated with combined anterior and posterior osteotomies. As an alternative to an SPO or PSO, some surgeons have advocated for anterior deformity correction combined with removal of any posterior spinal implants. Jang and colleagues19 reported on a series of patients treated using a posterior-anterior-posterior technique that consisted of removal of posterior hardware, followed by anterior strut grafting and deformity correction, and finalized with posterior compression instrumentation. Results showed sustained improvement in lumbar lordosis and sagittal vertical axis, and they revealed subjective improvements in function and pain at final follow-up. Anterior surgery plays a significant role in the treatment of flat back syndrome, although posterior extension-type osteotomies are the most widely used procedures, alternatives are available, and anterior body work is frequently needed for adequate correction.

Patient Outcomes Complication rates are high following surgical correction of flat back syndrome. Rates in the literature range from 25% to 60%.4,5,10,12 Early postoperative complications include neurologic injury, dural tears, postoperative myocardial infarction, massive transfusion requirements, wound infection, and deep venous thrombosis. The most common late complications are pseudarthrosis, hardware failure, and degeneration of adjacent spinal segments.4,5,10,12 Despite the high rate of complications, patients do report subjective improvement postoperatively. In Lagrone’s4 series that reported a 60% complication rate and a 36% rate of significant residual pain, 95% of patients reported benefit from the procedure in terms of pain relief and posture correction. More recent series have reported lower overall complication rates and have continued to echo subjective improvement in a large percentage of patients in regard to pain, function, and overall self-image.20,21 Bridwell’s16 series reported statistically significant improvement in postoperative pain and Owestry scores, and 88% of patients stated that they would undergo the procedure again. Clearly, surgical correction is beneficial for patients with flat back syndrome; however, patients should be counseled preoperatively about high rates of potential complications and residual pain. Patient expectations should be focused on improvements in function and pain relief, but they must be apprised that a complete resolution of symptoms is unlikely.4,5,11,12,14,16,19,21

Summary Flat back deformity most often results from postsurgical fusion and distraction into the lower lumbar spine. Patients come to medical attention complaining of pain and fatigue and are unable to stand erect without bending their legs, and a loss of the normal lumbar lordosis with a fixed positive sagittal imbalance of the spine is appreciable on radiography. All but the mildest symptomatic cases are best treated with surgical deformity correction; the most common surgical procedures are the SPO and PSO, with or without a supplemental anterior procedure. The goal of

these corrective surgeries is to increase lumbar lordosis and ultimately restore neutral spinal alignment as measured by the plumb line, or sagittal vertical axis. These osteotomies are technically challenging and lengthy, and they carry the potential for a high rate of morbidity. Despite the surgical risks and persistence of symptoms in a large portion of treated patients, with careful preoperative planning and close attention to surgical detail, a high percentage of patients will achieve overall improvement following surgical correction.

References 1. Doherty J: Complications of fusion in lumbar scoliosis. Proceedings of the Scoliosis Research Society. J Bone Joint Surg Am 55:438, 1973. 2. Moe J, Denis F: The iatrogenic loss of lumbar lordosis. Orthop Trans 1, 1977. 3. Grobler L, Moe J, Winter R, et al: Loss of lumbar lordosis following surgical correction of thoracolumar deformities. Orthop Trans 2:239, 1978. 4. Lagrone MO, Bradford DS, Moe JH, et al: Treatment of symptomatic flatback after spinal fusion. J Bone Joint Surg Am 70(4):569–580, 1988. 5. Farcy JP, Schwab FJ: Management of flatback and related kyphotic decompensation syndromes. Spine (Phila Pa 1976) 22(20):2452– 2457, 1997. 6. Aaro S, Ohlén G: The effect of Harrington instrumentation on the sagittal configuration and mobility of the spine in scoliosis. Spine (Phila Pa 1976) 8(6):570–575, 1983. 7. Casey MP, Asher MA, Jacobs RR, et al: The effect of Harrington rod contouring on lumbar lordosis. Spine (Phila Pa 1976) 12(8):750– 753, 1987. 8. Swank S, Lonstein JE, Moe JH, et al: Surgical treatment of adult scoliosis: a review of two hundred and twenty-two cases. J Bone Joint Surg Am 63(2):268–287, 1981. 9. van Dam BE, Bradford DS, Lonstein JE, et al: Adult idiopathic scoliosis treated by posterior spinal fusion and Harrington instrumentation. Spine (Phila Pa 1976) 12(1):32–36, 1987. 10. Booth KC, Bridwell KH, Lenke LG, et al: Complications and predictive factors for the successful treatment of flatback deformity (fixed sagittal imbalance). Spine (Phila Pa 1976) 24(16):1712–1720, 1999. 11. Chen IH, Chien JT, Yu TC: Transpedicular wedge osteotomy for correction of thoracolumbar kyphosis in ankylosing spondylitis: experience with 78 patients. Spine (Phila Pa 1976) 26(16):E354– E360, 2001. 12. Cho KJ, Bridwell KH, Lenke LG, et al: Comparison of Smith-Petersen versus pedicle subtraction osteotomy for the correction of fixed sagittal imbalance. Spine (Phila Pa 1976) 30(18):2030–2037.discussion 2038, 2005. 13. Potter BK, Lenke LG, Kuklo TR: Prevention and management of iatrogenic flatback deformity. J Bone Joint Surg Am 86-A(8):1793–1808, 2004. 14. Berven SH, Deviren V, Smith JA, et al: Management of fixed sagittal plane deformity: results of the transpedicular wedge resection osteotomy. Spine (Phila Pa 1976) 26(18):2036–2043, 2001. 15. Lu DC, Chou D: Flatback syndrome. Neurosurg Clin N Am 18(2):289– 294, 2007. 16. Bridwell KH, Lewis SJ, Lenke LG, et al: Pedicle subtraction osteotomy for the treatment of fixed sagittal imbalance. J Bone Joint Surg Am 85A(3):454–463, 2003. 17. Bernhardt M, Bridwell KH: Segmental analysis of the sagittal plane alignment of the normal thoracic and lumbar spines and thoracolumbar junction. Spine (Phila Pa 1976) 14(7):717–721, 1989. 18. Moskowitz A, Moe JH, Winter RB, et al: Long-term follow-up of scoliosis fusion. J Bone Joint Surg Am 62(3):364–376, 1980. 19. Jang JS, Lee SH, Min JH, et al: Surgical treatment of failed back surgery syndrome due to sagittal imbalance. Spine (Phila Pa 1976) 32(26):3081–3087, 2007. 20. Bridwell KH, Lenke LG, Lewis SJ: Treatment of spinal stenosis and fixed sagittal imbalance. Clin Orthop Relat Res (384):35–44, 2001. 21. Kostuik JP, Maurais GR, Richardson WJ, et al: Combined single-stage anterior and posterior osteotomy for correction of iatrogenic lumbar kyphosis. Spine (Phila Pa 1976) 13(3):257–266, 1988.

62  •  Surgical Treatment of Flat Back Deformity 22. Mac Millan MM, Cooper R, Haid R: Lumbar and lumbosacral fusions using Cotrel-Dubousset pedicle screws and rods. Spine (Phila Pa 1976) 19(4):430–434, 1994. 23. Rinella A, Bridwell K: Iatrogenic fixed sagittal imbalance, Vol 2, ed 5. Philadelphia, 2006, Saunders Elsevier. 24. Stagnara P, De Mauroy JC, Dran G, et al: Reciprocal angulation of vertebral bodies in a sagittal plane: approach to references for the evaluation of kyphosis and lordosis. Spine (Phila Pa 1976) 7(4):335– 342, 1982. 25. Jackson RP, McManus AC: Radiographic analysis of sagittal plane alignment and balance in standing volunteers and patients with low back pain matched for age, sex, and size: a prospective controlled clinical study. Spine (Phila Pa 1976) 19(14):1611–1618, 1994. 26. Gelb DE, Lenke LG, Bridwell KH, et al: An analysis of sagittal spinal alignment in 100 asymptomatic middle and older aged volunteers. Spine (Phila Pa 1976) 20(12):1351–1358, 1995. 27. Cochran T, Irstam L, Nachemson A: Long-term anatomic and functional changes in patients with adolescent idiopathic scoliosis treated by Harrington rod fusion. Spine (Phila Pa 1976) 8(6):576–584, 1983. 28. Takahashi S, Delécrin J, Passuti N: Changes in the unfused lumbar spine in patients with idiopathic scoliosis: a 5- to 9-year assessment after Cotrel-Dubousset instrumentation. Spine (Phila Pa 1976) 22(5):517–523; discussion 524, 1997. 29. Smith-Peterson M, Larson C, Aufranc O: Osteotomy of the spine for the correction of flexion deformity in rheumatoid arthritis. J Bone Joint Surg Am 27:1–11, 1945. 30. Voos K, Boachie-Adjei O, Rawlins BA: Multiple vertebral osteotomies in the treatment of rigid adult spine deformities. Spine (Phila Pa 1976) 26(5):526–533, 2001.

31. Shufflebarger HL, Clark CE: Thoracolumbar osteotomy for postsurgical sagittal imbalance. Spine (Phila Pa 1976) 17(8 Suppl):S287–S290, 1992. 32. Kuklo T, Potter B: Surgical management of flatback syndrome. Philadelphia, 2006, WB Saunders. 33. Bridwell KH: Decision making regarding Smith-Petersen vs. pedicle subtraction osteotomy vs. vertebral column resection for spinal deformity. Spine (Phila Pa 1976) 31(19 Suppl):S171–S178, 2006. 34. Herbert J: Vertebral osteotomy: technique, indications, and results. J Bone Joint Surg Am 30:680–689, 1948. 35. LaChapelle E: Osteotomy of the lumbar spine for correction of kyphosis in a case of ankylosing spondylarthritis. J Bone Joint Surg Am 28:851–858, 1946. 36. Weatherley C, Jaffray D, Terry A: Vascular complications associated with osteotomy in ankylosing spondylitis: a report of two cases. Spine (Phila Pa 1976) 13(1):43–46, 1988. 37. Devlin V: Smith-Peterson-type osteotomy. New York, 2003, Thieme. 38. Thiranont N, Netrawichien P: Transpedicular decancellation closedwedge vertebral osteotomy for treatment of fixed flexion deformity of spine in ankylosing spondylitis. Spine (Phila Pa 1976) 18(16):2517– 2522, 1993. 39. Brown C, Wong D: Pedicle subtraction osteotomy. New York, 2003, Thieme. 40. Noun Z, Lapresle P, Missenard G: Posterior lumbar osteotomy for flat back in adults. J Spinal Disord 14(4):311–316, 2001. 41. Van Royen BJ, De Gast A: Lumbar osteotomy for correction of thoracolumbar kyphotic deformity in ankylosing spondylitis: a structured review of three methods of treatment. Ann Rheum Dis 58(7):399– 406, 1999.

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63

Surgical Management of Degenerative Lumbar Scoliosis REX A.W. MARCO and ROBERT J. WOODRUFF

Overview Adult degenerative scoliosis remains a challenging problem for patients and spine surgeons. Treatment decisions can be complicated by social, psychologic, and medical factors. Patient outcomes can be optimized by understanding the natural history of degenerative scoliosis as well as the various nonoperative and operative treatment options. Adult degenerative scoliosis can develop de novo as a result of asymmetric disk and facet degeneration in a spine with relatively normal alignment, or it can occur as a result of asymmetric disk and facet degeneration associated with adolescent idiopathic scoliosis (AIS). The natural progression of adult scoliosis varies from individual to individual. Glassman and colleagues1 showed that patients with degenerative scoliosis have significantly lower SF-36 scores in 7 of 8 categories than age-matched controls. These patients also scored lower in 7 of 8 categories compared with patients who had back pain, sciatica, and hypertension. The decision to continue with nonoperative treatment or to pursue operative intervention remains complex and difficult, despite the fact that these patients have lower health-related quality of life scores.1 These patients must balance issues of progressive deformity, pain, cosmesis, overall medical condition, and the extent of potential intervention in their decision making.

Natural History The true natural history of degenerative scoliosis, either from previously existing AIS or de novo scoliosis, is not fully understood. The recommendation for fusion of AIS curves during adolescence comes in large part from the hope that the surgery will prevent curve progression. Forty-year follow-up data out of Iowa suggest that thoracic curves measuring more than 50 degrees and lumbar curves measuring more than 30 degrees will progress at a rate of approximately 1 degree per year.2,3 However, these data represent an average of all subjects, thus not every patient will demonstrate curve progression. In fact, many patients’ curves remain stable throughout their entire life. Scoliosis has been associated with psychosocial consequences, slightly higher rates of back pain, and decreased cardiac and pulmonary function in curves measuring over 100 degrees. In adults with de novo scoliosis, the natural history is even more poorly understood. The constellation of symptoms varies greatly among patients and cannot be 610

determined based on the size of the curve. However, with aging, the natural tendency is for progressive loss of disk height through dessication, decreased lumbar lordosis, increased sagittal imbalance, and decreased motion. This process is further complicated with coronal and sagittal changes related to osteoarthritis and osteoporosis, which lead to compression fractures and hypertrophy of the facet joints and ligamentum flavum in some patients. The combination of facet and ligamentum flavum hypertrophy, coupled with disk protrusions commonly seen anteriorly, can lead to central and lateral recess stenosis with resultant radiculopathy. However, even with these changes, some patients remain remarkably asymptomatic, whereas others with seemingly mild radiologic changes may complain of debilitating pain. Regardless of the patient’s symptoms, frank paralysis from compression and worsening alignment is rare, therefore surgical treatment of the disorder is almost never an emergency. It is thus prudent to spend adequate time on the patient’s workup to fully understand the source of the complaints, to exhaust nonoperative measures prior to pursuing surgery, and to have an extensive preoperative discussion to fully address the risks and benefits of proceeding with any sort of operative correction.

History and Physical Examination The assessment of these patients begins with a detailed history and physical exam. Clarification of the patient’s primary complaint should be elucidated, and it should be determined whether these symptoms are worsening.4 Patients who come to medical attention with worsening, intractable pain or neurogenic claudication may require different intervention than someone concerned with cosmesis alone. A history of vascular claudication can mimic neurogenic claudication; however, patients with vascular claudication often have improvement of their symptoms while standing still or sitting, whereas patients with neurogenic claudication show improvement while leaning forward. Patients with adult scoliosis can come to medical attention with multiple medical problems. A patient with a history of cardiopulmonary disease may not tolerate a prolonged operation and anesthesia, similarly, diabetes will adversely affect the cardiovascular system and wound healing, which in turn can increase the incidence of postoperative complications such as infection, deep venous thrombosis (DVT) and/or pulmonary embolism (PE), and pneumonia. Similarly, a history of smoking should be addressed, and every attempt should be made to institute a

63  •  Surgical Management of Degenerative Lumbar Scoliosis

smoking cessation program at least 1 month prior to surgery that continues 6 months after surgery, because tobacco use correlates with a higher risk of pseudarthrosis and pulmonary complications, poor wound healing, slower rate of recovery, and overall poorer outcome of the procedure.5-7 A personal or family history of bleeding problems or blood clots is extremely important and may warrant a preoperative hematologic evaluation. A history of susceptibility to infection should also be obtained to determine whether the patient may be more prone to developing perioperative wound complications. Rheumatologic disorders are not uncommon in this population, and the current diseasemodifying antirheumatic drugs (DMARDs) need to be altered if any surgery is being planned. Medications that inhibit coagulation, such as nonsteroidal antiinflammatory drugs (NSAIDs), acetylsalicylic acid, clopidogrel, anticoagulants, vitamin E, and fish oil should be stopped prior to surgery to decrease intraoperative bleeding and decrease the likelihood of developing postoperative wound and epidural hematomas. Assessing patients’ social support structure is invaluable in determining their ability to tolerate the postoperative demands during recovery. Patients without an extensive family support system may not be ideal surgical candidates. Elicit any history of previous treatments, such as physical therapy and injections; although these may have been previously tried, patient compliance and the quality of the injections vary greatly, so a history of either does not automatically mean that nonoperative treatment has failed. The physical exam begins with observation of the patient. Facial expressions are noted, because patients may occasionally grimace and appear uncomfortable while sitting, standing, or walking. Standing coronal and sagittal alignment, shoulder height, waist asymmetry, and pelvic obliquity are evaluated. Paraspinous rib and lumbar humps are evaluated with the Adam’s forward bend test. Significant loss of lumbar lordosis may present with a forward pitch of the trunk, which impairs forward gaze of the eyes, and patients compensate by flexing the hips and knees to maintain forward gaze. Asking the patient to stand sideways with straight legs further accentuates the severity of the sagittal imbalance. Observation of the gait is used to identify any limitations and signs of weakness or myelopathy. A thorough neurologic exam is necessary, including an assessment of strength, sensation, and the reflexes. Assessment of the distal pulses evaluates for evidence of vascular insufficiency, and examination of the hips and knees can assess for signs of symptomatic osteoarthritis, which can alter treatment recommendations.

Radiologic Evaluation The radiologic evaluation begins with full-length 36-inch anteroposterior (AP) and lateral scoliosis films. The patient’s position during these films must be standardized to negate any compensatory positioning. Patients should stand with their feet together and their hips and knees fully straightened; arms should be in 30 to 45 degrees of forward flexion with elbows flexed and hands resting on the clavicles. Standardizing this positioning prevents inaccurate representation of the sagittal vertical axis.8

In the AP projection, the coronal curves are measured using the Cobb technique, and the coronal alignment is measured using the C7 plumb line. Any deviation of the C7 plumb line from the central sacral vertical line (CSVL) suggests coronal imbalance. Shoulder asymmetry, waist asymmetry, pelvic obliquity, and vertebral body lateral listhesis may also be present. The appearance of an outlet view of the pelvis suggests that the patient has decreased lumbar lordosis and retroversion of the pelvis. In the lateral view, the overall sagittal alignment is examined by drawing the C7 plumb line and then determining the distance from this line to the lateral sacral vertical line (LSVL), a vertical line drawn from the posterosuperior corner of S1. This line ideally overlaps the C7 plumb line and transects the T12–L1 disk space as well as the C7–T1 disk space. The regional sagittal alignment of the thoracic, thoracolumbar, and lumbar spine is also measured. An oversimplified method to remember the normal sagittal alignment of these regions is the 0/30/60 rule, which states that the thoracolumbar alignment should be around 0 degrees, the thoracic kyphosis should be around 30 degrees, and the lumbar lordosis should be around 60 degrees. The pelvic incidence (PI) and pelvic tilt (PT) are also measured (Fig. 63-1). The PI is an angle made by the intersection between a line drawn perpendicular to the S1 end plate at its midpoint and a line from this point to the center point of a line drawn between the centers of the femoral heads.

Sacral Slope

Pelvic Tilt

Pelvic Incidence

Overhang Figure 63-1  Pelvic parameters measured on lateral radiograph. Sacral slope (SS) is the angle from horizontal made by the superior end plate of S1. Pelvic tilt (PT) is defined as the angle formed by a line drawn vertically from the center of the femoral head and one drawn from this point to the center of the S1 end plate; PT is a measure of the relative amount of pelvic retroversion. Pelvic incidence is the angle formed by drawing a line perpendicular to the S1 end plate at its center and one from that point to the center of the femoral heads. In most cases, the femoral heads do not perfectly overlap. In that case, find the center of each femoral head, draw a line between these points, and measure to the midpoint of this line.

611

612

SECTION F  •  Spinal Deformity

Schwab and Lafage9 discussed the importance of the relationship between PI and the ideal degree of lumbar lordosis (LL; Fig. 63-2). They suggested that the ideal LL can be estimated with the following formula: LL = PI + 9 deg rees (±9) Whereas PI remains fairly constant as pelvic retroversion increases, PT increases (Fig. 63-3). PT is an angle formed by the intersection of a vertical line drawn from the center point of a line drawn between the centers of the femoral heads and the line drawn from the midpoint of the S1 end plate to the center point of the line between the centers of the femoral heads (see Figs. 63-1 and 63-2). Lafage and Schwab10 showed that with increasing PT, pain and disability increase as measured by the Oswestry Disability Index, Short-Form 12 questionnaire, and Scoliosis Research Society 22 questionnaire scores. Similarly, Schwab and colleagues11 showed the disability caused by adult scoliosis in general. If surgery is planned, full-length supine AP bending and supine lateral radiographs can help assess curve flexibity in the coronal and sagittal planes. Patients with degenerative scoliosis can come to medical attention with symptoms suggestive of spinal stenosis and radiculopathy. Other pathologies, such as tumor and infection, may also be affecting the alignment of the spine; therefore further imaging may be indicated. Magnetic resonance imaging (MRI) can be useful in assessing the degree of spinal stenosis, disk desiccation and protrusion, ligamentum flavum hypertrophy, and facet pathology, and it may help identify signs of osteomyelitis, diskitis, and neoplasm. The MRI should be performed with gadolinium in patients who have had previous surgery to help differentiate scar tissue from disk material. However, MRI can be difficult to interpret in patients with a coronal deformity greater than 40 degrees or retained metallic implants. In these cases, a CT myelogram may be more useful. Both of these studies can be used for more advanced preoperative planning, such as vascular mapping, bone quality assessment, planning of

screw lengths and trajectory, and identification of levels for decompression.

Nonoperative Management In the absence of progressive neurologic deficit, nonoperative measures should be pursued first. This treatment consists of NSAIDs, physical therapy for strengthening and stretching exercises, cardiovascular conditioning, avoidance of painful activities, corticosteroid injections, and modalities such as heat and ice for symptom relief. Bracing

T1 T4

L1 T12

SVA thoracic

Primary CNS lymphoma

Rare

Typically diffuse disease

Germinoma

Rare

Insufficient data

Melanoma

Rare

Insufficient data

Gross total resection if possible; radiation and/or chemotherapy if unresectable Gross total resection rarely possible; biopsy to guide treatment and for prognosis; chemotherapy and/or radiation Gross total resection if possible; radiation and/or chemotherapy if unresectable Gross total resection if possible; radiation and chemotherapy data lacking Biopsy only; surgical debulking not indicated; chemotherapy mainstay of treatment Biopsy only; typically sensitive to chemotherapy and radiation Gross total resection if possible (rare); radiation and/or chemotherapy if unresectable

10% to 30% of patients with spinal hemangioblastoma have von Hippel-Lindau syndrome. Prognosis is excellent if gross total resection is achieved. Prognosis is poor.

Image entire neuroaxis to rule out disease elsewhere. Prognosis is poor.

*Percent of intramedullary tumors. CNS, central nervous system. From Chamberlain MC, Tredway TL: Adult primary intradural spinal cord tumors: a review. Curr Neurol Neurosci Rep 11:320–328, 2011.

Table 66-2  Primary Intradural, Extramedullary Tumors Tumor

Prevalence*

Location

Treatment

Notes

Meningioma

~50%

Thoracic (~80%) ≫ cervical > lumbosacral

Schwannoma

~25%

Cervical > cauda equina > thoracic > conus

Surgical if symptomatic; may be observed with serial imaging; radiotherapy an option for incomplete resection or recurrence Surgical if symptomatic; may be observed with serial imaging

Neurofibroma

~25%

Surgical if symptomatic; usually observed with serial imaging

MPNST

Rare

Gross total resection if possible (rare); radiation and/or chemotherapy if unresectable

Gross total excision may be curative; 80% occur in females Increased incidence in NF2; almost uniformly histologically benign Increased incidence in NF1; plexiform subtype carries poor prognosis (may progress to MPNST), but otherwise benign Associated with NF1 and poor prognosis

*Percent of intradural-extramedullary tumors. MPNST, malignant peripheral nerve sheath tumor; NF1, neurofibromatosis type 1; NF2, neurofibromatosis type 2. From Chamberlain MC, Tredway TL: Adult primary intradural spinal cord tumors: a review. Curr Neurol Neurosci Rep 11:320–328, 2011.

or a Cobb dissector with gauze to minimize tissue injury and bleeding (Fig. 66-2). ■ If unfamiliar with anterolateral or anterior approaches, have an access surgeon, either a general surgeon or a cardiothoracic surgeon, provide the exposure. ■ Wide osseous removal is the goal, although laminectomies, vertebrectomies, and rib resections should be performed without destabilizing the spinal column when possible. ■ Because of cord traction with change in position, thoracolumbar intramedullary tumors are generally localized approximately 1 cm more rostral when the patient is prone than when supine; radiographic study is commonly done supine.8

DURAL OPENING If not already present, the operative microscope is brought into the field for this portion of the procedure. Hemostasis is ensured before incising the dura to minimize the morbidity caused by spinal subarachnoid blood and to avoid obscuring the operative field. Intraoperative ultrasound may help precisely localize the tumor in real time.9 After the tumor is localized, and good hemostasis is achieved, moistened cotton pledgets are placed on either side of the planned dural opening to prevent blood from entering the subarachnoid space (Fig. 66-3). The anesthesiologist is made aware of imminent dural opening and possible rapid loss of a substantial quantity of cerebrospinal

66  •  Surgical Technique for Resection of Intradural Tumors

Figure 66-1  Magnetic resonance imaging (MRI) shows an intradural-extramedullary homogeneously enhancing lesion consistent with a schwannoma (left to right, Sagittal T1-, T2-, and T1- weighted MRI with contrast and axial T1-weighted MRI with contrast).

Figure 66-2  Posterior approach to T10–T11 schwannoma, subperiosteal dissection.

Figure 66-3  Posterior approach to T10–T11 schwannoma, dural exposure.

fluid (CSF). Using the microforceps to hold the dura, a No. 15 scalpel blade is used to incise the dura in the midline without opening the arachnoid layer. Next, a Woodson dissector is placed between the dural opening and the arachnoid layer. The dura is opened further with the scalpel to provide adequate visualization of the region of interest; if more lateral visualization is desired, the dura may be incised laterally in a “T” shape toward the nerve root. Also, the operating table may be rotated as needed to facilitate an ergonomically sound approach for the neurosurgeon. We use 4-0 braided nylon sutures placed in the dural edges for lateral retraction to keep the operative field exposed and to prevent blood from bone edges and retracted muscle from entering the subarachnoid space (Fig. 66-4). Intradural exposure is maintained by tying the sutures to the paraspinal musculature or surgical drape or

by clamping a hemostat to the two free ends of the suture and allowing the hemostat to hang over the side of the patient. Finally, if still intact, the arachnoid layer is opened sharply. Electrophysiologic monitoring may both facilitate identification of neural element function and provide medicolegal documentation of spinal cord function during the operation.10

APPROACH TO INTRADURALEXTRAMEDULLARY TUMOR The borders of the intradural-extramedullary tumor are defined using microinstruments, such as from a Rhoton tray, to minimize direct pressure or manipulation of the spinal cord. Caudal to the conus medullaris, the nerve roots may be gently retracted either medially or laterally

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Figure 66-4  Posterior approach to T10–T11 schwannoma. Dural opening reveals bulging spinal cord with underlying ventral mass.

Figure 66-6  Posterior approach to T10–T11 schwannoma internally debulked with the Cavitron ultrasonic surgical aspirator (ValleyLab, Boulder, CO) and teased out of the canal with minimal retraction on the spinal cord.

debulk the lesion internally (Fig. 66-6). Bipolar electrocautery should be used at a very low current setting and should be limited to avoid thermal injury to the cord. In the case of meningioma, all involved dura mater is exposed to facilitate gross total resection. Gross total resection of meningioma is important for the long-term prognosis in World Health Organization (WHO) grade 2 or higher meningiomas. However, achieving gross total resection may not be as important with WHO grade 1 meningiomas, because their recurrence rate is low.11

APPROACH TO INTRAMEDULLARY TUMOR Figure 66-5  Posterior approach to T10–T11 schwannoma. Moistened cotton pledgets are used to expose and demarcate the dissection plane between the tumor and the spinal cord.

to facilitate visualization of the mass. Moistened cotton pledgets are used to demarcate the tumor border and separate it from the spinal cord (Fig. 66-5). A biopsy may be taken for intraoperative frozen pathologic analysis. For a neurofibroma or schwannoma, the involved nerve root is stimulated to determine what portion of the mass is safely resectable. While resecting a tumor, any damage to neural structures that produces reproducible extremity or anal motor function on intraoprative stimulation should be avoided. In such cases, gross total resection may not be possible. For lesions caudal to the conus medullaris and attached to filum terminale, the proximal cut should be made first to prevent retraction of the lesion cranially. If the attachment is identified and can be easily separated, the tumor can be removed in a piecemeal fashion with biopsy forceps or as one piece. Because of the small working corridor, piecemeal resection is preferred to avoid applying undue pressure on the cord. A Cavitron ultrasonic surgical aspirator (CUSA) may also be used to resect the tumor in a piecemeal fashion and

Intradural tumors are almost exclusively approached posteriorly. The initial approach is exactly as described previously in this chapter for intradural-extramedullary tumors. Under microscopic magnification, the dura is incised in the midline over the entire length of the lesion. If a biopsy alone is planned, the exposure may be very limited to avoid the morbidity of a larger exposure. The lesion may not be apparent at the pial surface, so the approach must be planned based on the preoperative imaging. Ultrasound may be useful in locating the lesion intraoperatively to plan the myelotomy.9 Lesions situated centrally are approached via a midline myelotomy; lesions situated more laterally are approached via the dorsal root entry zone or midline myelotomy. Keep in mind that the posterior median sulcus may be difficult to identify for the midline myelotomy because of edema. In such cases, the superficial vessels also may not serve as reliable markers to identify the midpoint between the bilateral dorsal root entry zones. The myelotomy may be made with either a No. 11 blade knife or a carbon dioxide laser (Fig. 66-7). At this point there may be a loss of SSEPs. The remainder of the surgery depends on the surgical goal, whether it is to merely obtain a biopsy, to debulk, or to achieve a gross total excision. In general, a diffusely infiltrative mass, such as an astrocytoma, cannot be safely excised; a more discrete mass, such as an ependymoma, may allow for a gross total resection.

66  •  Surgical Technique for Resection of Intradural Tumors

Figure 66-7  Posterior approach to C3 ependymoma. Midline myelotomy with a No. 11 blade scalpel (left) and separation of the edges using Rhoton dissectors (right).

Figure 66-8  Posterior approach to C3 ependymoma. Sagittal T2-weighted magnetic resonance imaging shows a hyperintense lesion (left); midline myelotomy reveals an encapsulated intramedullary tumor with a reddish to purplish appearance (right).

Before attempting this, the mass should be internally de­ bulked to create a safe working space. This is achieved using microdissectors, bipolar electrocautery, and/or the CUSA. We do not recommend the use of electrocautery because of the potential for neural damage from dissipating current. The key to safely excising an intradural tumor is to identify the plane of dissection between the mass and the normal surrounding neural tissue. This plane is carefully developed using gentle retraction with microdissectors and microforceps (Fig. 66-8). If this plane is apparent, but the tumor is adherent to normal-appearing neural tissue, centrifugal resection should be performed with the goal of maximum subtotal resection. Care must be taken at all times not to apply direct or indirect traction to the spinal cord, and care must be taken not to pull on the tumor adherent to the spinal cord. When the surgical goal has been met, the pia

mater may be closed with interrupted 8-0 nonabsorbable monofilament or equivalent sutures.

HEMOSTASIS When operating in the intradural space, hemostasis is achieved in multiple ways. A moistened cotton pledget or Surgifoam may be placed on bleeding neural tissue and left in place for a few seconds or minutes, and bleeding often stops with this alone. Absorbable gelatin sponges either soaked in saline or in recombinant human thrombin may also be placed on top of bleeding neural tissue to achieve hemostasis. Only when nondestructive measures have failed to stop bleeding should the neurosurgeon resort to electrocautery, which damages intervening neural tissue. We do not recommend monopolar electrocautery; bipolar

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electrocautery minimizes the current spread and the consequent unnecessary neural injury. Saline irrigation should be used with bipolar cautery to limit the heat transference.

CLOSURE Once the lesion is excised, the area should be inspected for any residual lesion and active bleeding (Fig. 66-9). Blood products should be evacuated with copious warm irrigation to minimize the risk of postoperative chemical meningitis. Ultrasound can be used to assess the extent of resection of the tumor. The lateral traction sutures are removed from the dural edges, and the dura is closed using either interrupted or running suture. This may either be braided (4-0 nylon) or monofilament (5-0 or 6-0 nylon or Gore-Tex) suture (Fig. 66-10). For minimally invasive approaches, nitinol U-clips (Medtronic, Minneapolis, MN) can be used for dural closure.12 In the case of meningioma, a dural substitute must be used to repair the defect caused by excision of the mass. Many products are commercially available. Alternatively, autologous fascia lata may be harvested and used as a patch graft. The dural closure should be watertight to prevent the development of a pseudomeningocele, and this is tested by having the anesthesiologist hold a positive pressure of 30 to 40 mm H2O in the patient’s lungs while inspecting the dural suture line for leaks. Leaks may be addressed by primary repair with the aforementioned suture or by patch grafting with the materials discussed here or with locally harvested muscle. If the dura mater cannot be closed in a watertight fashion, a lumbar drain should be placed, and CSF should be drained postoperatively to reduce intrathecal pressure at the dural repair. Placement of an overlying collagen matrix could also be considered in this case to reduce the risk of pseudomeningocele (Fig. 66-11). Alternatively, a sealant approved by the Food and Drug Administration (FDA), such as DuraSeal spine sealant, can be used to reinforce watertight closure of the

Figure 66-9  Posterior approach to T10–T11 schwannoma. The tumor is excised, and hemostasis is achieved. No gross injury to the cord is observed.

dura. This may be supplemented with a back brace to increase intraabdominal pressure to counteract the CSF leak.13 Finally, the wound is closed in multiple layers. The overlying muscle is loosely approximated with size 0 absorbable suture. The muscle fascia is tightly closed with either interrupted or running size 0 absorbable suture. Finally, the dermis and epidermis are closed according to surgeon preference.

Postoperative Care The extent of resection should be confirmed with contrast MRI (Fig. 66-12). ■ Oral opiates or intravenous patient-controlled analgesics should be considered for postoperative pain control. ■

Figure 66-10  Posterior approach to T10–T11 schwannoma. Primary closure with 6-0 Gore-Tex suture in running locking fashion.

Figure 66-11  Posterior approach to T10–T11 schwannoma. Placement of an overlying collagen matrix over the primary dural closure can reduce the possibility of delayed pseudomeningocele.

66  •  Surgical Technique for Resection of Intradural Tumors

Figure 66-12  Magnetic resonance imaging (MRI) after posterior approach for resection of schwannoma shows no evidence of residual lesion (left to right, sagittal T1-, T2-, and T1-weighted MRI with contrast and axial T1-weighted MRI with contrast).

Early mobilization, physical therapy, and rehabilitation are recommended. ■ Follow-up should include x-rays; spinal instability or delayed deformity may occur after laminectomy that involves the lower cervical or cervicothoracic region, especially in younger patients. ■

Complications Common transitory postoperative symptoms: spinal headache, motor changes, and/or sensory changes, especially when myelotomy is performed ■ Permanent neurologic deficits ■ Epidural hematomas ■ Pseudomeningocele/CSF leak, wound infection, meningitis, or postlaminectomy spinal deformity ■

Conclusion Most common approaches used for the majority of intradural-extramedullary or intramedullary tumors are described here. With posterior exposures with varying degrees of lateral bone resection, dentate ligament division and gentle cord rotation may allow for safe removal of a majority of lesions irrespective of their location in reference to the cord.14 However, an anterior approach may be necessary for some ventral tumors. Use of spinal instrumentation should be considered preoperatively if the exposure or the resection could lead to instability of the spine.

References 1. Chamberlain MC, Tredway TL: Adult primary intradural spinal cord tumors: a review. Curr Neurol Neurosci Rep 11:320–328, 2011. 2. Bazan C: Imaging of lumbosacral spine neoplasms. Neuroimaging Clin North Am 3:591–608, 1993. 3. Shapiro R: Myelography, ed 4, Chicago, 1984, Yearbook Medical Publishers. 4. Haji FA, Cenic A, Crevier L, et al: Minimally invasive approach for the resection of spinal neoplasm. Spine (Phila Pa 1976) 36:E1018–E1026, 2011. 5. Lu DC, Chou D, Mummaneni PV: A comparison of mini-open and open approaches for resection of thoracolumbar intradural spinal tumors. J Neurosurg Spine 14:758–764, 2011. 6. Mannion RJ, Nowitzke AM, Efendy J, et al: Safety and efficacy of intradural extramedullary spinal tumor removal using a minimally invasive approach. Neurosurgery 68:208–216; discussion 216, 2011. 7. Tredway TL, Santiago P, Hrubes MR, et al: Minimally invasive resection of intradural-extramedullary spinal neoplasms. Neurosurgery 58:ONS52–ONS58; discussion ONS-8, 2006. 8. Pompili A, Caroli F, Telera S, et al: Minimally invasive resection of intradural-extramedullary spinal neoplasms. Neurosurgery 59:E1152, 2006. 9. Zhou H, Miller D, Schulte DM, et al: Intraoperative ultrasound assistance in treatment of intradural spinal tumours. Clin Neurol Neurosurg 113:531–537, 2011. 10. Malhotra NR, Shaffrey CI: Intraoperative electrophysiological monitoring in spine surgery. Spine (Phila Pa 1976) 35:2167–2179, 2010. 11. Setzer M, Vatter H, Marquardt G, et al: Management of spinal meningiomas: surgical results and a review of the literature. Neurosurg Focus 23:E14, 2007. 12. Park P, Leveque JC, La Marca F, et al: Dural closure using the U-clip in minimally invasive spinal tumor resection. J Spinal Disord Tech 23:486–489, 2010. 13. Hawk MW, Kim KD: Review of spinal pseudomeningoceles and cerebrospinal fluid fistulas. Neurosurg Focus 9:e5, 2000. 14. Angevine PD, Kellner C, Haque RM, et al: Surgical management of ventral intradural spinal lesions. J Neurosurg Spine 15:28–37, 2011.

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Vascular Lesions of the Spinal Cord NIKOLAY L. MARTIROSYAN, SERGEY NECKRYSH, FADY T. CHARBEL, NICHOLAS THEODORE, and G. MICHAEL LEMOLE JR

Overview Four topics will be addressed in this chapter: 1) normal vascular anatomy of the spinal cord; 2) vascular neoplastic lesions, represented by hemangioblastomas and cavernous malformations; 3) arteriovenous malformations (AVMs) and arteriovenous fistulas; and 4) spinal cord aneurysms.

Normal Vascular Anatomy of the Spinal Cord The vascular anatomy of the spinal cord is divided into extrinsic and intrinsic spinal arteries and veins.1 The intrinsic arteries are further divided into central and peripheral arterial systems, which are supplied by central arteries anteriorly, and the pial network.1,2 More specifically, the central system supplies the anterior two thirds of the spinal cord through the anterior spinal artery (ASA).2 The posterior spinal artery (PSA) consists of the peripheral system and supplies the posterior component of the spinal cord.3 Overlaps between these two systems are found only in the terminal branches, which are not true anastomoses; in the inner white matter; and at the periphery of the gray matter.4 The extrinsic arteries are metameric in nature, integrating tissues with one source of supply.1

rootlets of the cauda equina.2,3 The PSA is fed by the 10 to 20 ipsilateral posterior radiculomedullary arteries.6,7 Nevertheless, in a few instances, a single radiculomedullary artery does supply both posterior spinal arteries.7,8 Anatomically, the PSA has a characteristic single-vessel appearance; however, it can form several anastomosing channels. The PSA has a plexiform design, and it can become so small that it is difficult to see (Fig. 67-2; see also Fig. 67-1).9

PIAL ARTERIAL PLEXUS The pial arterial plexus is formed by the surface anastomoses of the ASA and the PSA systems, and it is responsible for blood supply of the spinal cord surface.6 It supplies the peripheral sections of the spinal cord and includes the posterior horns and substantia gelatinosa.4 The pial arterial plexus branches infiltrate the dorsal midline of the spinal cord and then proceed inward in a perpendicular fashion.10 The plexus is fed on the lateral surfaces by the posterior radicular arteries, which are also responsible for supplying the dura mater, spinal ganglia, PSA, and the nerve roots (see Fig. 67-1).7

RADICULAR ARTERIES

The ASA supplies the anterior two thirds of the spinal cord.5 Rostrally it originates from the vertebral arteries, before they join to form the basilar artery.4 The ASA travels through the anterior median fissure,3 and its diameter decreases as it proceeds rostrally.2,3 The diameter of the ASA becomes consistent once it reaches the thoracic region. The size variation is anatomically explicit: the ASA gets progressively smaller until it joins with the artery of Adamkiewicz, at which point it becomes very prominent. Lastly, the terminal branches of the ASA allow it to form several anastomoses (Fig. 67-1).6

Radicular arteries originate from segmental vessels that arise from such larger tributaries as the aorta or the subclavian artery. The 31 pairs of radicular arteries are responsible for supplying numerous structures that include the dura mater, spinal ganglia, PSA, and ASA.11 Radicular arteries are classified into those that divide into 1) arteries that do not reach the dura of the spinal cord; 2) arteries that penetrate the dura but end early; and 3) radiculomedullary arteries that actually vascularize the spinal cord.11 It is important to make a note about the artery of Adamkiewicz, also known as the arteria radicularis magna or the great radicular artery, which is the largest radiculomedullary artery, with a diameter of 1.0 to 1.3 mm.7 Nearly 80% of the time, it is present on the left side, anastomoses with the ASA, and then divides into small ascending and large descending branches (see Fig. 67-1).3,12

POSTERIOR SPINAL ARTERY

CENTRAL ARTERIES

The vertebral artery gives off the paired posterior spinal arteries (PSA); however, the PSA sometimes originates from a posterior radicular artery. The arteries proceed rostrally and travel posterolaterally; they terminate near the end of the spinal cord after providing several branches to posterior

The central arteries arise from the ASA and pierce the anterior median fissure to enter the spinal cord. The 210 central arteries form a centrifugal system that supplies the middle of the spinal cord, the central sulcus, anterior and posterior gray horns, and periphery of the white matter.11,13,14 Once

ANTERIOR SPINAL ARTERY

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67  •  Vascular Lesions of the Spinal Cord

Aorta PSA Adamkiewicz a.

Segmental a.

ASA

PSA Central a.

A

B

ASA

Adamkiewicz a.

Figure 67-1  A, Anterolateral view of lumbar spinal cord. B, Vascularization of lumbar spinal cord. Contribution of the anterior spinal artery and posterior spinal artery in supplying the blood to the spinal cord. (Courtesy Nicholas Theodore, MD.)

it reaches the anterior gray matter, it divides into short ascending and descending branches that supply the edges of the gray matter.2 The number of central arteries present at specific segments of the spinal cord also differs.15 The central arteries are most numerous in the cervical and lumbosacral region and are least numerous in the thoracic region. Lastly, the acute angle formed by these arteries in the lumbosacral region permits for a wider perfusion of the spinal cord.13,16

VEINS OF THE SPINAL CORD The veins of the spinal cord follow a pattern similar to the arteries of the spinal cord. The intrinsic spinal cord veins are formed by two groups. First is the longitudinal anteromedian group, which collects into the central veins. The second group is collected through radial veins to coronal veins.17,18 Three anterior and posterior spinal veins drain the spinal cord and are in turn drained by the anterior and posterior radicular veins. The internal vertebral venous plexus integrates the venous drainage in the epidural space; this plexus communicates with the dural sinuses and external vertebral venous plexus.19 The spinous Batson venous plexus is valveless, which allows blood to pass into the systemic venous system. This network provides an easy route of dissemination for metastases.20 This can be quite significant in cases of prostate cancer, in which increased intraabdominal pressure

facilitates spread of metastatic tumor in the vertebrae, brain, or skull through this venous plexus.21

CAPILLARIES OF THE SPINAL CORD The capillaries of the spinal cord differ according to location. The capillary bed is at least five times denser in the gray matter of the spinal cord than in the white matter, because other arterial structures provide the white matter. It is greatest near the site of cell bodies, which reflects their increased metabolic requirements. The capillary beds of the white matter are robust, as are the nerve fiber routes. When the capillary density of the white matter alone is compared with the transition zone of the gray and the white matter, the latter has been shown to have a higher density.16

Hemangioblastoma GENETICS Hemangioblastoma is sporadic in nature or is inherited in an autosomal dominant fashion with von Hippel–Landau (VHL) syndrome.22 The VHL gene is located at the locus of 3p25-p26.23-27 Mutations such as point and frameshift mutations and large deletions have been identified within the VHL gene. A mutation within codon 238 is specifically implicated in retinal and CNS hemangioblastoma.27 A loss

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of function mechanism of a single tumor suppressor gene has also been attributed in development of hemangioblastoma pathology, and several molecular factors have been associated with hemangioblastoma. Increased hypoxia-induced factor (HIF) and vascular endothelial growth factor (VEGF) transcripts have been found in ocular hemangioblastoma.28-30 Increased expression of VEGF in part is responsible for tumor growth through abundant neovascularization. Other HIF-induced molecules— including transforming growth factor (TGF), platelet-derived growth factor (PDGF), fibroblast growth factor (FGF), and epidermal growth factor (EGF)—are increased in hemangioblastoma and are all factors associated with angiogenesis.29 Presence of erythropoietin (Epo) and Epo receptor (EpoR) also alludes to the presence of involvement of progenitor cells in VHL-associated lesions.29,31,32 The origin of the stromal, neoplastic component of hemangioblastoma33 continues to elude researchers; however, immunohistochemical studies have consistently identified the following epitopes: neuron-specific enolase,22,34 neural cell adhesion molecule (CD56),35,36 and vimentin.35-38 The vascular endothelial cells in hemangioblastoma are also characterized by expression of von Willebrand factor, platelet–endothelial cell adhesion molecules, and Weibel– Palade bodies.27,39-41

EPIDEMIOLOGY Spinal cord hemangioblastomas (Fig. 67-3; see also Fig. 67-2) are rare lesions that represent 1% to 3% of all intramedullary spinal cord tumors, and men are affected twice as often as women. Central nervous system (CNS) hemangioblastomas are present in 21% to 72% of patients with VHL disease, and approximately 40% are located in the spinal cord. Multiple lesions may be present in 25% to 33% of patients with CNS hemangioblastomas,42 although this

figure may underestimate the actual incidence, because not all patients undergo a full workup for VHL disease. Spinal hemangioblastomas are intramedullary (75%) or have extramedullary or intradural extension (10% to 15%). Approximately 96% of spinal hemangioblastomas are located posterior to the dentate ligament.43 Extradural hemangioblastomas are rare and may arise from the vertebral bodies. By location, 50% of spinal hemangioblastomas occur in the thoracic cord, 40% are in the cervical cord, and 6% are in the lumbar region. Hemangioblastomas have also been rarely reported in the conus medullaris,44 filum terminale,45 nerve roots, and peripheral nerves.46 Typical age at presentation is between 40 and 50 years in patients with sporadic hemangioblastomas (lesions are more often intracranial); patients with VHL disease are usually seen in their late twenties to early thirties. Hemangioblastomas usually present with nonspecific signs of intramedullary mass and syrinx, and syrinx is seen in approximately 50% to 70% of patients. Initial symptoms can be divided into three major groups: 1) sensory changes, which occur in 38.9% of patients, mostly as numbness and involvement of posterior columns; 2) weakness in 27.8%; and 3) pain in 33% (in these cases the tumor frequently extends into or originates from the dorsal root entry zone).47 Patients may also come to medical attention with signs of myelopathy and urinary incontinence. Surprisingly, spontaneous hemorrhage from spinal hemangioblastomas is quite rare; although the majority of patients had subarachnoid hemorrhage (SAH), intramedullary hemorrhage was less common.48

PATHOLOGY The typical spinal cord hemangioblastoma usually enlarges the cord, is well demarcated, and consists of a highly vascular nodule with an associated cyst; leptomeningeal vessels are prominent. Histologically, these tumors are composed of an intricate vascular network of irregular and often dilated capillaries with intervening stromal cells. These stromal cells can produce erythropoietin, resulting in erythrocytosis. Immunostaining for epithelial markers is negative for hemangioblastoma; these markers are important when differentiating between hemangioblastoma and metastatic renal cell carcinoma, which may also develop in patients with VHL syndrome.49,50 A recent study showed high Ki67 activity in intramedullary–extramedullary hemangioblastomas, whereas the Ki67 activity was less than 1% in intramedullary lesions.51

IMAGING

Figure 67-2  Hemangioblastoma.

Dilated, tortuous feeding arteries and draining pial veins can be seen on a myelogram in approximately 50% of cases. Angiography demonstrates a highly vascular mass with dense vascular blush and draining vessels, which can mimic an AVM. Preoperative embolization is a valid option. Magnetic resonance imaging (MRI) findings are consistent with diffuse cord expansion with high signal intensity on T2-weighted imaging with prominent foci of high-velocity signal loss. Cyst formation and syrinx are seen in 50% to 70% of cases.42,43 The tumor nodule is strongly enhanced with contrast administration, and intraoperative use of

67  •  Vascular Lesions of the Spinal Cord

A

B

Figure 67-3  Spinal hemangioblastoma. A, T1-weighted sagittal magnetic resonance image demonstrates hemangioblastoma in the ventral portion of the spinal cord at the T1–T2 level. Flow voids from the dilated venous plexus of the spinal cord surrounding the lesion at the corresponding levels. B, Selective spinal angiogram of the same patient demonstrates a lobulated, highly vascular lesion that was found to be hemangioblastoma on pathologic examination after surgical resection.

indocyanine green angiography facilitates lesion delineation to ensure completeness of resection.52

SURGICAL CONSIDERATIONS Progressive neurologic deterioration caused by mass effect of the tumor and enlarging syrinx and acute neurologic deficit caused by hemorrhage are indications to surgically intervene. In patients with VHL disease, lesions may be multiple, and it is very important to pinpoint the deficit to the particular symptomatic location. Ultimately, multiple surgical interventions may be needed in these patients to treat the disease over their lifetime. Hemangioblastomas are considered in the discussion of vascular spinal cord malformations, because they often behave like AVMs during surgical resection. Presurgical embolization can be implemented to reduce the risk of intraoperative bleeding.53

SURGICAL TECHNIQUE The patient is positioned depending on the location of hemangioblastoma, and the appropriate approach is performed to extend one level above and one level below the margins of the tumor. Bone removal (laminectomy, laminoplasty, or corpectomy) must be adequate to allow exposure of tumor margins along with associated feeding and draining vessels. ■ The dura mater is incised in the midline, elevated, and retracted the entire length of the exposure with preservation of the arachnoid membrane. Sharp or blunt “tearing” ■

techniques can be used to extend the dural opening. Cotton pads or balls are sometimes used to protect the underlying spinal cord during dural opening; recall that spinal dura has only one layer, unlike cranial dura. Cottonoid strips can be packed into the lateral paraspinal gutters to maintain a bloodless operative field, and dural leaflets are tacked up to adjacent muscles or drapes with 4-0 braided nylon suture. ■ The microscope is brought into the operative field, and the arachnoid is sharply dissected from the surface of the hemangioblastoma and associated vessels. In general, the tumor is approached in much the same manner as an AVM, and special attention is paid to feeding and draining vessels. ■ Pial vessels that cross the margin of the tumor at its junction with the pia mater are coagulated using bipolar cautery at a low setting and are sharply divided to clearly expose the margin of the tumor at the pial surface. Sensory rootlets embedded into the tumor may be dissected free or interrupted if the tumor is to be completely resected. ■ The plane of dissection is developed in a circumferential manner using bipolar cautery, microscissors, and small cottonoid strips. The tumor capsule is normally prominent. It is important that dissection be performed in a completely bloodless field, so that each feeding and draining vessel can be distinguished from en passant vessels and interrupted as it reaches the surface of tumor capsule. Again, surgical technique mirrors that used for AVM resection.

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Traction on the spinal cord, including “tenting,” should be avoided while reflecting the poles of the tumor. ■ Bipolar electrocautery must be used judiciously and at low voltage to avoid thermal injury to adjacent neural tissue. If bleeding occurs from the tumor capsule, coagulation often makes it worse. Hemostasis can be obtained by application of a variety of hemostatic agents, such as Gelfoam soaked in thrombin. ■ Piecemeal resection of the tumor often causes vigorous bleeding; thus it should not be attempted unless the tumor is large and cannot otherwise be safely removed. In this scenario, meticulous coagulation and hemostasis are imperative. A portion of the tumor can be removed to afford additional exposure. ■ The operative bed is directly inspected to make certain no tumor remains and that hemostasis is complete. ■ Dural closure is performed in a watertight manner with monofilament 4-0 or 5-0 suture on a tapered needle. Some surgeons apply fibrin glue over the suture line. ■ Multiple-layer closure of the wound is performed in a standard fashion. ■

OUTCOMES Hemangioblastomas can be safely removed without significant new postoperative deficit. Approximately 96% of patients will remain unchanged or will improve neurologically, and 4% will worsen. A recent National Institutes of Health (NIH) study published on surgical outcomes after hemangioblastoma resection demonstrated the following54,55: Location of the tumor anterior to the dentate ligament carries a higher risk of new postoperative neurologic deficit. ■ Likelihood of new permanent postoperative neurologic deficit increases with lesions larger than 500 mm.3 ■ Cysts associated with hemangioblastoma diminish or resolve in almost all patients. Presence of a cyst preoperatively does not alter the surgical outcome, and further surgical manipulations on the tumor cyst during resection are not needed.54 ■

EPIDEMIOLOGY Cavernous malformations (Fig. 67-4) can be considered neoplastic lesions based on their features and growth pattern. These lesions can occur sporadically or in a familial pattern and have an identifiable genetic abnormality with an autosomal dominant pattern of inheritance and incomplete penetrance. Spinal cord cavernous malformations represent 5% to 12% of all spinal cord vascular malformations and 3% to 15% of all cavernous malformations that occur in the CNS. There is slight female predominance, and symptomatic presentation and diagnosis usually occur in the fourth decade of life. The thoracic cord is affected more often than the cervical, and lesions in the conus medullaris and cauda equina are rare.

CLINICAL PRESENTATION AND NATURAL HISTORY The clinical course of spinal cord cavernous malformations is variable. Patients can develop acute symptoms attributed to hemorrhage, or they may come to medical attention with stepwise deterioration, which can mimic demyelinating disorders. Acute presentation is characterized by pain that corresponds to the level of the cavernous malformation and neurologic deterioration that can occur over several days. This is different from the typical hemorrhage caused by an AVM of the spinal cord, which is typically more acute, and neurologic deficit is concomitant with the onset of pain. Initial hemorrhage from a cavernous malformation can cause paraplegia or quadriplegia, although incomplete neurologic deficit followed by some degree of recovery, which is rarely complete, is more common. In untreated lesions, repeated hemorrhages may occur months to years after the initial hemorrhage. A more subtle presentation can occur when the lesion is primarily localized on the

Spinal Cord Cavernous Malformations GENETICS Cavernous malformations have a strong genetic predisposition, and some familial and sporadic forms have incomplete penetrance and variable expressivity.56,57 Nearly 150 types of mutations are reported, and frameshift and nonsense mutations are the most prominent. Sporadic cases account for 80% of the cavernous malformations, with an incidence of 1 in 200, and these cases demonstrate great locus and allelic heterogeneity.58 Several rare causes have also been reported, such as a balanced translocation between chromosomes 3 and X in a female with skewed X inactivation.59

Figure 67-4  Spinal cavernous malformation.

67  •  Vascular Lesions of the Spinal Cord

dorsal aspect of the spinal cord, and patients initially complain of intermittent paresthesias. Radiculopathy is more common with lesions in the dorsal root entry zone. With the widespread use of MRI, cavernous malformations are often discovered at an early symptomatic stage or even while asymptomatic.

PATHOLOGY Spinal cord cavernous malformations are identical in appearance and histopathology to intracranial cavernous malformations, and grossly they may be described as soft and spongy with a dark blue to red-brown hue. Cavernous malformations are usually well circumscribed, and hemosiderin staining of the surrounding tissues as a result of repeat bleeding can clearly define the plane of dissection. This discoloration is sometimes the only visual clue that a cavernous malformation may be located under the pial surface. Microscopically, cavernous malformations consist of endothelium-lined channels filled with blood with no intervening brain tissue. Vessel walls lack elastic and muscular layers, and calcifications are rare. A gliotic, often hemosiderin-laden plane usually is evident around the malformation. Tonguelike extensions of the cavernous malformation can extend into the surrounding gliotic plane, and this should be kept in mind during resection to achieve complete excision.

IMAGING Findings on MRI include signs of hemorrhage in different stages of blood product degradation with a mixture of highand low-intensity signals. The typical appearance of a cavernous malformation is an inhomogeneous high-intensity signal on both T1- and T2-weighted images with a surrounding dark ring of hemosiderin and appearing hypointense on T1- and T2-weighted images. Enhancement is not typical for cavernous malformations. Unlike their intracranial counterparts, the diagnosis of spinal cord cavernous malformations with MRI is not always straightforward, especially with small lesions. The classic “popcorn” appearance is not always seen in spinal cord cavernous malformations. In some cases, spinal MRI, particularly T2-weighted images, can be misleading for surgical planning when trying to estimate where the malformation comes closest to the pial surface. Malformations that appear to be located superficially on MRI may be found to lie deeper in the spinal cord during surgical exploration. Nevertheless, MRI represents an invaluable imaging technique, compared with more traditional imaging modalities, and with emergence of more powerful MR scanners, the quality of spinal cord imaging is rapidly improving. Angiography has very little value in diagnosing these angiographically occult lesions. The angiogram may demonstrate a venous anomaly associated with a cavernous malformation; the cavernous malformation, not the venous anomaly, is felt to be the source of recurrent hemorrhage. The venous anomaly represents an anatomic variant that should be preserved during surgical resection, because it provides venous drainage to the surrounding normal tissues. Preoperative embolization is not an option with cavernous malformations.

SURGICAL CONSIDERATIONS The increasing experience with surgical excision of intramedullary spinal cord cavernous malformations and the high probability of neurologic deterioration if these are left untreated have expanded the role for surgical treatment. Studies clearly demonstrate that progression of neurologic symptoms in patients with spinal cord cavernous malformations is the rule rather than the exception. Neurologic outcome is most dependent on the preoperative neurologic status of the patient, and best outcomes are achieved in patients with good neurologic status preoperatively. Given its small cross-sectional area and high eloquence, the spinal cord is unlikely to tolerate even minor expansions from hemorrhage or from growth of the malformation, and this is an important consideration. Modern microsurgical technique can provide good outcomes with an acceptable level of postoperative morbidity in patients with spinal cord cavernous malformations. A recent study showed the effectiveness of a carbon dioxide laser in spinal cord cavernous malformation resection; the laser allows the surgeon to perform delicate myelotomies safely and to shrink cavernous malformations away from eloquent spinal cord tissue.60 Surgery may be recommended for appropriate candidates with symptomatic lesions, especially when the cavernous malformation extends to the pial surface. However, this decision is significantly more difficult in patients with asymptomatic or minimally symptomatic lesions and in patients with deep-seated lesions. In these cases, recommendations for radical surgical resection should be tailored to each individual case. Young patients and patients with large lesions are the most appropriate candidates in this group, because they are most likely to experience long-term benefit from early surgical intervention.

SURGICAL TECHNIQUE Dorsally Located Lesions (Fig. 67-5) ■ Preoperative localization is an important part of surgical planning and can be done using techniques such as external skin marking or image guidance with fiducial application. ■ Most cavernous malformations can be exposed and resected via a posterior approach. Laminectomy or laminoplasty should provide adequate exposure for dorsally located lesions. Laminoplasty has been recommended for cervical or upper thoracic lesions to prevent postsurgical kyphotic deformity. ■ Laminoplasty in patients without significant degenerative disease or spinal cord expansion can be performed with a pneumatic drill and a footplate attachment with laminar cuts on both sides. Ligamentous structures are sharply divided, and the laminae and spinous processes are removed en bloc over the levels of interest. Absolute hemostasis should be obtained before opening the dura. ■ The intraoperative microscope is brought into the operative field, and the dura mater is incised in the midline with preservation of the underlying arachnoid layer as described in previous sections. The dural edges are tacked up to the drapes or paraspinous muscles using 4-0 braided nylon sutures.

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Figure 67-5  Surgical corridors to the lesions in the spinal cord. Straight arrow: Certain lesions in the spinal cord located posteriorly and extending to the pial surface in the midline could be approached safely by performing an incision through the dorsal median septum of the spinal cord. Curved arrow: Lesions located paramedially and extending to the pial surface of the spinal cord at the dorsal root entry zone could be approached via the dorsolateral sulcus of the spinal cord. Dotted line: The two-point method is used to design a surgical approach to lesions of the spinal cord located laterally, when anatomic sulci of the spinal cord cannot be used. The first point is placed in the center of the lesion; the second point is placed where the lesion comes closest to the pial surface. The line connecting the two points indicates the shortest trajectory to the lesion.

The arachnoid is opened sharply in the midline, and the edges are secured to the ipsilateral dural leaflet. ■ The spinal cord is examined under high magnification; malformations that extend toward the pial surface may be visible at the surface, and in other cases, blue or redbrown discoloration of the spinal cord caused by hemosiderin deposits will be visible and will point to the location of the malformation. Image guidance or intraoperative ultrasound could be used to localize those lesions that leave no clues as to their location. ■ A two-point method is used to determine the optimal entry point and trajectory through the spinal cord to the cavernous malformation: a line is drawn through the center of the lesion to the point where it comes closest to the surface. For deeper lesions, this technique is modified in the spinal cord to avoid eloquent tracts and to take advantage of better tolerated avenues of approach (see Fig. 67-5). ■ For deep-seated lesions, myelotomy is performed under high magnification, either through the dorsal median sulcus or along the dorsal root entry zone, whichever offers a better trajectory to the malformation. ■ Care must be taken to avoid damaging the adjacent normal spinal cord parenchyma, and sharp dissection with judicious use of bipolar electrocautery is the standard of care. Myelotomies should be parallel to fiber tracts on the long axis of the spinal cord to minimize damage. ■ Resection of the lesion is performed using microcurettes and gentle suction aspiration. Handheld suction devices with thumb apertures offer controlled suction strength, ■

which is critical to avoid injury to surrounding tissues. Typically, lesions will be removed in a piecemeal fashion, although some can be resected en bloc. Although not truly encapsulated, cavernous malformations have a well-defined gliotic plane that separates them from the surrounding spinal cord. ■ Bleeding is seldom a problem with cavernous malformations because of their low-flow nature, and hemostasis should be accomplished using hemostatic agents and gentle compression. Bipolar cautery use should be avoided unless absolutely necessary, and when used at all, it should be set to a low power. Venous draining anomalies are often associated with cavernous malformations and should be preserved, because they may provide venous drainage for adjacent eloquent tissues. ■ After hemostasis is obtained, careful inspection of the resection bed under high magnification is imperative to identify and further resect small “tongues” of the cavernous malformation that may extend into the adjacent tissue. Incompletely resected lesions can recur and hemorrhage; therefore every attempt should be made to resect these lesions fully during the first surgery. ■ Dura is closed in a watertight fashion as described in previous sections. A multilayer wound closure is performed using standard techniques.

Ventrally Located Lesions Lesions involving the anterior and lateral aspect of the spinal cord are much more difficult to approach (Fig. 67-6); however, if the lesion is symptomatic and reaches the anterior or lateral pial surface, surgery can be attempted. In these cases surgical morbidity is generally higher owing to the increased spinal cord eloquence and difficulty of the surgical approaches. Generally, only lesions that reach the pial surface are approached anteriorly; approaches through the dorsal median sulcus and dorsal root entry zone are better tolerated with deep lesions. Lesions located anteriorly in the cervical spinal cord can be approached via cervical corpectomy, which requires anterior interbody arthrodesis and instrumentation at the conclusion of the surgical procedure. The depth and narrowness of the surgical field in this approach is a challenge. Principles of dural opening, lesion localization and removal, and closure are similar to those of the posterior technique. In the thoracic region, access to the anterior spinal cord can be obtained via thoracotomy with a corpectomy. Although this approach allows adequate visualization of the anterolateral aspect of the spinal cord, the working angle and field depth make surgical conditions less ideal. Watertight dural closure is even more crucial in this location because of the potential to develop a cerebrospinal fluid leak into the pleural cavity. The posterolateral transpedicular approach described by Martin and colleagues11 can also be used to access lesions in the anterolateral thoracic spinal cord. Details of this approach are summarized here. Combined posterior midline and transverse incisions are performed over the appropriate levels, and the thoracic laminae are exposed on the side of the approach. ■ Bony elements of the posterolateral thoracic spine are removed using rongeurs and a high-speed drill. ■

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T2-weighted imaging. Patients should undergo MRI surveillance 6 to 12 months after the initial surgery and 2 to 3 years thereafter. If recurrence is suspected clinically and radiographically, reoperation can be considered. A recently published large case series analysis showed that 11% of patients worsen, 83% remain unchanged, and 6% improve after surgery.61

Spinal Cord Arteriovenous Malformations GENETICS

Figure 67-6  Approach to spinal cord lesions located ventrally. Lesions extending to or located on the anterior surface of the spinal cord represent the most challenging surgical approach. They could be accessed via vertebral corpectomy, or they could be exposed from a posterior approach. Dentate ligament closest to the lesion is cut, and 4-0 braided nylon suture is passed through the stump of the ligament. Suture is used to gently rotate the spinal cord to expose the anteriorly located lesion.

The ipsilateral pedicles at the corresponding levels are removed down to their insertion with the vertebral bodies to expose the lateral aspect of thoracic dura. ■ Dural opening is performed along the lateral thecal sac in a fashion similar to the one described for the posterior approach. ■ The critical part of the approach is to identify and section the dentate ligament several levels above and below the cavernous malformation. Stitches are placed in the proximal portion of the ligament to facilitate gentle rotation of the spinal cord and expose the ipsilateral ventral portion of the cord and the cavernous malformation, which extends to the pia. Resection of the malformation is then carried out as described in previous sections. ■ Limitations of this approach include inadequate visualization of anterior cord surface beyond the anterior midline and ASA. Bilateral posterolateral transpedicular approaches may be performed to expose a lesion that crosses the midline, although such aggressive bony resection will likely require stabilization with instrumentation and fusion at the completion of the procedure. ■

OUTCOMES Cavernous malformations of the spinal cord can be resected using contemporary microsurgical techniques with overall improvement in patient condition and natural history. Morbidity and recovery after surgical resection usually mimics a bleeding episode and can be justified if the risk of future bleeding is eliminated. If surgical intervention is attempted, every possible effort should be made to resect the lesion fully to prevent lesion recurrence, regrowth, and rehemorrhage. MRI immediately after surgery can be ambiguous if blood in the operative bed obscures the presence of residual cavernous malformation. This is particularly the case with

Several contributing factors to AVM pathology have been isolated, yet the exact mechanisms still bewilder researchers and physicians. Repression of VEGF and angiopoeitin 1 and 2 and their receptor Tie2 have been shown to result in AVM pathology through downstream effects on tumor growth factor β (TGF-β) and vascular instability.62 Moreover, mutation or deletion of integrin-β8 has an effect on the proper signaling pathway of TGF-β, which causes AVM.63 The downregulation of endothelin-1 (ET-1) mRNA has also been shown to be involved in the pathophysiology of AVM through anomalous vascular remodeling and dysautoregulation of vessel injury.64-68 Another molecular factor involved in AVM is endoglin (Eng), which has several roles in vascular physiology, including remodeling of capillary plexi and proliferation of endothelial cells. Patients with type 1 hereditary hemorrhagic telangiectasia also have an Eng mutation and subsequently develop AVM pathology, which provides further evidence for its role in AVM.69 Furthermore, stromal cell–derived factor 1 (SDF-1), a chemokine, is found in the AVM-affected vessels and causes increases in the migration and deposition of endothelial cell progenitors in the involved vessels.70

CLASSIFICATION Historic classification schemes for rare spinal cord AVMs were often confusing, but as case numbers and surgical experience grew, more coherent systems of thought were devised. The classification proposed by Rosenblum and collegues71 in 1987 defined four major types of spinal AVMs based on angiographic findings and hemodynamic features (Table 67-1). With later modifications, this system became the most widely accepted system in use. Recent attempts to simplify and offer a more-inclusive system of thought for all AVMs that affect the spinal cord led to a new classification by Spetzler and colleagues,72 and this system is used for the discussion that follows here.

EPIDEMIOLOGY AND NATURAL HISTORY Extradural Arteriovenous Fistulas Extradural-arteriovenous fistulas (Fig. 67-7) are rare lesions. A direct connection between an extradural artery and vein results in venous hypertension, enlargement of the epidural venous complex, mass effect on the spinal cord, and impaired venous outflow. Sometimes these lesions

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Table 67-1  Classification Systems for Spinal Arteriovenous Malformations (AVMs)

Traditional Classification*

Spetzler† and Traditional Classifications* of Extradural Arteriovenous (AV) Fistulas

I. AV fistulas located in the dura of the nerve root

1.  Extradural AV fistulas, an AVM subtype

IV. Intradural AV fistulas with medullary artery on the pial surface, communicating directly with the pial vein without intervening nidus III. Juvenile AVM with abnormal tangle of blood vessels filling the spinal cord at the involved levels and containing neural parenchyma within the nidus of the AVM II. Glomus AVM with localized and tightly coiled intraparenchymal nidus supplied by medullary artery and drained via normal venous routes

2.  Intradural dorsal AV fistulas Single feeders (subtype A) Multiple feeders (subtype B) 3.  Intradural ventral AV fistulas Type A (small shunt, low flow) Type B (medium shunt,   higher flow) Type C (large shunt, highest flow) 4.  Extradural-intradural AVM Figure 67-8  Intradural dorsal arteriovenous fistulas. (From Spetzler RF, Meyer FB, editors: Youman’s neurological surgery, vol 2, ed 5, St Louis, 2004, Elsevier.) 5.  Intramedullary AVM

6.  Conus AVM *Rosenblum B, Oldfield EH, Doppman JL, et al: Spinal arteriovenous malformations: a comparison of dural arteriovenous fistulas and intradural AVMs in 81 patients. J Neurosurg 67(6):795–802, 1987. † Spetzler RF, Detwiler PW, Riina HA, et al: Modified classification of spinal cord vascular lesions. J Neurosurg Spine 96(2):145–156, 2002.

Figure 67-9  Intradural ventral arteriovenous fistulas. (From Spetzler RF, Meyer FB, editors: Youman’s neurological surgery, vol 2, ed 5, St Louis, 2004, Elsevier.)

Figure 67-7  Extradural arteriovenous fistulas. (From Spetzler RF, Meyer FB, editors: Youman’s neurological surgery, vol 2, ed 5, St Louis, 2004, Elsevier.)

present with acute epidural hemorrhage, which requires urgent surgical intervention.73 When treated promptly, these patients generally have a good prognosis.

Intradural Dorsal Arteriovenous Fistulas Intradural arteriovenous fistula (Fig. 67-8) is the most common type of spinal vascular malformation, responsible for approximately 30% to 80% of spinal vascular malformations. Men are affected approximately three to five times more often than women.74 These lesions predominantly

occur in the lower thoracic spinal cord and conus medullaris and usually consist of a plexiform low-flow shunt from intervertebral (radicular) arterial feeders or, less frequently, from sacral and hypogastric arteries. The connection to the medullary venous system is within the dural leaflet of the nerve root or immediately adjacent to it; there is no intervening nidus.73 The shunt produces venous hypertension in the medullary veins, which constitute the sole venous outflow from the coronal venous plexus of the spinal cord. Symptoms are nonspecific and include back pain, weakness, sensory symptoms, and bowel or bladder dysfunction. Hemorrhage is rare, and patients rarely come to medical attention with acute symptoms. Once patients become symptomatic, 90% will become disabled within 5 years if treatment is not initiated.

Intradural Ventral Arteriovenous Fistulas Intradural ventral arteriovenous fistulas (Figs. 67-9 and 67-10) account for 15% to 30% of spinal vascular malformations and occur in both men and women with equal

67  •  Vascular Lesions of the Spinal Cord

A

B

Figure 67-10  Ventral arteriovenous fistula supplied by Adamkiewicz artery. A, Non–digital subtraction angiography (DSA) superselective image of the artery forming an arteriovenous fistula. B, DSA image of the same patient demonstrates dilated coronal venous plexus of the spinal cord with engorgement of the draining veins.

Figure 67-11  Extradural-intradural arteriovenous malformations. (From Spetzler RF, Meyer FB, editors: Youman’s neurological surgery, vol 2, ed 5, St Louis, 2004, Elsevier.)

frequency. Mean age at presentation is 45 years; The most typical location is in the thoracolumbar spinal cord and conus medullaris, but these fistulas may be found anywhere; midline lesions derive their blood supply from the ASA or, less frequently, from the PSA with a fistulous component into the superficial venous system of the spinal cord.75 Patients present with myelopathy, weakness, sensory deficits, pain, or sphincter problems. The incidence of hemorrhage is 10% to 20%, and a progressive course is more typical than an acute presentation.

Extradural-Intradural Arteriovenous Malformations Extradural-intradural AVMs (Fig. 67-11) are large but rare. Also known as juvenile AVMs, they are typically found in the cervical spinal cord in adolescents and young adults. The vascular supply may arise from anterior and posterior spinal arteries and from arteries that feed extradural tissues. These lesions present with hemorrhage, pain, and rapidly progressive neurologic deficit; they may occupy the entire lumen of the spinal canal, and they may extend into the surrounding tissues and bone.76 It is theorized that these AVMs arise embryologically from a single metamere. They can have an aggressive clinical course, are difficult to treat, and are often considered inoperable. Despite multimodal

Figure 67-12  Intramedullary arteriovenous malformations. (From Spetzler RF, Meyer FB, editors: Youman’s neurological surgery, vol 2, ed 5, St Louis, 2004, Elsevier.)

intervention, prognosis is poor, and as one researcher put it, “their rarity is perhaps the only favorable aspect.”74

Intramedullary Arteriovenous Malformations Intramedullary AVMs (Figs. 67-12 and 67-13) are a true AVM but with a nidal component located within the parenchyma of the spinal cord; this type accounts for 15% to 20% of all spinal cord vascular malformations. No gender predilection is apparent, and lesions may be located anywhere in the spinal cord; occasionally, they will extend to a pial surface. The main presenting symptom is acute or progressive myelopathy with or without radiculopathy. These highflow and high-pressure lesions may harbor aneurysms in approximately 20% to 50% of cases. This leads to a higher

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A

B

C

Figure 67-13  Intramedullary arteriovenous malformations (AVMs). A, T2-weighted sagittal magnetic resonance imaging demonstrates intramedullary AVM at C3–C4 levels with associated hematoma and flow voids from arterialized coronal venous plexus of the spinal cord. B, Selective spinal angiogram of the same patient demonstrates intramedullary AVM supplied mainly by the feeders arising from the left vertebral artery. C, Intraoperative image of the same patient. The spinal cord at C3–C4 levels was exposed via laminectomy. Note arterialized venous plexus of the spinal cord.

PATHOPHYSIOLOGY

Figure 67-14  Conus arteriovenous malformation. (From Spetzler RF, Meyer FB, editors: Youman’s neurological surgery, vol 2, ed 5, St Louis, 2004, Elsevier.)

By definition, shunting of arterial blood flow into a venous bed without an intervening capillary network is the main feature of any AVM. Histopathologic analysis of a recovered specimen will demonstrate vascular tissue with varying degrees of vessel wall breakdown, particularly in the venous elastic lamina. Shunting of arterial flow results in the cascade of pathophysiologic mechanisms that are responsible for neurologic symptoms. These mechanisms include subarachnoid and intraparenchymal hemorrhage, venous hypertension, vascular steal, arachnoiditis, and mass effect with compression of the spinal cord or nerve roots Depending on the type of vascular malformation, its location, and the nature of the arterial feeders and venous outflow, one or several of these mechanisms may be present. A detailed discussion of AVM pathophysiology is beyond the scope of this chapter.

IMAGING incidence of acute presentation as a result of subarachnoid or intraparenchymal hemorrhage.

Conus Arteriovenous Malformations Conus AVMs (Fig. 67-14) are location-specific lesions that are rare and complex; they involve the conus medullaris or cauda equina and consist of multiple feeders and multiple nidi with complex venous drainage. The arterial supply arises from the ASA or branches of the PSA.72 Presentation is nonspecific, and myeloradiculopathy is attributed to mass effect, hemorrhage, or venous hypertension.

Although conventional myelography and computed tomographic (CT) myelography have been described as an imaging modality of some value in the past, today the patient is most likely to get an MRI of the spine and spinal cord as an initial imaging step. MRI can demonstrate a dilated, tortuous venous system with flow void signals, enlargement of the cord at the level of the nidus, products of blood degradation in cases of prior hemorrhage, and changes in the cord attributed to venous hypertension, vascular steal, and prior hemorrhage. Current MRI resolution usually does not demonstrate the nidus or fistula, nor can

67  •  Vascular Lesions of the Spinal Cord

it clearly delineate the feeding and outflow vascular anatomy precisely; thus selective and superselective angiography remain the gold standards for evaluation of spinal cord vascular malformations. Endovascular treatment has a role in management of spinal vascular malformations and sometimes is the only treatment option.

SURGICAL CONSIDERATIONS It is crucial that the vascular anatomy and flow characteristics of these lesions be understood exquisitely before attempting to treat them surgically. Angiography allows precise localization of the nidus or fistula and allows identification of the vascular supply and venous drainage patterns. It is useful to perform angiography using external markers that will later serve as a reference for the surgical approach. Intraoperative monitoring of somatosensoryevoked potentials (SSEPs) has been demonstrated to improve outcomes after endovascular and surgical stages of treatment. The surgical approach is selected based on the location of the lesion: dorsally located lesions are approached via laminotomy, laminectomy, or hemilaminectomy with facetectomy; intraoperative angiography can be extremely useful, both to locate a lesion and to demonstrate its obliteration. Before patient positioning, the femoral sheath for angiography is usually placed and secured. The patient is generally positioned prone on chest rolls or a frame, and careful positioning will avoid abdominal compression, which can increase venous pressure in the venous plexus of the spinal cord; venous hypertension can make hemostasis problematic. Alternative positions, such as sitting and lateral positions, can be considered for appropriate lesions. The skin incision is planned two levels above and below the level of interest. Laminae are exposed using standard techniques, and skin edges and paraspinous musculature are retracted using self-retaining retractors. Alternatively, fishhooks can be used by securing them to Leila bars on either side of the incision; this will depress the edges of the incision, offer a shallower surgical field, and facilitate surgical technique under the microscope. Laminotomy is performed en bloc using a high-speed pneumatic drill with a pediatric footplate tip. Laminae can be reimplanted at closure and secured with either plates or sutures. The dural opening is performed without violation of the arachnoid membrane, and the dural edges are secured to the drapes or paraspinous tissues with 4-0 Neurolon sutures. The microscope is usually brought into the field at this point, although microscopic technique may also facilitate dural opening. Occasionally, a hemilaminectomy with unilateral facet­ ectomy can be used to gain adequate exposure to dorsolateral lesions, such as intradural dorsal arteriovenous fistulas. Stability is usually not an issue after unilateral facetectomy, but a stabilization procedure can be performed at the time of initial surgery, or as a second stage, after assessment of stability in the postoperative period. The surgical approach to the ventrally located lesions is more difficult. Corpectomy is generally used to gain exposure to the ventral dura. The approach for anterior cervical lesions is similar to that used for anterior cervical corpectomies. Thoracic lesions can be approached via thoracotomy, and a retroperitoneal

approach is used for lumbar lesions. Approaches to ventrally located lesions require a surgical stabilization procedure at the completion of the operation.

SURGICAL TECHNIQUE Extradural Arteriovenous Fistulas Surgical treatment of extradural arteriovenous fistulas is focused on interrupting the shunt into the venous plexus of the cord. The lesion is exposed posteriorly using one of the approaches previously described. The feeding vessel is identified and sacrificed using electrocautery and is interrupted with microscissors. Intradural Dorsal Arteriovenous Fistulas ■ The goal of surgical treatment is to eliminate venous hypertension by interrupting communication between the fistula and venous plexus of the spinal cord. ■ Rarely, these lesions may be considered for endovascular obliteration, but in general, they are considered surgical cases. ■ After the dura is opened, the operative microscope is brought into the surgical field. ■ The arachnoid is opened with microscissors, and the edges are secured to the dura using small hemoclips or sutures. The underlying veins of the coronal venous plexus can be quite dilated, and caution should be exercised while opening the arachnoid over them. ■ Vascular anatomy should be explored to differentiate the efferent vein from the fistula, which is generally located in the dural leaflet along the nerve root sleeve. Temporary interruption of the fistula can be accomplished using temporary aneurysm clips. ■ The coronal venous plexus is observed for decreased venous distension as a result of interruption of the shunt. If this phenomenon does not occur, it means additional vascular contribution to the coronal venous plexus may exist, and intraoperative angiography can be used to identify it. ■ Once the fistula site is confirmed, the fistula itself is cauterized using bipolar cautery, and it is sharply sectioned. Temporary clips are removed, and the venous plexus is inspected for resumption of normal venous color and distension. ■ The dura is closed in a standard watertight fashion, followed by standard multilayer soft tissue and skin closure. ■ General anesthesia is reversed at the end of the case, and the patient’s neurologic function is assessed in the operating room. ■ Patients should undergo an intraoperative or postoperative angiogram on the first postoperative day to evaluate the completeness of the surgical intervention. If the fistula is not completely obliterated, serious consideration must be given to reexploration. Intradural Ventral Arteriovenous Fistulas ■ The goal of surgery is to interrupt the communication between the arterial feeder—or, rarely, feeders—that arise most often from the ASA and draining veins on the pial surface. These lesions do not have a formal nidus and are superficial.

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Many surgeons agree that type A and some type B lesions should be approached surgically, not endovascularly, because the fistula is very small, and attempting embolization can result in occlusion of the ASA with devastating neurologic sequelae. ■ Anterior approaches to the spinal cord are described in preceding sections. The dura and arachnoid are opened in the usual manner. ■ The ventral surface of the spinal cord is explored using the operative microscope, and the location of the fistulous connection is established. Feeders that arise from the posterior spinal arteries must also be interrupted. The veins on the pial surface drain normal tissue and should be preserved during dissection. ■ Whenever possible, the fistula should be interrupted using clip ligation, rather than bipolar electrocautery, because of possible current spread and coagulation of the ASA with devastating neurologic consequences. ■ Veins in the ventral surface of the cord are observed for color change and collapse after fistula obliteration. If the veins remain arterialized, additional feeders must be located and ligated. ■ Dural closure is performed in a standard watertight fashion, and soft tissues and skin are closed in a multilayer fashion. ■

Extradural-Intradural Arteriovenous Malformations ■ Surgical experience with extradural-intradural AVMs is limited owing to their rarity. Only a few cases of successful treatment of extradural-intradural AVMs appear in the literature. ■ Many surgeons accept these lesions as inoperable, and endovascular treatment predominates in their management. Surgical or endovascular treatment is often palliative in nature and aimed at reducing shunt flow to ameliorate neurologic symptoms from venous hypertension or mass effect. ■ When surgery is an option, it is performed in a staged fashion in combination with preoperative embolization. The surgical techniques used are described in the sections of this chapter for the other types of vascular malformations. Intramedullary Arteriovenous Malformations ■ A combined endovascular and surgical approach is considered to be most effective for the management of intramedullary AVMs. ■ Laminectomy and dural and arachnoid openings are performed as described earlier. ■ Sharp arachnoid opening and dissection are performed, because use of bipolar electrocautery may result in current spread to the adjacent dilated veins that drain the normal spinal cord. ■ Arachnoid dissection should be performed carefully to avoid damage to the underlying distended veins. Because these AVMs are high-flow and high-pressure lesions, hemostasis can be very problematic, and all attempts should be made to avoid violating the integrity of the distended venous vasculature. ■ No vessel should be coagulated and interrupted until it has been clearly determined to supply the nidus of the AVM. This can be best ascertained by intraoperative



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■



■



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■

exploration or angiography. As with cerebral AVMs, arterial feeders must be sacrificed before the venous outflow is disconnected; otherwise, a devastating rupture of the nidus could ensue. Midline or paramedian myelotomy is performed if nidus of the AVM is deep and does not reach the pial surface. The paramedian myelotomy can be considered if the patient already has fixed sensory deficit. A very thin gliotic plane often surrounds the nidus of the AVM. Resection of the nidus is undertaken using bipolar electrocautery within this plane by interruption of the small penetrating vessels. Penetrating vessels should be cauterized and cut with microscissors as close to the nidus as possible, because proximal portions of the vessel tend to retract into the cord parenchyma and continue bleeding. Chasing these vessel stumps with electrocautery risks damaging the adjacent spinal cord tissue. Many AVMs harbor aneurysms, which can be obliterated using bipolar electrocautery during the early stages of nidus resection. This maneuver gains additional working space for nidus dissection. When contribution from the ASA is significant, hemostasis may become an issue, because these feeders may be deep to the nidus. Early identification and interruption of these feeders may decrease the amount of intraoperative bleeding and volume of the nidus. Extreme caution must be used when working near the ASA. Very meticulous hemostasis and minimal cord manipulation is imperative for successful resection with minimal neurologic deficit. Closure is performed in the standard fashion.

Conus Arteriovenous Malformations Because of their complexity, conus AVMs often require a staged, combined endovascular and neurosurgical approach. Embolization could be used as either a definitive treatment or as an adjunct to surgical resection. Operative technique incorporates approaches and surgical techniques described earlier for intramedullary malformations and intradural fistulas. Spinal Cord Aneurysms Spinal cord aneurysms are extremely rare, and only sporadic cases are described in the literature. Spinal cord aneurysms can be classified into two basic groups: those that arise within the abnormal vasculature of preexisting vascular malformations and isolated aneurysms that form without any associated vascular anomalies. Aneurysms are also rooted in other pathologies, such as Marfan syndrome, and they represent the major cause of mortality in Marfan syndrome. Ehlers-Danlos syndrome pathology is strongly associated with cerebrovascular complications, namely aneurysms,77 although intracranial aneurysms are the prevalent form of aneurysm in patients with Ehlers-Danlos syndrome type IV.77,78 Patients with spinal cord aneurysms usually come to medical attention with subarachnoid or intraparenchymal hemorrhage. Treatment of the aneurysms within the nidus of an AVM was described earlier. Isolated aneurysms can be clipped or treated using endovascular techniques. Surgical approaches to specific spinal regions are described in previous sections.

67  •  Vascular Lesions of the Spinal Cord

References 1. Baik MW: Vascular anatomy of spinal cord. Korean J Cerebrovasc Dis 2:144–148, 2000. 2. Tveten L: Spinal cord vascularity. III. The spinal cord arteries in man. Acta Radiol Diagn (Stockh) 17:257–273, 1976. 3. Turnbull IM: Blood supply of the spinal cord: normal and pathological considerations. Clin Neurosurg 20:56–84, 1973. 4. Turnbull IM, Brieg A, Hassler O: Blood supply of cervical spinal cord in man: a microangiographic cadaver study. J Neurosurg 24:951–965, 1966. 5. Zeitlin H, Lichtenstein BW: Occlusion of the anterior spinal artery: clinicopathologic report of a case and a review of the literature. Arch Neurol Psychiat 36:96–111, 1936. 6. Gillilan LA: The arterial blood supply of the human spinal cord. J Comp Neurol 110:75–103, 1958. 7. Sliwa JA, Maclean IC: Ischemic myelopathy: a review of spinal vasculature and related clinical syndromes. Arch Phys Med Rehabil 73:365– 372, 1992. 8. Lasjaunias PL, Berenstein A, Brugge KGT: Surgical neuroangiography, Berlin–New York, 2001, Springer. 9. Griffiths IR: Spinal cord blood flow after acute experimental cord injury in dogs. J Neurol Sci 27:247–259, 1976. 10. Martirosyan NL, Feuerstein JS, Theodore N, et al: Blood supply and vascular reactivity of the spinal cord under normal and pathological conditions. J Neurosurg Spine 15:238–251, 2011. 11. Lazorthes G, Gouaze A, Zadeh JO, et al: Arterial vascularization of the spinal cord: recent studies of the anastomotic substitution pathways. J Neurosurg 35:253–262, 1971. 12. Parke WW, Whalen JL, Bunger PC, et al: Intimal musculature of the lower anterior spinal artery. Spine (Phila Pa 1976) 20:2073–2079, 1995. 13. Hassler O: Blood supply to human spinal cord: a microangiographic study. Arch Neurol 15:302–307, 1966. 14. Mawad ME, Rivera V, Crawford S, et al: Spinal cord ischemia after resection of thoracoabdominal aortic aneurysms: MR findings in 24 patients. AJR Am J Roentgenol 155:1303–1307, 1990. 15. Woollam DH, Millen JW: The arterial supply of the spinal cord and its significance. J Neurol Neurosurg Psychiatry 18:97–102, 1955. 16. Turnbull IM: Microvasculature of the human spinal cord. J Neurosurg 35:141–147, 1971. 17. Gillilan LA: Veins of the spinal cord: anatomic details; suggested clinical applications. Neurology 20:860–868, 1970. 18. Aminoff MJ, Barnard RO, Logue V: The pathophysiology of spinal vascular malformations. J Neurol Sci 23:255–263, 1974. 19. Lin VW, Bono CM: Spinal cord medicine principles and practice, New York, 2010, Demos Medical. 20. Batson OV: The function of the vertebral veins and their role in the spread of metastases. Ann Surg 112, 1940. 21. Geldof AA: Models for cancer skeletal metastasis: a reappraisal of Batson’s plexus. Anticancer Res 17:1535–1539, 1997. 22. Gläsker S, Li J, Xia JB, et al: Hemangioblastomas share protein expression with embryonal hemangioblast progenitor cell. Cancer Res 66:4167–4172, 2006. 23. Bonner T, O’Brien SJ, Nash WG, et al: The human homologs of the raf (mil) oncogene are located on human chromosomes 3 and 4. Science 223:71–74, 1984. 24. Crossey PA, Maher ER, Jones MH, et al: Genetic linkage between von Hippel–Lindau disease and three microsatellite polymorphisms refines the localisation of the VHL locus. Hum Mol Genet 2:279–282, 1993. 25. Latif F, Modi W, Tory K, et al: A MspI polymorphism and linkage mapping of the human protein-tyrosine phosphatase G (PTPRG) gene. Hum Mol Genet 2:91, 1993. 26. Richards FM, Phipps ME, Latif F, et al: Mapping the Von Hippel– Lindau disease tumour suppressor gene: identification of germline deletions by pulsed field gel electrophoresis. Hum Mol Genet 2:879– 882, 1993. 27. Wizigmann-Voos S, Plate KH: Pathology, genetics and cell biology of hemangioblastomas. Histol Histopathol 11:1049–1061, 1996. 28. Chan CC, Chew EY, Shen D, et al: Expression of stem cells markers in ocular hemangioblastoma associated with von Hippel–Lindau (VHL) disease. Mol Vis 11:697–704, 2005. 29. Chan CC, Collins AB, Chew EY: Molecular pathology of eyes with von Hippel–Lindau (VHL) disease: a review. Retina 27:1–7, 2007.

30. Chan CC, Vortmeyer AO, Chew EY, et al: VHL gene deletion and enhanced VEGF gene expression detected in the stromal cells of retinal angioma. Arch Ophthalmol 117:625–630, 1999. 31. Lee YS, Vortmeyer AO, Lubensky IA, et al: Coexpression of erythropoietin and erythropoietin receptor in von Hippel–Lindau disease– associated renal cysts and renal cell carcinoma. Clin Cancer Res 11:1059–1064, 2005. 32. Vortmeyer AO, Yuan Q, Lee YS, et al: Developmental effects of von Hippel–Lindau gene deficiency. Ann Neurol 55:721–728, 2004. 33. Catapano D, Muscarella KA, Guarnieri V, et al: Hemangioblastomas of central nervous system: molecular genetic analysis and clinical management. Neurosurgery 56:1215–1221; discussion 1221, 2005. 34. Lach B, Gregor A, Rippstein P, et al: Angiogenic histogenesis of stromal cells in hemangioblastoma: ultrastructural and immunohistochemical study. Ultrastruct Pathol 23:299–310, 1999. 35. Ishizawa K, Komori T, Hirose T: Stromal cells in hemangioblastoma: neuroectodermal differentiation and morphological similarities to ependymoma. Pathol Int 55:377–385, 2005. 36. Kleihues P, Cavenee WK: Centre international de recherche sur le centre: Pathology and genetics of tumours of the nervous system, Lyon, 2000, IARC Press. 37. Cruz-Sánchez FF, Rossi ML, Rodríguez-Prados S, et al: Haemangioblastoma: histological and immunohistological study of an enigmatic cerebellar tumour. Histol Histopathol 5:407–413, 1990. 38. Omulecka A, Lach B, Alwasiak J, et al: Immunohistochemical and ultrastructural studies of stromal cells in hemangioblastoma. Folia Neuropathol 33:41–50, 1995. 39. Lampugnani MG, Resnati M, Raiteri M, et al: A novel endothelialspecific membrane protein is a marker of cell–cell contacts. J Cell Biol 118:1511–1522, 1992. 40. Wagner DD, Olmsted JB, Marder VJ: Immunolocalization of von Willebrand protein in Weibel–Palade bodies of human endothelial cells. J Cell Biol 95:355–360, 1982. 41. Weibel ER, Palade GE: New cytoplasmic components in arterial endothelia. J Cell Biol 23:101–112, 1964. 42. Osborn AG: Diagnostic neuroradiology, St. Louis, 1994, Mosby. 43. Wanebo JE, Lonser RR, Glenn GM, et al: The natural history of hemangioblastomas of the central nervous system in patients with von Hippel–Lindau disease. J Neurosurg 98:82–94, 2003. 44. Brisman JL, Borges LF, Ogilvy CS: Extramedullary hemangioblastoma of the conus medullaris. Acta Neurochir (Wien) 142:1059–1062, 2000. 45. Tibbs RE, Jr, Harkey HL, Raila FA: Hemangioblastoma of the filum terminale: case report. Neurosurgery 44:221–223, 1999. 46. Escott EJ, Kleinschmidt-DeMasters BK, Brega K, et al: Proximal nerve root spinal hemangioblastomas: presentation of three cases, MR appearance, and literature review. Surg Neurol 61:262–273; discussion 273, 2004. 47. Murota T, Symon L: Surgical management of hemangioblastoma of the spinal cord: a report of 18 cases. Neurosurgery 25:699–707; discussion 708, 1989. 48. Minami M, Hanakita J, Suwa H, et al: Cervical hemangioblastoma with a past history of subarachnoid hemorrhage. Surg Neurol 49:278–281, 1998. 49. Fuller GN, Goodman JC: Practical review of neuropathology, Philadelphia, 2001, Lippincott Williams & Wilkins. 50. Graham DI, Bell JE, Ironside JW: Color atlas and text of neuropathology, London–Baltimore, 1995, Mosby–Wolfe. 51. Imagama S, Ito Z, Wakao N, et al: Differentiation of localization of spinal hemangioblastomas based on imaging and pathological findings. Eur Spine J 20:1377–1384, 2011. 52. Ueba T, Abe H, Matsumoto J, et al: Efficacy of indocyanine green videography and real-time evaluation by FLOW 800 in the resection of a spinal cord hemangioblastoma in a child: case report. J Neurosurg Pediatr 9:428–431, 2012. 53. Clark AJ, Lu DC, Richardson RM, et al: Surgical technique of temporary arterial occlusion in the operative management of spinal hemangioblastomas. World Neurosurg 74:200–205, 2010. 54. Lonser RR, Weil RJ, Wanebo JE, et al: Surgical management of spinal cord hemangioblastomas in patients with von Hippel–Lindau disease. J Neurosurg 98:106–116, 2003. 55. Mehta GU, Asthagiri AR, Bakhtian KD, et al: Functional outcome after resection of spinal cord hemangioblastomas associated with von Hippel–Lindau disease. J Neurosurg Spine 12, 233–242, 2010.

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SECTION G  •  Spinal Tumors and Vascular Lesions 56. Riant F, Tournier-Lasserve E, Bergametti F, et al: Recent insights into cerebral cavernous malformations: the molecular genetics of CCM. FEBS J 277:1070–1075, 2010. 57. Washington CW, McCoy KE, Zipfel GJ: Update on the natural history of cavernous malformations and factors predicting aggressive clinical presentation. Neurosurg Focus 29:E7, 2010. 58. Mosca L, Pileggi S, Avemaria F, et al: De novo MGC4607 gene heterozygous missense variants in a child with multiple cerebral cavernous malformations. J Mol Neurosci 47:475–480, 2012. 59. Gianfrancesco F, Esposito T, Penco S, et al: ZPLD1 gene is disrupted in a patient with balanced translocation that exhibits cerebral cavernous malformations. Neuroscience 155:345–349, 2008. 60. Consiglieri GD, Killory BD, Germain RS, et al: Utility of the CO(2) laser in the microsurgical resection of cavernous malformations. World Neurosurg 2011 [Epub ahead of print]. 61. Mitha AP, Turner JD, Abla AA, et al: Outcomes following resection of intramedullary spinal cord cavernous malformations: a 25-year experience. J Neurosurg Spine 14:605–611, 2011. 62. Hashimoto T, Emala CW, Joshi S, et al: Abnormal pattern of Tie-2 and vascular endothelial growth factor receptor expression in human cerebral arteriovenous malformations. Neurosurgery 47:910–918; discussion 918–919, 2000. 63. Su H, Kim H, Pawlikowska L, et al: Reduced expression of integrin alphavbeta8 is associated with brain arteriovenous malformation pathogenesis. Am J Pathol 176:1018–1027, 2010. 64. Benigni A, Zoja C, Corna D, et al: A specific endothelin subtype A receptor antagonist protects against injury in renal disease progression. Kidney Int 44:440–444, 1993. 65. Douglas SA, Louden C, Vickery-Clark LM, et al: A role for endogenous endothelin-1 in neointimal formation after rat carotid artery balloon angioplasty. Protective effects of the novel nonpeptide endothelin receptor antagonist SB 209670. Circ Res 75:190–197, 1994. 66. Giaid A, Yanagisawa M, Langleben D, et al: Expression of endothelin-1 in the lungs of patients with pulmonary hypertension. N Engl J Med 328:1732–1739, 1993.

67. Lerman A, Edwards BS, Hallett JW, et al: Circulating and tissue endothelin immunoreactivity in advanced atherosclerosis. N Engl J Med 325:997–1001, 1991. 68. Rhoten RL, Comair YG, Shedid D, et al: Specific repression of the preproendothelin-1 gene in intracranial arteriovenous malformations. J Neurosurg 86:101–108, 1997. 69. Mahmoud M, Allinson KR, Zhai Z, et al: Pathogenesis of arteriovenous malformations in the absence of endoglin. Circ Res 106:1425– 1433, 2010. 70. Gao P, Chen Y, Lawton MT, et al: Evidence of endothelial progenitor cells in the human brain and spinal cord arteriovenous malformations. Neurosurgery 67:1029–1035, 2010. 71. Rosenblum B, Oldfield EH, Doppman JL, et al: Spinal arteriovenous malformations: a comparison of dural arteriovenous fistulas and intradural AVMs in 81 patients. J Neurosurg 67:795–802, 1987. 72. Spetzler RF, Detwiler PW, Riina HA, et al: Modified classification of spinal cord vascular lesions. J Neurosurg 96:145–156, 2002. 73. Riina HA, Spetzler RF: Classification of vascular lesions affecting the spinal cord. Operative Tech Neurosurg 6:106–115, 2003. 74. Martin NA, Khanna RK, Batzdorf U: Posterolateral cervical or thoracic approach with spinal cord rotation for vascular malformations or tumors of the ventrolateral spinal cord. J Neurosurg 83:254–261, 1995. 75. Barrow DL, Colohan AR, Dawson R: Intradural perimedullary arteriovenous fistulas (type IV spinal cord arteriovenous malformations). J Neurosurg 81:221–229, 1994. 76. Spetzler RF, Zabramski JM, Flom RA: Management of juvenile spinal AVMs by embolization and operative excision. Case report. J Neurosurg 70:628–632, 1989. 77. Savasta S, Merli P, Ruggieri M, Bianchi L, et al: Ehlers-Danlos syndrome and neurological features: a review. Childs Nerv Syst 27:365– 371, 2011. 78. Pepin M, Schwarze U, Superti-Furga A, et al: Clinical and genetic features of Ehlers-Danlos syndrome type IV, the vascular type. N Engl J Med 342:673–680, 2000.

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Ankylosing Spondylitis: Posterior Approaches (Osteotomy) to the Cervical and Lumbar Spine in the Management of a Fixed Sagittal Plane Deformity ALAN HILIBRAND, MAURICE GOINS, and CHRISTOPHER KEPLER

Overview Ankylosing spondylitis (AS) is a chronic inflammatory disease of unknown etiology that affects approximately 197 people per 100,000 per year in the United States with a male-to-female predominance of approximately 3 : 1. An idiopathic seronegative spondyloarthropathy, AS is strongly associated with the class I antigen HLA-B27. The sacroiliac joints and the axial skeleton are most commonly affected by AS, but clinically significant peripheral joint involvement may also occur. The chronic inflammatory nature of the condition causes stiffness and loss of lordosis or increased kyphosis of the spine through destruction and autofusion of the vertebral motion segments. This can ultimately lead to a dramatic imbalance of sagittal alignment, causing severe deformities throughout the cervical, thoracic, and lumbosacral spine (Fig. 68-1).

Osteotomy for Correction of Kyphotic Deformity of Ankylosing Spondylitis INDICATIONS Involvement of the cervical spine in patients with AS is often overlooked, because lumbar spine and appendicular sequelae may be more obvious. Cervical kyphosis may slowly progress in an insidious fashion, resulting in the development of a chin-on-chest deformity. When cervical kyphosis progresses to the point of causing difficulty with function and hygiene, a corrective cervical osteotomy is indicated. Functional difficulty may present as dysphagia or inability to lift the head to allow forward gaze. Inability to achieve forward gaze inhibits activities of daily living, such as forward ambulation and ascending and descending stairs. Also, difficulty swallowing solids may cause malnourishment. In addition to the cervical spine, the thoracic 662

and lumbar spine may contribute to the kyphotic deformity. Kyphosis of the ankylosed thoracic spine usually does not progress sufficiently to require surgical intervention. When it occurs in AS, increased thoracic kyphosis often goes unnoticed owing to the naturally occurring thoracic kyphosis. The combination of this natural kyphosis and the relatively small thoracic spinal canal places the thoracic spinal cord at higher risk of traction and ischemic injury with osteotomy. In the lumbar spine, AS presents as low back pain for more than 3 months duration, stiffness, diminished range of motion, and hypolordosis. Osteotomy is the procedure of choice to address severe, fixed kyphotic deformities in the lumbar spine that result from AS. The midportion of the lumbar spine is the safest area for correction, below the termination of the spinal cord (i.e., the conus medullaris at the L1–L2 level). Correction of kyphotic deformity of the lumbar spine via osteotomy may be safer than in the cervical spine because of the potential to perform the correction below the level of the spinal cord. In cases of coexisting deformities of the cervical and lumbar spine, osteotomy of the lumbar spine is generally preferred for this reason, and also because it can simultaneously correct the forward gaze and lumbar kyphosis. Patients with preexisting cervical kyphosis who come to medical attention with acute cervical spine fractures that require surgical stabilization may occasionally be treated with osteotomy to simultaneously stabilize the acute fracture and correct the functionally limiting deformity.

CONTRAINDICATIONS Extraarticular manifestations of AS include aortic incompetence, cardiac conduction defects, fibrotic lung disease, and renal amyloidosis. These extraskeletal expressions of AS can present a significant risk for serious perioperative complications, including cardiopulmonary compromise and renal insufficiency. In some instances, the severity of these concomitant medical conditions may result in an

68  •  AS: Posterior Approaches (Osteotomy) to the Cervical and Lumbar Spine in the Management of a Fixed Sagittal Plane Deformity

Flexion deformity cervical spine: osteotomy C8–T1

Thoracolumbar kyphosis: osteotomy L3

Fixed flexion deformity of hips: total hip replacement

Figure 68-1  A patient with ankylosing spondylitis.

unacceptably high level of morbidity for the patient to tolerate surgery, and careful preoperative evaluation is warranted. Appendicular skeletal manifestations of AS, such as hipflexion contractures and osteoarthritis, may exaggerate a kyphotic spinal deformity by tipping the patient forward, thereby worsening effective sagittal balance. Correction of hip pathology in AS is safe and efficacious and should be addressed before spinal management.

POSTERIOR CERVICAL OSTEOTOMY FOR CORRECTION OF KYPHOTIC DEFORMITY OF ANKYLOSING SPONDYLITIS Advantages ■ High degree of correction ■ Single-level surgery for correction ■ Availability of segmental internal fixation for precise control and maintenance of osteotomy correction Disadvantages ■ Risk of neurologic injury (infrequent) ■ Risk of vascular injury ■ Technically demanding ■ Inability to correct concomitant lumbar deformities Preoperative Evaluation Preoperative evaluation begins with a thorough history and physical evaluation. The medical history should focus on premorbid conditions that may compromise surgical

Figure 68-2  Anatomic sites of deformity in ankylosing spondylitis and their surgical correction.

treatment and recovery. In addition to evaluating the entire spinal column, the musculoskeletal examination should also evaluate the hip joints, which are often affected by osteoarthritis in AS. As a result, loss of the normal chinbrow vertical angle either occurs as a result of flexion deformity throughout the spine or through fixed hip-flexion contractures (Fig. 68-2). Surgical correction should be planned for the area of the major deformity after conducting a thorough medical evaluation. Measurement of the chin-brow and sagittal vertical angles is necessary for preoperative planning of the degree of correction needed from the osteotomy (Fig. 68-3). In addition, the inion-wall angle can also be helpful in preoperative planning; it is measured by standing the patient against the wall and measuring the distance between the wall and the inion at the base of the skull. This provides another useful tool for monitoring the progression and subsequent correction of cervical kyphosis. Once the chin-brow angle has been determined, the angle necessary to bring the face to within 10 degrees of horizontal gaze can be calculated. The goal is to provide a reasonably safe correction to improve the patient’s ability to perform the activities of daily living that rely on forward gaze, such as grooming, eating, reading, and ambulation. Correction beyond neutral (overcorrection) is not recommended, because a fixed gaze above the horizon creates significant difficulty for the patient during straightforward ambulation and stair descent.

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Figure 68-3  Measurement of sagittal-vertical and chin-brow angles in preparation for ankylosing spondylitis deformity correction surgery.

To view the entire spine and assist with determining the level for corrective osteotomy, lateral radiographs of the entire cervical, thoracic, and lumbar spine on a 36-inch cassette are necessary. A sketch of the spinal osteotomy can be drawn on tracing paper, which can also be used to outline the surgical algorithm. Alternatively, the osteotomy and operative plan can be written on radiographs with a wax pen (Fig. 68-4). One day before surgery, the patient should be admitted to the hospital. This allows for the application of a halo cast with a contoured plaster jacket. After the halo cast is applied, the patient is placed in a seated position to evaluate for potential areas of undue pressure that will be placed on the patient intraoperatively. If necessary, areas of the cast that could contact pressure points are trimmed, and these are well padded. The restrictive nature of a kyphotic posture causes many patients with AS to have a protuberant abdomen, which affects their breathing (Fig. 68-5); therefore the abdominal portion of the contoured body cast must avoid compression that might inhibit respiratory function. The cast is also modified posteriorly to allow access to the cervical and upper thoracic spine. Preadmission also allows for the establishment of central venous access, which is necessary for intraoperative hemodynamic monitoring by the anesthesiologist. Completing these procedures before surgery maximizes patient safety and surgical efficiency when the patient arrives in the operating room.

Intraoperative Technique 1. After awake fiberoptic intubation and induction of anesthesia, the patient should be placed in a beach chair position.

2. It is imperative to have the appropriate neurophysiologic monitoring available throughout the entire procedure; if available, this should include transcranialevoked motor potentials, somatosensory-evoked potentials, and C8 dermatomal-evoked potentials. 3. If neurophysiologic monitoring is unavailable, the procedure should be performed under local anesthesia. 4. The patient is positioned on the operating table in the seated position, and the halo cast is secured to the table. Cervical traction is then applied to the halo to stabilize the head and cervical spine (Fig. 68-6). The posterior support bars of the halo may be removed if they hinder the approach to the cervical spine. 5. Following the induction of general anesthesia, transesophageal echocardiographic monitoring should be established to assist with detection of a possible air embolus, which may occur secondary to the patient’s upright position. Air can be removed via the central venous pressure line if necessary. 6. The posterior cervical spine is approached through a standard midline incision, and Gelpi retractors are used to provide exposure. Meticulous hemostasis is essential. Subperiosteal dissection should widely expose the laminae, facet joints, and transverse processes. 7. The C7–T1 interval is identified with intraoperative radiographs. Performing the osteotomy at the cervicothoracic junction minimizes the risk of injury to the vertebral artery, which enters the transverse foramina at the C6 level in the majority of patients (Fig. 68-7). 8. The incision should be long enough to allow placement of fixation in four spinal segments proximally and distally from the osteotomy level.

68  •  AS: Posterior Approaches (Osteotomy) to the Cervical and Lumbar Spine in the Management of a Fixed Sagittal Plane Deformity

B A

C

D

Figure 68-4  A, Anteroposterior (AP) schematic of preoperative planning for posterior cervical osteotomy. B, AP radiograph shows preoperative planning for posterior cervical osteotomy. C, Lateral schematic of preoperative planning for posterior cervical osteotomy. D, Lateral radiograph shows preoperative planning for posterior cervical osteotomy.

9. To minimize the amount of time the osteotomy will be vulnerable to displacement, internal fixation points should be established before resection of bony elements and osteotomy. Segmental instrumentation is usually placed to before lateral mass screw fixation at C3, C4, and C5 and pedicle screw fixation distal to the osteotomy site, typically at T2 to T4. 10. A wide laminectomy of C7 and a partial laminectomy of C6 and T1 should be performed. This will prevent cord compression that can occur after closing the oste-

otomy because of impingement by the laminae of adjacent levels (Fig. 68-8). 11. After performing the laminectomy, remove the C7 pedicles using a rongeur and motorized burr. This should be done very carefully to avoid iatrogenic nerve injury to C8 or C7. 12. Next, any remaining soft tissue or bone that contacts the C7 and C8 nerve roots should be resected (Fig. 68-9). 13. Osteoclasis is now performed with extreme caution by gradually extending the patient’s cervical spine from its

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Figure 68-6  Patient with ankylosing spondylitis in upright position and cervical traction in preparation for posterior cervical osteotomy. Figure 68-5  Patient with ankylosing spondylitis with protuberant abdomen secondary to pulmonary restriction.

Figure 68-7  Schematics show the location of the prominent vasculature in the cervical spine relative to the posterior cervical osteotomy site.

Figure 68-8  Posterior cervical osteotomy with wide laminectomy of C7 and partial laminectomy of C6 and T1.

68  •  AS: Posterior Approaches (Osteotomy) to the Cervical and Lumbar Spine in the Management of a Fixed Sagittal Plane Deformity

Figure 68-9  Lateral cervical schematic following removal of tethering bone and soft tissue near C8 nerve root following osteotomy and osteoclasis.

Figure 68-10  Closed posterior osteotomy with local bone graft supplementation.

kyphotic position. It is imperative that neurophysiologic monitoring be performed before, during, and after osteoclasis. Special attention must be paid to avoiding anterior or posterior translation of C7 onto T1, which may lead to spinal cord compression. 14. The head should be positioned such that the gaze will be directed approximately 10 degrees downward from standing horizontal gaze after the correction is secured. This will minimize the risk of overcorrection. Having the patient seated in an upright position allows easy visual assessment of the patient’s horizontal gaze. 15. As the desired amount of correction is approached, the spinous processes of C6 and T1 should approximate each other, yielding adequate bony apposition of the remaining transverse processes of C7 and T1 to promote fusion. At this time, readjust and secure the halo in position to stabilize the cervical spine. 16. Internal fixation points should now be connected via longitudinal rods. 17. After closing the osteotomy and securing it in position with instrumentation, autologous bone graft from the resected posterior elements may be used to supplement the arthrodesis (Fig. 68-10). 18. Closure of the wounds is often difficult. We recommend fascial closure and meticulous skin closure using interrupted vertical mattress sutures. Retention sutures may also be needed to assist with approximation of wound edges. 19. The posterior aspect of the halo–vest may be replaced to provide further mechanical support.

potentially lead to airway compromise. Dramatic fluid shifts also occur postoperatively as patients go from an upright operative position to a supine postoperative position. In addition, many patients have underlying pulmonary compromise as a result of restrictive lung disease, and large fluid shifts in these patients create an environment in which congestive heart failure can develop. As a result, we recommend that patients with restrictive lung disease remain intubated in an intensive care unit until airway and cardiopulmonary function have stabilized. Because the fulcrum of rotation for the osteotomy is along the posterior vertebral cortex, the anterior column of the spine is lengthened. Structures anterior to the spine, therefore, are very vulnerable to stretch and traction injuries, including the esophagus. This often leads to postoperative dysphagia that may necessitate a period of parenteral nutrition. For prolonged dysphagia, we recommend placement of a feeding tube. In addition, we also recommend that the surgical team keep a cast saw at the patient’s bedside in the event that rapid removal of the halo-vest is required. Postoperative immobilization in a halo-vest is mandatory for 6 to 12 weeks. After this, the patient is placed in a standard Philadelphia collar for another 6 to 8 weeks. Radiographs are taken at 1-, 3-, and 6-month intervals to evaluate fusion and graft incorporation.

Postoperative Management The sudden change in cervical positioning may cause formation of a retropharyngeal hematoma, which can

Complications Significant neurovascular complications may occur following cervical osteotomies, including spinal cord compression or traction that causes paraparesis or paraplegia, vascular injury to the spinal cord that causes anterior spinal cord ischemic injury, and nerve-root impingement that results in radiculopathy. Performing the operative procedure in the seated position also brings the additional risk of air entering the low-pressure venous system and causing an air embolus.

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If this occurs, the wound should be immediately filled with irrigant and moist sponges to prevent air from entering the low-pressure venous system. Additional complications such as infection, nonunion, malunion, dysphagia, halopin loosening, and loss of fixation with recurrence of kyphotic deformity may potentially occur in the postoperative period.

PEDICLE SUBTRACTION OSTEOTOMY FOR KYPHOTIC DEFORMITY OF THE THORACOLUMBAR SPINE Advantages ■ Achieves posterior correction via a single osteotomy ■ Avoids anterior approach ■ Avoids anterior gap that may occur after Smith-Peterson technique ■ Eliminates need for multiple osteotomies ■ Reduces distraction/stretch of abdominal structures ■ May improve forward gaze and avoid or delay the need for correction of cervical kyphosis in patients with deformities of both regions Disadvantages ■ Potential for excessive blood loss ■ Potential for neurologic injury Preoperative Evaluation Localize any levels of deformity: cervical, thoracic, or lumbar. Full-length radiographs to review spinal alignment Specialized views to assess for correction  Traction  Hyperextension  Radiographic assessment  Sagittal vertical axis  Regional assessment of lordosis and kyphosis  Chin–brow angle  Trace deformity and plan corrective osteotomy site  Plan hardware insertion  

■ ■ ■ ■ ■ ■ ■ ■

Bechman-Adson retractor Adson cerebellar retractor Gelpi retractors Osteotomes Scoville nerve root retractor Pedicle screw fixation system Red blood cell recovery system Neurophysiologic monitoring

Patient Positioning.  Once intubation, general anesthesia induction, and placement of appropriate hemodynamic and neurophysiologic monitors are complete, the patient is carefully turned onto the operating table into the prone position. Proper surgical positioning for a patient with a severe kyphotic deformity is challenging but not impossible. We recommend using a radiolucent table that flexes to accommodate the patient’s posture. Extension of the table will assist with reduction after completion of the osteotomy (Fig. 68-11). It is critical to meticulously pad all bony prominences and ensure that no undue pressure is exerted on the ocular region. In addition to evaluating these areas at regular intervals, they must also be evaluated after a change in table position from a flexed to an extended posture. Alternatively, to accommodate the kyphotic posture, the patient’s trunk could be placed on a four-poster frame, omitting the thigh supports (Fig. 68-12). This will assist with positioning by allowing the hips to flex and the knees to touch the table at the level of the kidney rest. Elevation of the kidney rest later in the procedure will assist with reduction of the patient’s deformity. Pillows should also be used to maintain knee flexion; this will decrease the amount of tension placed on the sciatic nerve when the reduction maneuver is eventually performed.

Location of Osteotomy Osteotomies performed in the lumbar spine in patients with AS often provide sufficient correction such that additional osteotomies in the cervical or thoracic spine are usually unnecessary. Ideally, lumbar osteotomy is performed at or below L2. This places the osteotomy below the level of the conus medullaris and the rib cage and above the level of the aortic bifurcation, thus minimizing surgical complications. Operative Technique Equipment  ■ Fluoroscopy- and radiography-compatible table ■ Fluoroscopy ■ Straight and angled curettes ■ Kerrison punches ■ Rongeurs ■ Stille-Horsley bone-cutting forceps ■ Impactor

Figure 68-11  Patient positioning for lumbar pedicle subtraction osteotomy shows table extension to close the osteotomy site.

68  •  AS: Posterior Approaches (Osteotomy) to the Cervical and Lumbar Spine in the Management of a Fixed Sagittal Plane Deformity

Figure 68-12  Alternative patient positioning for lumbar pedicle subtraction osteotomy to accommodate kyphotic posture with hip flexion and kidney rest supports.

Another option is to perform the procedure on a Jackson lordosing table. The head may be suspended with cranial tongs to prevent undue pressure on the face. On this table, the patient’s pelvis and iliac crests may be suspended above the bed but will be reduced down toward the hip bolsters once the correction is performed. The lordotic nature of the frame will provide the reduction force to reduce the osteotomy. Location of Incision.  The spine should be exposed through a midline posterior approach, centering over the level of the osteotomy; this is usually done at the center of the lumbar lordosis (L3–L4), although recent study has shown that the level of osteotomy has little effect on the degree of correction achieved. The skin incision is marked in a longitudinal fashion to allow exposure from T12 to the sacrum. Intraoperative Technique.  After the skin incision is marked, the surgical area is cleaned and draped in the usual sterile fashion. The area is widely prepped to include the iliac crest, in case autograft bone harvesting is necessary because of insufficient local bone graft. 1. Incision is made, and soft-tissue dissection is performed. 2. The lumbar spine is exposed through a standard posterior midline approach. 3. The incision is taken down through the subcutaneous tissues to the fascia, which is incised over the spinous processes. 4. The paraspinal muscles are dissected off the spinous processes and laminae subperiosteally with a combination of Bovie cautery and a Cobb periosteal elevator. 5. Sponges are packed into the wound to assist with dissection of soft tissue and also to provide hemostasis. 6. Elevation of the paraspinal muscles and soft tissue should continue laterally over the facets and out to the tips of the transverse processes. 7. If needed, large Gelpi retractors can replace cerebellar retractors to provide a wider, deeper exposure.

8. Intraoperative radiographs or fluoroscopy is used to ensure that the osteotomy will be performed at the correct level. 9. Pedicle screws should be placed before the bony resection and osteotomy. If the procedure is performed on a Jackson table, a provisional rod should be placed as lateral as possible to connect fixation points above and below the osteotomy at this time. 10. For an L3 osteotomy, a complete resection of the posterior elements of L3 along with the caudal half of the lamina of L2 and the cephalad half of the lamina of L4 will be necessary. It is imperative that portions of L2 and L4 be resected to prevent a pincer effect, in which the correction maneuver causes the laminae of L2 and L4 to compress the thecal sac. 11. A Horsley bone rongeur is used to remove the spinous processes from L2 through L4, and a Leksell rongeur is used to thin the laminae. 12. A large curette may be used to resect the ligamentum flavum from the laminae, allowing entrance into the spinal canal. 13. Kerrison punches are used to perform a wide laminectomy of L3 out to the pedicles. Caution should be used when resecting the laminae in fixed kyphotic deformities, because the dura may be adherent to the lamina. A Penfield elevator is useful to free the dura from the lamina. 14. Using a combination of Leksell rongeurs and Kerrison punches, resection of the posterior elements proceeds to include the pars interarticularis, superior and inferior facets, and the transverse processes of L3. At this point the pedicles are the only remaining posterior elements of the L3 vertebra. 15. The inferior facets of L2 and the superior facets of L4 must also be resected. 16. Curettes are used to remove the cancellous bone from within the pedicles and to begin decancellation of the L3 vertebral body. 17. The lateral aspect of the pedicle can be removed with Kerrison punches and rongeurs so that curettes can be placed into the posterior portion of the vertebral body to remove cancellous bone. 18. The posterior vertebral cortex is left in place, while the cancellous bone is removed. Leaving the posterior vertebral wall intact provides a bony barrier that protects the thecal sac, which lies immediately adjacent to the posterior vertebral wall. 19. Once the cancellous bone has been removed from the posterior two thirds of the vertebral body, the thecal sac is retracted, along with the nerve root, toward the contralateral side. This will allow access to the posterior wall of the vertebra, which is now cut using a quarterinch osteotome. 20. Bone tamps are used to implode the posterior wall into the defect within the vertebral body created by previously removing cancellous bone (Fig. 68-13). 21. The displaced posterior cortical wall is removed with pituitary rongeurs and Kerrison punches. 22. The bony resection creates a large surface area of exposed cancellous bone that may bleed tremendously. Hemostatic agents such as Gelfoam and FloSeal should be readily available to place onto bleeding surfaces.

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SECTION H  •  Inflammatory Disease

which typically occurs after approximately 3 months. Radiographs are taken at monthly intervals to evaluate fusion healing.

Figure 68-13  “Eggshell” procedure for removal of lumbar vertebral body in closing wedge osteotomy.

23. Once the bleeding is controlled, excess hemostatic agent should be removed because it may be extruded into the canal during osteotomy reduction, which can cause neurologic compression. 24. The previously flexed table is now gradually brought into extension, thereby closing the osteotomy. If a Jackson table is used, the provisional rod is loosened, and the connecting fixation points are allowed to approach one another to close down the posterior bony resection. 25. Rods are contoured and placed into the previously placed pedicle screws to secure the reduction of the osteotomy. 26. The osteotomy edges are brought into close contact by compressing across the pedicle screws. Careful neurologic monitoring should be performed while closing the osteotomy site. If there are any changes in neurologic monitoring, the site should be reopened. 27. The canal should be inspected carefully for sites of impingement by extruded bony fragments or hemostatic agents. After inspection, the osteotomy site should be closed and secured into position using the previously placed fixation construct. 28. The bony surfaces are decorticated, and local bone graft is placed. The wound is then closed in layers over a drain.

Postoperative Care Postoperatively, the patient is placed in a custom thoracolumbosacral orthosis until the osteotomy site is healed,

Complications As noted earlier, the complications of thoracolumbar pedicle subtraction osteotomy are principally neurologic and vascular. Translation across the osteotomy site may cause severe compression of the cauda equina, resulting in paraparesis and bowel and bladder dysfunction. Another possible cause of postoperative paresis may be due to decreased blood flow to the thoracic spinal cord itself as a result of hemodynamic instability, an event that can cause an anterior spinal cord injury because of ischemia. Blood loss during this procedure can be quite high, typically over 2 liters, and anesthesia personnel must be prepared to rapidly infuse blood products and crystalloid to maintain spinal cord perfusion pressures. In addition, patients may also require concomitant replacement of clotting factors because of heavy bleeding and dilution effects. Although the risks of abdominal stretch and the potential for superior mesenteric artery syndrome are lower with this procedure than with the traditional Smith-Peterson osteotomy, the patient’s abdomen must be carefully evaluated for signs of an extended postoperative ileus. Large fluid shifts may occur in the first 3 days after surgery such that the patient’s hemodynamic status must be carefully monitored. Other postoperative complications may include nonunion, loss of correction, and wound infection.

Conclusion Patients who have kyphotic deformities as a result of AS are often extremely disabled. They have difficulty with activities of daily living because of an inability to sustain a forward gaze to view the horizon. This poses a unique challenge for the patient and also for the treating spine surgeon. Fixed kyphosis of the cervical spine is often further complicated by profound osteopenia. Serious complications or unsatisfactory results have often caused patients and doctors alike to be hesitant in choosing surgery for treatment of AS. Although the techniques for correction of fixed flexion deformity remain demanding, advancements in surgical techniques, instrumentation, neurophysiologic monitoring, and medical management have minimized the risk of intraoperative complications and have made surgical treatment of kyphotic deformities of the ankylotic spine a safer option. In all such patients, the goals of surgical management remain the correction of forward gaze to the horizon and improvement of gait and ambulation by restoring the C7 plumb line over the sacrum.

SECTION

I Spinal Infection

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Bacterial, Fungal, and Tuberculosis Diskitis and Osteomyelitis of the Cervical, Thoracic, and Lumbar Spine MICHAEL J. VIVES and AMIT SOOD

Overview The management of spinal infections involves several general considerations. The ultimate goals in management are eradication of the infection, preservation of neurologic function, and prevention of sequelae such as progressive deformity and chronic pain. A systematic approach is used in the diagnosis and treatment of spinal infections; early diagnosis is of the utmost importance, before the onset of neurologic sequelae or spinal instability. These infections are evaluated according to the location, pathogen (bacterial vs. fungal), route of infection (direct inoculation, contiguous spread from an adjacent infection, or hematogenous seeding), age of the patient, and immune status of the host. In the setting of diskitis or spinal osteomyelitis (Fig. 69-1), these goals can often be achieved without operative intervention. A presumptive diagnosis is established by the combination of suggestive laboratory findings, which include elevated erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP), along with plain radiographs and advanced imaging studies such as computed tomography (CT) and magnetic resonance imaging (MRI). A definitive tissue diagnosis of the offending pathogen can often be made using percutaneous CT-guided biopsy. After determination of the organism’s sensitivity profile, a 6-week course of the appropriate intravenous (IV) antibiotics is usually sufficient. Bracing is often prescribed as adjuvant treatment to optimize the environment for eradication of the infection as well as for structural stability. Often patients are immunocompromised and/or malnourished; thus a multidisciplinary approach toward treatment with infectious disease and nutritional services is important.

Indications and Contraindications for Surgical Management of Spinal Infection INDICATIONS Neurologic deficit from spinal cord injury or progressive root-level deficit

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672

Significant deformity, instability, or bone destruction/ pathologic fracture ■ Persistent sepsis or abscess formation ■ Inability to identify the offending pathogen by closed methods ■ Inability to eradicate the infection by medical management alone ■ Intractable pain localized to the involved area of the spine ■

CONTRAINDICATIONS Medical comorbidities that make operative intervention prohibitive ■ Uncorrected coagulopathies ■ Medically stable, immunocompetent patients with early involvement, none of the above indications, and diagnosis made by biopsy ■

Operative Technique GENERAL CONSIDERATIONS When surgical treatment is deemed necessary, several concepts appear to be generally accepted: Thorough débridement, decompression (if necessary), and establishment or maintenance of spinal stability are critical steps in treatment. ■ In most cases, if the microbiologic diagnosis has not been established, preoperative antibiotics should be held until adequate tissue is obtained. ■ The location of the lesion is usually anterior; therefore anterior procedures are usually preferred with the exception of selective lower lumbar lesions, in which the neural elements can be safely manipulated to permit anterior débridement and reconstruction. ■ Systemic illness and malnutrition are often present and must be addressed concurrently. ■

Conversely, several issues in the surgical management of spinal infections remain controversial. Choice of structural graft. Owing to the attendant morbidity of harvesting large structural autografts (tricortical iliac crest, fibula, and vascularized rib), alternative methods of reconstructing the weight-bearing anterior

■

69  •  Bacterial, Fungal, and Tuberculosis Diskitis and Osteomyelitis of the Cervical, Thoracic, and Lumbar Spine

similar to those used for the anterior treatment of degenerative and traumatic conditions. Because these methods have been described in separate, detailed sections, this chapter will review each technique more generally, and it will highlight important considerations for applying these methods to the management of spinal infections.

CERVICAL DISKITIS AND OSTEOMYELITIS

Figure 69-1  In the setting of diskitis or spinal osteomyelitis, treatment goals can often be achieved without operative intervention.

column are increasingly used. Despite concerns about the risk of sequestration and delayed healing, recent studies have demonstrated good outcomes, and without the aforementioned complications, using both allograft and titanium cages for spinal reconstruction after débridement of active infection. ■ Use of recombinant human bone morphogenetic protein (rhBMP). Over the past several years, use of rhBMP has increased in a variety of orthopedic procedures to enhance bone formation. Specifically, it is being used with increased frequency for spinal fusion procedures given its potent osteoinductive properties. Studies thus far have not demonstrated an increase in morbidity or mortality associated with the use of rhBMP in the setting of local infection1-5; however, such application is off label. ■ The use of instrumentation in the infected spine. Concerns have led to the common and effective practice of performing the anterior reconstruction with a strut graft and instrumenting the spine through a separate, posterior approach. Recent studies, however, have demonstrated successful management of pyogenic and granulomatous infections using anterior instrumentation. ■ Same-day anterior–posterior versus staged procedures. Some have advocated staging the posterior placement of hardware to prevent “seeding” of the hardware by bacteremia produced by the anterior débridement. Although this advice is well reasoned, it is unclear whether it is necessary. The authors feel that the decision should be made on a case-by-case basis, predicated primarily on the patient’s overall physiologic condition on completion of the anterior procedure. The techniques for treatment of diskitis and osteomyelitis of the cervical, thoracic, and lumbar spine are generally

Positioning ■ The patient is positioned supine with a bump under the buttocks if autograft harvesting is planned. ■ A roll placed between the shoulder blades may facilitate visualization of the lower cervical spine. ■ Gardner-Wells tongs may be applied for distraction once the patient has been appropriately positioned. Taping the shoulders with judicious caudal distraction may improve radiographic visualization and increase working space. ■ Somatosensory-evoked and transcranial motor-evoked potentials are used when patients’ neurologic function is preserved. ■ If the offending organism has not been previously identified, clear instructions to hold preoperative antibiotics are given to the anesthesia team. Approach ■ A left-sided approach is favored by many, although studies have failed to firmly establish an association between the side of approach and the incidence of recurrent laryngeal nerve symptoms.6,7 ■ Transverse skin incisions are preferred if three or fewer vertebral bodies must be visualized. For more extensive procedures, an oblique incision just anterior to the anterior border of the sternocleidomastoid muscle is used. ■ A standard anterolateral approach to the subaxial cervical spine is performed (Fig. 69-2). ■ Location with fluoroscopy should be performed to clearly identify the levels of interest. ■ A self-retaining retractor is used with blades placed beneath the elevated medial borders of the longus colli muscle. Débridement and Decompression ■ Great care should be taken to maintain orientation with respect to the midline, because the anatomy in the region of the active infection may be distorted. Exposure of an uninvolved level above and below may be helpful. ■ Much of the initial débridement can be performed piecemeal using pituitary rongeurs and curettes. Generous sampling of pathologic material should be sent for Gram stain; culture for aerobic, anaerobic, acid-fast, and fungal organisms; and histologic evaluation. ■ The remainder of the decompression is accomplished in standard fashion, with a high-speed burr used to sequentially thin the bone from anterior to posterior. The thin remaining shell of bone is then removed with microcurettes (Fig. 69-3).

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SECTION I  •  Spinal Infection

Figure 69-2  A standard anterolateral approach to the subaxial cervical spine.

Figure 69-4  With distraction applied, the graft is rotated and tamped into the slot in the inferior vertebra.

Distraction across the defect using the Caspar distractor alone or in addition to Gardner-Wells tongs is helpful for seating the graft. ■ With distraction applied, the graft is rotated and tamped into the slot in the inferior vertebra (Fig. 69-4). ■

Strut Graft with Anterior Instrumentation.  If this technique is selected, grafting is done in the manner previously described for cervical corpectomy. Specifics for applying this technique in the infected spine include the following: Preservation of end plate integrity is achieved by gentle preparation with a high-speed burr or rasps and curettes. ■ Screws are inserted into uninvolved bone by correlating preoperative imaging with intraoperative findings. Reliance of screw purchase in pathologic bone is not recommended. A preoperative CT scan may be helpful to evaluate bone quality at the levels considered for screw fixation. ■ The anterior vertebral body surfaces often undulate with convexities in the peridisk areas. Flattening any anterior prominences with a high-speed burr will allow the plate to sit flush against the bone and decrease the overall profile. ■

Figure 69-3  The thin remaining shell of bone is removed with microcurettes.

Reconstruction Strut Graft Without Anterior Instrumentation To prevent dislodgment, the graft is countersunk into the vertebral bodies above and below. ■ A high-speed burr is used to create slots in the bone above and below. The graft is placed in the slot in the superior vertebra first. ■

69  •  Bacterial, Fungal, and Tuberculosis Diskitis and Osteomyelitis of the Cervical, Thoracic, and Lumbar Spine

Posterior Instrumentation If noninstrumented strut grafting was performed anteriorly, we favor the addition of posterior instrumentation to increase stability of the construct and decrease postoperative immobilization requirements. Posterior instrumentation is also used in most cases of three-level corpectomy owing to concerns of inadequate stability with anterior plating. ■ Posterior instrumentation is done using standard techniques described elsewhere in this book. Lateral mass screws are generally used from C3 to C6, and pedicle screws are used caudally at C7 at the end of long constructs, as anatomy permits. Some favor extension of long posterior constructs to the upper thoracic spine. ■ If the posterior procedure is performed under the same anesthesia, a separate set-up table of instruments to be used for the posterior procedure is requested in advance and kept separate from instruments used during the anterior stage. ■

Illustrative Case

Figure 69-6  T2-weighted sagittal magnetic resonance imaging.

■

Lateral cervical radiograph of cervical diskitis/ osteomyelitis in a middle-aged man with insulindependent diabetes (Fig. 69-5) ■ T2-weighted sagittal MRI (Fig. 69-6) ■ Postoperative lateral radiograph after anterior débridement and decompression, allograft fibula strut grafting with anterior plating, and posterior lateral mass fixation (Fig. 69-7) ■ Postoperative anterior–posterior (AP) radiograph of the same patient (Fig. 69-8)

Figure 69-7  Postoperative lateral radiograph after anterior debridement and decompression, allograft fibula strut grafting with anterior plating, and posterior lateral mass fixation.

Figure 69-5  Lateral cervical radiograph of a middle-aged man with insulin-dependent diabetes and cervical diskitis/osteomyelitis.

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SECTION I  •  Spinal Infection

Figure 69-9  Care is taken to stabilize the patient at an angle perpendicular to the floor, using padded attachments to the table or a beanbag and tape.

If the patient is to be placed in the lateral decubitus position, a high-quality plain radiograph is obtained before positioning to correlate the rib with the vertebral body of interest. The ribs are then manually palpated and counted. The incision is based over the rib, one or two levels above the vertebrae to be resected, to permit adequate direct access to the cephalad vertebrae if instrumentation is planned.

■

Figure 69-8  Postoperative anteroposterior radiograph.

THORACIC DISKITIS AND OSTEOMYELITIS Anesthesia ■ The thoracolumbar junction can be approached using standard, two-lung ventilation; higher transthoracic approaches may be facilitated by selected intubation and one-lung ventilation with a double-lumen endotracheal tube. ■ An arterial line, central venous line, and Foley catheter are typically placed for continuous blood pressure and fluid status monitoring. ■ Somatosensory and transcranial motor-evoked potentials are used when patients have preservation of neurologic function. ■ Antibiotics are withheld until specimens are obtained to establish the microbiologic diagnosis. Patient Positioning ■ For anatomic reasons, a left-sided approach is favored by many. The thick-walled aorta can be manipulated with less risk than the thin-walled vena cava. In addition, because of the right-sided location of the liver, less caudal access is available to the thoracolumbar junction without a transdiaphragmatic approach. Midthoracic levels can be adequately approached from either side. ■ For anterior approaches to the upper thoracic spine, the patient is positioned supine as described earlier. ■ For access to the middle and lower thoracic spine, the patient is positioned in a true lateral decubitus position. Care is taken to stabilize the patient at an angle perpendicular to the floor, using padded attachments to the table or a beanbag and tape (Fig. 69-9). ■ An axillary roll is placed just below the dependent axilla to protect the neurovascular supply to the arm. Localization ■ If the patient is supine, localization with fluoroscopy is performed to identify the levels of interest.

Surgical Approach ■ For access to T1 through T4, posterior and posterolateral approaches are typically used. However, anterior decompression requires a low anterior cervical approach combined with either a sternotomy or partial clavicle resection, which is associated with significant perioperative morbidity. For access to the upper thoracic spine, another technique has been described, a modified low anterior cervical dissection combined with a partial manubriotomy; this spares the sternoclavicular joints and the sternum, decreasing the morbidity from these additional procedures.8,9 ■ For access to T4 through T10, a transthoracic-transpleural approach is typically performed through the bed of the resected rib (Fig. 69-10). ■ For exposure of the thoracolumbar junction, a transpleural-retroperitoneal thoracoabdominal approach, with detachment of the diaphragm, is commonly used. The thoracolumbar junction can also be exposed through an extrapleural-retroperitoneal approach, which avoids incision of the diaphragm and may be associated with less pulmonary morbidity. ■ In selected cases of thoracic level osteomyelitis, costotransversectomy and lateral extracavitary approaches may be options; these are described elsewhere. Whereas such approaches are effective for decompression and bony débridement, debulking and débridement of anterior paraspinal collections may be incomplete. This may result in a higher load of pathogens in the vicinity of cages used for anterior column reconstruction. Decompression and Reconstruction Supine Position ■ After the initial exposure, either a manubriotomy or resection of the sternum or distal clavicle is performed. After lateral reflection of the thymus, the tracheoesophageal bundle is retracted medially, and the brachiocephalic trunk is retracted laterally. The prevertebral fascia may then be divided.

69  •  Bacterial, Fungal, and Tuberculosis Diskitis and Osteomyelitis of the Cervical, Thoracic, and Lumbar Spine

Figure 69-10  For access to T4 through T10, a transthoracictranspleural approach is typically performed through the bed of the resected rib. Figure 69-11  After the initial exposure, the lung is gently retracted superomedially, away from the spine.

An operating microscope may be used for optimal visualization. ■ Corpectomy of the pathologic vertebrae is then performed, as described in earlier sections, using a combination of osteotomes, rongeurs, punches, and a high-speed burr. Infected and necrotic bone and disk material may be easily removed with rongeurs and curettes and sent for microbiologic analysis. ■

Lateral Decubitus ■ After the initial exposure, the lung is gently retracted superomedially, away from the spine (Fig. 69-11). ■ Confirmation of the involved level is performed by intraoperative imaging. The anatomy of the involved segments may be severely distorted, so careful correlation to the localizing film and preoperative imaging studies is necessary. ■ Ligation of the segmental vessels overlying the vertebral bodies to be instrumented, as well as those at the corpectomy level, is generally required (Fig. 69-12). The parietal pleura is typically thickened and inflamed, making vessel identification difficult. ■ Corpectomy of the pathologic vertebrae may then be performed as described above. Removal of the involved disks can provide orientation before the bloodier portion of the corpectomy proper. ■ If formal neurologic decompression is required, removal of retropulsed tissue should continue across the spinal canal until the contralateral pedicle is identified. Based on preoperative imaging, the posterior longitudinal ligament may require opening to débride epidural components of infection.

Figure 69-12  Ligation of the segmental vessels overlying the vertebral bodies to be instrumented, as well as those at the corpectomy level, is generally required.

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SECTION I  •  Spinal Infection

Reconstruction of the anterior weight-bearing column can be performed with structural autograft, typically the iliac crest; structural allograft; or cages packed with morcellized autograft, allograft, or a combination of both (Fig. 69-13). ■ If anterior strut grafting without anterior instrumentation is preferred, the graft should be countersunk into the vertebral bodies above and below (Fig. 69-14). If anterior instrumentation is to be used, the graft should be fit to span from the inferior end plate of the proximal vertebra to the superior end plate of the inferior vertebra; this will facilitate screw placement into the adjacent vertebral bodies. ■

Anterior Instrumentation ■ If anterior instrumentation is to be used, standard techniques for plate or screw-rod devices can be applied. This should be performed after thorough débridement and irrigation of the field. ■ Reliance of screw purchase in pathologic bone is not recommended. Where possible, bicortical purchase of normal, uninvolved segments is preferable (Fig. 69-15).

Illustrative Case ■

A 50-year-old man with a history of IV drug use came to medical attention with thoracic back pain and rapidly progressive cord-level neurologic deficit. ■ T2-weighted sagittal MRI demonstrates T6–T7 diskitis/ osteomyelitis with pathologic fracture, epidural extension, and spinal cord compression (Fig. 69-16). ■ Postoperative AP radiograph is taken after anterior débridement and decompression involving T6 and T7 corpectomies with instrumentation at T5 through T8 (Fig. 69-17).

Figure 69-13  Reconstruction of the anterior weight-bearing column can be performed with structural autograft, typically iliac crest; structural allograft; or cages packed with morcellized autograft, allograft, or combinations of both.

Figure 69-14  If anterior strut grafting without anterior instrumentation is preferred, the graft should be countersunk into the vertebral bodies above and below.

Figure 69-15  Where possible, bicortical purchase of normal, uninvolved segments is preferable.

69  •  Bacterial, Fungal, and Tuberculosis Diskitis and Osteomyelitis of the Cervical, Thoracic, and Lumbar Spine

Posterior Instrumentation ■ Posterior stabilization is generally recommended after noninstrumented anterior strut grafting. Standard techniques described in earlier sections are applicable. We favor segmental fixation with hook or pedicle screw constructs. ■ In selected cases involving multilevel anterior corpectomies, the addition of posterior instrumentation is utilized to achieve greater initial stability, increase the fusion rate, and decrease postoperative bracing requirements. In most cases, more limited posterior constructs appear sufficient when combined with anterior plate or screw-rod devices.

Illustrative Case ■

Postoperative lateral radiograph after addition of posterior instrumentation to the patient presented in Figures 69-16 through 69-18 ■ Axial CT scan that demonstrates appropriate position of the pedicle screws selected for the posterior construct (Fig. 69-19)

Figure 69-16  T2-weighted sagittal magnetic resonance imaging demonstrates T6–T7 diskitis/osteomyelitis with pathologic fracture, epidural extension, and spinal cord compression.

Figure 69-17  Postoperative anteroposterolateral radiograph after anterior débridement and decompression involving T6 and T7 corpectomies with instrumentation at T5 through T8.

Figure 69-18  Postoperative lateral radiograph after addition of posterior instrumentation to the patient presented in Figures 69-16 and 69-17.

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SECTION I  •  Spinal Infection

Figure 69-20  The patient is placed in a lazy, right lateral decubitus position with a bump under the left side.

Figure 69-19  Axial computed tomography scan demonstrates the appropriate position of the pedicle screws selected for the posterior construct.

LUMBAR DISKITIS AND OSTEOMYELITIS Positioning and Anesthesia ■ For approaches that involve levels proximal to L4, a retroperitoneal flank approach is utilized. The patient is placed in a lazy, right lateral decubitus position with a bump under the left side (Fig. 69-20). ■ To approach the lumbosacral junction, the patient is positioned supine, and a retroperitoneal approach is performed through a midline vertical incision. A roll may be placed beneath the lumbar spine to maintain lordosis, and the legs are slightly flexed and abducted to relax the iliopsoas. ■ Transpsoas approaches have also been described but may be best suited for cases where only limited anterior débridement and no formal anterior decompression are required.10 ■ If the organism has not been identified, antibiotics are withheld until specimens are obtained. Exposure ■ A standard retroperitoneal approach to the lumbar spine is performed. The flank approach involves division of the external oblique, internal oblique, and transversus abdominis muscles (Fig. 69-21). The vertical midline approach involves splitting the rectus abdominis muscle in the midline linea alba. ■ The retroperitoneal space is entered laterally by identification of the retroperitoneal fat. Blunt finger dissection along the anterior surface of the left psoas muscle should lead to the great vessels. ■ At L4 and higher, ligation and division of the segmentals allow the great vessels to be gently retracted toward the right, with the psoas mobilized toward the left to expose the spine (Fig. 69-22). The local anatomy may be distorted by the infection, and the vessels may be difficult to mobilize secondary to inflammation. Blunt dissection

Figure 69-21  The flank approach involves division of the external oblique, internal oblique, and transversus abdominis muscles.

Figure 69-22  After ligation and division of the segmentals, the great vessels can be gently retracted toward the right with the psoas mobilized toward the left to expose the spine.

69  •  Bacterial, Fungal, and Tuberculosis Diskitis and Osteomyelitis of the Cervical, Thoracic, and Lumbar Spine

with firm, controlled pressure on the surface of the disks is most effective. ■ The L5–S1 level is exposed through the bifurcation of the great vessels after ligation and division of the middle sacral vessels. The L4–L5 disk can be exposed by two techniques: both the left iliac artery and vein can be carefully retracted from left to right, or the disk can be approached between the left iliac artery and vein; with this latter method, the left iliac artery is mobilized to the left, and the iliac vein is retracted across the midline toward the right after careful ligation and division of the ascending lumbar segmental vein. ■ A spinal needle is inserted into the appropriate disk, and an intraoperative image is obtained to verify the local anatomy.

Débridement and Decompression ■ Removal of severely affected bone and disk is readily performed using rongeurs and curettes. ■ To increase yield, generous amounts of tissue should be sent for analysis. After adequate specimens have been obtained, empiric antibiotic coverage should be started. ■ The remainder of the decompression is performed in routine fashion as described in previous sections. All gross purulence and necrotic bone should be removed back to a margin of healthy, bleeding tissue. ■ If an epidural abscess is present anterior to the dural sac, a formal decompression is performed from pedicle to pedicle. The abscess can be gently débrided with a Penfield dissector, and careful suction and irrigation are performed.

Figure 69-23  Strut grafting to achieve stability after corpectomy can be performed using iliac crest autograft or allograft.

Anterior Reconstruction ■ The orientation of the great vessels in the lower lumbar spine should be evaluated if stabilizing anterior plates or screw-rod constructs are being considered. ■ Strut grafting to achieve stability after corpectomy can be performed using iliac crest autograft (Fig. 69-23) or allograft. If anterior stabilizing implants are not being used, the graft should be countersunk in the upper end plate above and in the lower end plate below.

Illustrative Case ■

A 68-year-old man developed severe, unrelenting back pain several months after experiencing bacteremia from a chronic lower extremity infection. ■ Sagittal T1-weighted MRI demonstrated diskitis and osteomyelitis involving L4–L5 (Fig. 69-24). Sagittal T2-weighted MRI demonstrated bony involvement with pathologic fracture of L4 (Fig. 69-25). ■ The patient was treated with IV antibiotics after CT-guided biopsy but experienced increasing pain and evidence of further bone loss. ■ Sagittal reconstruction of CT scan was performed after anterior débridement, decompression, and reconstruction with an iliac crest strut graft. Posterior stabilization was performed under a separate anesthesia (Fig. 69-26).

Figure 69-24  A 68-year-old man developed severe, unrelenting back pain several months after experiencing bacteremia from a chronic lower extremity infection. Sagittal T1-weighted magnetic resonance imaging demonstrates diskitis and osteomyelitis involving L4–L5.

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SECTION I  •  Spinal Infection

Figure 69-25  Sagittal T2-weighted MRI demonstrates bony involvement with pathologic fracture of L4.

Figure 69-27  Pedicle screw constructs can be applied in routine fashion as described in earlier sections.

Pedicle screw constructs can be applied in routine fashion as described in earlier sections. After supplemental posterior fusion, postoperative AP radiography was performed in the patient discussed in Figures 69-24 to 69-27. ■ The decision to perform both procedures under the same anesthesia, versus operating in a staged manner, should be made on a case-by-case basis. ■ In selected cases, posterior techniques may be used in the lower lumbar spine to treat diskitis and osteomyelitis. Posterior lumbar interbody fusion (PLIF) or transforaminal lumbar interbody fusion (TLIF) may be applicable as described elsewhere. Cases with more-limited bony involvement, with infection confined mostly to the disk space and end plate interface, are better suited to this approach. More extensive bony débridement and reconstruction are more readily performed with the AP approach. ■ The use of expandable cages for anterior column reconstruction is gaining popularity. This technology may allow selected cases to be stabilized from a posterior first approach, followed by a second-stage anterior débridement. In cases associated with neurologic deficit as a result of epidural abscess (see below), this permits timely decompression from a posterior approach. If appropriate alignment has already been achieved and/or maintained, the cage can then be expanded to fit the defect and achieve stable seating. ■

Figure 69-26  Sagittal reconstruction of computed tomographic scan performed after anterior débridement, decompression, and reconstruction with an iliac crest strut graft. Posterior stabilization was performed under a separate anesthesia.

Posterior Stabilization ■ We routinely perform supplemental posterior fusion after noninstrumented anterior decompression and strut grafting in the lower lumbar spine. Such an approach allows early mobilization with minimal bracing requirements, and it promotes fusion.

69  •  Bacterial, Fungal, and Tuberculosis Diskitis and Osteomyelitis of the Cervical, Thoracic, and Lumbar Spine

TUBERCULOSIS AND FUNGAL INFECTIONS OF THE SPINE Fungal infections of the spine are managed in similar fashion to pyogenic infections. Antimicrobial therapy must be adjusted based on the culture results. ■ Patients who experience fungal infections of the spine are commonly immunocompromised and malnourished. Consultation with medical and nutritional specialists is recommended. ■ Tuberculosis (TB) infections of the spine commonly respond well to medical treatment with combinations of isoniazid, rifampin, pyrazinamide, ethambutol, and/or streptomycin. The diagnosis must be confirmed by biopsy. New testing methods that use polymerase chain reaction can decrease the amount of time required to definitively establish the diagnosis. ■ Surgical indications are similar to those for pyogenic infections, although medical treatment appears effective even in the presence of large soft-tissue abscesses associated with TB. ■

Figure 69-28  Sagittal T2-weighted magnetic resonance imaging demonstrates presumed Pott disease with anterior soft-tissue abscess, two-level involvement (including pathologic fracture), and preservation of the intervening disk.

Operative techniques for management of TB spinal infections are similar to those used for pyogenic infections. As with pyogenic infections, recent studies have demonstrated the safety and efficacy of anterior instrumentation for treatment of TB infections, although this continues to be an area of controversy.

■

Illustrative Case ■

A 49-year-old man came to medical attention with back pain and new-onset lower extremity paralysis. ■ Sagittal T2-weighted MR demonstrated presumed Pott disease with anterior soft-tissue abscess, two-level involvement (including pathologic fracture), and preservation of the intervening disk (Fig. 69-28). ■ The patient underwent anterior débridement and reconstruction involving two-level corpectomy, cage placement, and anterior instrumentation (Fig. 69-29). In a staged fashion, posterior stabilization was performed to increase the probability of fusion and decrease postoperative bracing needs (Fig. 69-30).

Figure 69-29  This patient underwent anterior debridement and reconstruction involving two-level corpectomy, cage placement, and anterior instrumentation.

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Empiric antibiotic coverage should continue until culture and sensitivity information is available. ■ Appropriate antibiotic treatment should continue for approximately 6 weeks in pyogenic infections and 6 months to 1 year for TB. Infectious disease consultation is recommended to help manage antibiotic selection, dosing, and scheduling. ■ Effectiveness of treatment should be monitored by serial evaluation of ESR and CRP. Postoperative radiographs and CT scans to monitor for evidence of hardware failure, pseudarthrosis, or recurrent abscesses may be helpful. The roles of MRI and nuclear studies to assess the postoperative progress are unclear. ■

Complications Complications of the surgical treatment of spinal infections are similar to those reported after the use of these techniques for degenerative and traumatic conditions. Failure to eradicate the infection may be due to inadequate débridement or improper antibiotic selection, dosing, or duration, and graft dislodgment may occur secondary to improper technique or failure to achieve adequate stability. In addition, malnutrition may contribute to delayed wound healing, postoperative wound infections, and dehiscence.

■

References Figure 69-30  In a staged fashion, posterior stabilization was performed to increase the probability of fusion and to decrease postoperative bracing needs.

EPIDURAL ABSCESS Most often, epidural abscess presents with associated diskitis or osteomyelitis. Rarely it may result from direct hematogenous spread. ■ Although commonly focal in nature, the abscess may extend over multiple motion segments. Most occur in the thoracic (51%) and lumbar (35%) spine within the posterior epidural space. In the cervical spine, epidural abscesses tend to occur in the anterior epidural space. ■ Progressive neurologic deficits may develop if not addressed appropriately with early treatment. ■ Surgical evacuation is the recommended treatment. Nonoperative treatment with IV antibiotics for up to 6 weeks may be considered for lumbar abscesses, if no systemic sepsis or neurologic deficit is present.11 However, any signs of neurologic deterioration or lack of response to medical treatment warrants emergent surgical intervention using the techniques described in this chapter. ■ A pseudocapsule often surrounds the dura. This typically requires careful separation and elevation from the underlying dura for adequate removal. ■

Postoperative Care Postoperative management is similar to that prescribed after performance of these procedures for degenerative or traumatic conditions.

■

1. Miller CP, Simpson AK, Whang PG, et al: Effects of recombinant human bone morphogenetic protein 2 on surgical infections in a rabbit posterolateral lumbar fusion model. Am J Orthop (Belle Mead NJ) 38(11):578–584, 2009. 2. Allen RT, Lee YP, Stimson E, et al: Bone morphogenetic protein-2 (BMP-2) in the treatment of pyogenic vertebral osteomyelitis. Spine (Phila Pa 1976) 32(26):2996–3006, 2007. 3. Chen X, Schmidt AH, Tsukayama DT, et al: Recombinant human osteogenic protein-1 induces bone formation in a chronically infected, internally stabilized segmental defect in the rat femur. J Bone Joint Surg Am 88(7):1510–1523, 2006. 4. Govender S, Csimma C, Genant HK, et al: Recombinant human bone morphogenetic protein-2 for treatment of open tibial fractures: a prospective, controlled, randomized study of four hundred and fifty patients. J Bone Joint Surg Am 84-A(12):2123–2134, 2002. 5. Aryan HE, Lu DC, Acosta FL, Jr, et al: Corpectomy followed by the placement of instrumentation with titanium cages and recombinant human bone morphogenetic protein-2 for vertebral osteomyelitis. J Neurosurg Spine 6(1):23–30, 2007. 6. Beutler WJ, Sweeney CA, Connolly PJ: Recurrent laryngeal nerve injury with anterior cervical spine surgery risk with laterality of surgical approach. Spine (Phila Pa 1976) 26(12):1337–1342, 2001. 7. Haller JM, Iwanik M, Shen FH: Clinically relevant anatomy of recurrent laryngeal nerve. Spine (Phila Pa 1976) 37(2):97–100, 2012. 8. Lam FC, Groff MW: An anterior approach to spinal pathology of the upper thoracic spine through a partial manubriotomy. J Neurosurg Spine15(5):467–471, 2011. 9. Radek A, Maciejczak A, Kowalewski J, et al: [Trans-sternal approach to the cervicothoracic junction]. Neurol Neurochir Pol 33(5):1201– 1213, 1999. 10. Sofianos DA, Briseño MR, Abrams J, et al: Complications of the lateral transpsoas approach for lumbar interbody arthrodesis: a case series and literature review. Clin Orthop Relat Res 470(6):1621–1632, 2012. 11. Savage K, Holtom PD, Zalavras CG: Spinal epidural abscess: early clinical outcome in patients treated medically. Clin Orthop Relat Res 439:56–60, 2005.

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70

Surgical Management of Gunshot Wounds to the Spine GABRIEL TENDER

Overview

Mechanisms of Injury

Gunshot wounds (GSWs) to the spine represent a major health problem in U.S. metropolitan areas as well as in military hospitals. With the perpetually escalating levels of violence, civilian GSWs to the spine have increased to 13% to 17% of all spinal cord injuries.1,2 Because of the high potential for severe functional impairment, these patients require major socioeconomic expenditures.3,4 Because of the high velocity of the ordnance, military GSWs to the spine are typically more severe and usually result in complete injuries, with decreased likelihood of neurologic recovery.5 In both civilian and military spinal GSWs, thoracic injuries are most common, followed by lumbosacral and cervical injuries.5

The energy of any moving object is determined according to the formula E = ½ mv2, where E is kinetic energy, m is mass, and v is velocity. Therefore the bullet energy impacted to tissues increases exponentially with the velocity. Most civilian firearms, typically pistols and handguns, have muzzle velocities of less than 2000 feet per second and are considered “low energy,” whereas military assault rifles, such as AK-47s and M-16s, have muzzle velocities greater than 2000 feet per second and are considered “high energy.” The closer the range of a gunshot, the less energy will be lost during transit; thus more energy will be transferred to the victim in close-range shootings. Fragmentation of the bullet on impact, as occurs with hollow-point bullets, results in multiple trajectories and increased damage to tissues.9 Bullets may have a “jacket,” a thin metallic layer covering its surface. Fully jacketed bullets are designed to hit longrange targets, are highly precise, and may incur clean entry and exit wounds. Partially jacketed or nonjacketed bullets are designed to hit close-range targets and expand on impact, resulting in fragmentation and increased tissue damage. Most bullets are made of a lead core, whereas the jackets are made of copper, brass, or nickel. These materials can be toxic, particularly if the bullets are lodged in the intervertebral disk. Lead toxicity has been reported and can be determined by periodic measurements of the lead level or by indirect effects, such as hematopoietic or axonal changes. In animal studies, copper has also been shown to be toxic to the brain and spinal cord tissue when in direct contact with tissues.

Epidemiology Civilian GSWs have reached epidemic proportions in the United States, being 90 times more frequent than in any other industrialized nation.6 GSWs to the spine have increased proportionally and now represent the second most common cause of spinal cord injury in metropolitan areas. The typical GSW patient is likely to be young, single, African American or Hispanic, male, and unemployed, with a history of previous violent injuries or encounters with the criminal justice system.6 Despite the fact that handguns represent only about 25% of the firearms in the United States, they are responsible for about 80% of GSW injuries.1 Because of the increasing incidence of GSWs to the spine, most level 1 trauma centers have now become well versed in the treatment of these types of patients. In the past 10 years, the United States has been involved in two simultaneous conflicts within the global War on Terror: Operation Iraqi Freedom (2003 through 2012) and Operation Enduring Freedom.7,8 These two conflicts alone have resulted in over 50,000 casualties. Spine injuries are among the most disabling conditions affecting wounded soldiers. Associated injuries are frequent in this population, and these patients have higher rates of musculoskeletal, head, and chest trauma, as well as spine injuries at multiple levels, than their civilian counterparts. Delivery of medical care in a hostile combat environment can be challenging, and evacuation of the casualty and care provider to a safe location may take priority over a full medical evaluation while under fire. 686

Prehospital and Emergency Room Management The initial treatment of GSW victims targets the maintenance of airway, breathing, and circulation—the ABCs. All patients should receive tetanus prophylaxis as soon as possible, and specific issues must be addressed depending on the level of injury.9 Cervical wounds are frequently complicated by airway injuries and often require immediate intubation or tracheostomy. Similarly, injuries to the major arteries in the neck result in pulsatile bleeding and may require placement of temporary stents to restore cerebral blood flow. Lesions of

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the pharynx and esophagus have a higher rate of infection and may mandate emergent surgical exploration and repair. These interventions should not be delayed by attempts to obtain radiographic clearance of the cervical spine in patients without neurologic deficit, because GSWs to the spine are rarely unstable. In patients with hypotension and bradycardia (i.e., neurogenic shock), the sympathetic input is diminished and should be treated with pressors rather than volume-replacement agents. Because the diaphragm is innervated by the C3–C5 spinal cord segments, patients with high cervical spinal cord injuries are usually unable to breathe and typically require immediate intubation for ventilation. Thoracic GSWs are usually associated with lung injuries (hemothorax and/or pneumothorax) or cardiovascular injuries (heart perforation, cardiac tamponade, aortic disruption). The treatment of these lesions takes precedence over those of the spinal cord injury. Lumbar and sacral GSWs are typically associated with abdominal and pelvic injuries, respectively. Particular attention should be given to colonic perforations, because they carry a higher risk of infection if not treated with the appropriate antibiotics for an adequate period of time.

Neurologic Evaluation The neurologic examination begins with removing all the patient’s clothing and log-rolling the patient to protect the spinal cord in case of an unstable injury. The number of entrance and exit wounds is recorded, and the difference between the two accounts for the number of bullets retained in the body. Entry wounds typically have clean and welldefined margins, whereas exit wounds have a ragged, “blown out” appearance. After local wound care, the wounds can be marked with radiopaque markers for later radiographic deduction of the missile paths. Physical examination is focused on the level of injury and the presence of neurologic function below it. In the conscious patient, it is easy to determine the motor strength as well as sensory impairment. Comatose or sedated patients can be evaluated by their response to painful stimuli in the upper and lower extremities. Deep tendon reflexes are usually absent below the level of injury in patients with complete neurologic deficit (i.e., spinal shock). Particular attention should be given to the presence of the rectal sphincter tone and the bulbocavernosus reflex, which will determine whether the patient has a complete versus incomplete injury.

Radiologic Evaluation The initial radiologic evaluation typically consists of plain radiographs, anteroposterior (AP) and lateral, of the involved areas. If the wounds are tagged with radiopaque markers, the bullet trajectories can be inferred, as can the potential tissue damage incurred on that path. Bullet fragments retained in the body can also be identified. If spinal instability is suspected (e.g., a patient has neurologic symptoms), particularly in the cervical spine, active flexion– extension films can be obtained.

The radiologic examination of choice for GSW to the spine is computed tomography (CT). Thin-slice (1 to 2 mm) CT images permit accurate bullet localization within the spinal segment as well as assessment of associated bony destruction. Coronal and sagittal reconstruction allows evaluation of the integrity of the three spinal columns and of the presence of focal kyphosis and/or scoliosis at the injured level. Magnetic resonance imaging (MRI) has the potential of inducing bullet migration and thus worsening neurologic deficit. However, several studies have attested to the safety of MRI use in patients with spinal GSW. Advantages of MRI over CT include better definition of the soft tissues (disks, spinal cord, spinal nerves) and less artifact from the bullet.

Indications for Surgical Intervention Preoperatively, all patients should receive broad-spectrum antibiotics. In cases of colonic perforation, antibiotics should be continued for 7 to 14 days and should include Gram-negative and anaerobic coverage.10,11 In patients with visceral perforation and concomitant spinal injury, it appears that surgical débridement of the spinal lesion and bullet removal from the spine do not improve the outcome. Steroids are not indicated in GSW to the spine, because they do not improve neurologic function but do increase the rate of complications.

CEREBROSPINAL FLUID FISTULA Cerebrospinal fluid (CSF) fistulas are easily recognized by the clear nature of the fluid persistently coming out of a GSW entry or exit wound.12 In cases of occult leaks, β-2 transferrin analysis can confirm the diagnosis, because this protein is specific to CSF. Occasionally, patients may exhibit mental status changes and even cranial nerve palsies as a result of extreme loss of CSF. The first line of treatment for CSF leaks is placement of a lumbar drain. This allows for controlled drainage of 10 to 15 mL/hour, or until severe headache ensues, and sealing of the defect created by the GSW. Because of the risk of meningitis if left untreated, if the CSF leak persists, a laminectomy is typically required that should include repair of the dural defect, either primarily or with a dural graft. Lumbar drainage is usually continued postoperatively to facilitate the sealing of the dural repair.

SPINAL INSTABILITY A GSW to the spine rarely leads to instability. In the awake patient with no neurologic symptoms, it is safe to assume that the cervical spine is stable and to proceed with the emergent care without obtaining “radiographic clearance.” In these cases, immobilization in a hard cervical collar for 2 weeks allows for the pain and spasms to subside and permits a better evaluation by flexion–extension radiographs. Spinal instability is more likely in high-energy injuries, because missiles moving at higher speeds have a wider circumference of damage because of the shock wave.

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Spinal instability should be suspected in patients with comminuted fractures that involve the anterior and posterior elements, particularly if associated with abnormal focal angulation or subluxation. Progressive angulation over the course of weeks or months can also be interpreted as instability. Occasionally, MRI can identify the degree of ligamentous injury and can indirectly assist in the determination of the degree of instability. In patients with incomplete neurologic deficit, spine surgeons may choose to treat a potentially unstable fracture that may result in a worsening neurologic status if not surgically stabilized. This is particularly true for patients with retained bullet or bone fragments in the spinal canal, who can also undergo a surgical decompression at the same time. In patients with complete neurologic deficit, the surgical goal is to provide sufficient spinal stability to allow the patient to undergo the strenuous physical therapy and retraining necessary to use their preserved motor function to accommodate daily needs. The surgical approach typically involves instrumentation and depends on the particular configuration of the fracture. An unstable GSW that involves mostly the vertebral body can be addressed by performing a corpectomy and fixation, whereas those that predominantly involve the posterior elements are treated by a posterior multilevel fixation, with or without decompression. Occasionally, a circumferential fixation is required in severely comminuted fractures. The timing of surgery is usually between 5 and 10 days from the injury. Earlier operations have a high risk of CSF fistulas, whereas operations later than 2 weeks have a higher incidence of arachnoiditis and infection.

NEUROLOGIC DEFICIT Neurologic deficit is more often complete after a GSW to the spine (59%) than with blunt injuries (49%). The societal cost of these injuries is tremendous: not only do these patients have extensive stays in the intensive care unit (ICU), hospital, and rehabilitation facilities, they are frequently ventilator dependent for prolonged periods of time. In addition, they are typically young and were previously capable of independent living; often they are completely disabled after the GSW. Neurologic deficit after GSW to the spine can be progressive, incomplete, or complete. Progressive or delayed newonset neurologic deficit after GSW to the spine represents an indication for emergent decompression, but it is a relatively rare occurrence. Progressive neurologic deterioration may be due to a bullet or bone fragment in the spinal canal or to an expanding epidural hematoma. This neurologic progression is best detected if the serial examinations are documented in the chart following the same pattern of muscle groups (e.g., the American Spinal Injury Association [ASIA] scale chart), preferably by a single, experienced physician. Incomplete neurologic deficit typically involves various degrees of weakness of the legs and/or arms below the injury level, but occasionally it may present as BrownSequard, central cord, anterior cord, or even cruciate hemiparesis syndromes. The role of surgical decompression in these patients is still a matter of debate. Some authors

believe that decompressive operations should be done in all the patients with evidence of canal compromise,13 but others have suggested that removal of bullet or bone fragments is beneficial only in the T12–L4 region.14,15 Most authors have not found any benefit from spinal canal decompression after GSW. If surgery is performed, timing is optimal within the first 24 to 48 hours after injury. Complete neurologic deficit is characterized by complete absence of motor or sensory function below the level of injury. Most of these patients do not benefit from surgical decompression, because their chances of neurologic recovery are minimal. The only possible exception is the rare patient with a GSW to the cervical spine and imaging evidence of compressive pathology by bone fragments or a bullet. Early decompression in these cases may provide recovery of one or two cervical spinal segments, with major positive effects on their future recovery of independence with activities of daily living (ADLs).

SPECIAL INDICATIONS Disk Herniation GSW to the spine may result in disk herniations with spinal canal or foraminal compromise. In these rare cases, the indications for surgery are the same as for other acute disk herniations: emergent diskectomy for decompression. Bullet removal in these cases is not necessary, unless it is technically easy to perform and does not jeopardize adjacent neural structures. Lead Toxicity Lead toxicity is an unusual occurrence reported in GSW with the bullet lodged in the intervertebral disk space.16 The diagnosis is based on the presence of anemia and other hematopoietic alterations and requires determination of blood lead levels. The treatment consists of bullet removal and administration of lead-chelating agents. Bullet Migration Another rare situation is that of documented bullet migration. When associated with increased or new-onset neurologic deficit, surgical removal of the bullet is usually indicated.

Late Complications Besides neurologic deficit, the most common long-term complication in both complete and incomplete injuries is neuropathic pain. Various studies report an incidence of neuropathic pain after spinal cord injury between 30% and 90%. This typically occurs in young patients who have major difficulties with basic self-care tasks, such as grooming and cleaning, as well as driving, job-related duties, and social activities. Moreover, patients in severe pain are prone to emotional imbalances, such as depression and anxiety, and they report a lower overall satisfaction with life. Neuropathic pain in these patients has a complex etiology and involves changes in structure, biochemistry, and genes in the peripheral and central nervous systems. Current pharmacologic and surgical therapies are often ineffective over

70  •  Surgical Management of Gunshot Wounds to the Spine

time for these patients. Medications include neuroleptics, narcotics, antidepressants, and calcium-channel blockers (e.g., gabapentin). Surgical intervention for bullet removal has not been shown to improve the pain in this population. Other operations target the treatment of pain pathways (e.g., spinal cord stimulation or dorsal root entry zone ablative procedures) with variable reported successful outcomes.

Louisiana State University–New Orleans Experience Between January 2007 and October 2011, 147 patients were admitted and received level 1 trauma services at Louisiana State University in New Orleans. Patient age ranged between 14 and 66 years (mean, 27 years). Interestingly, the mean age for African American patients was 25, whereas for whites, the mean age was 36. The patient group was composed of 123 African Americans (84%) and 13 Caucasians (9%). Most of the patients were male (92%),

and most were single (97%). Interestingly, of the 88 patients tested for drugs, 73 (83%) tested positive, with the leading substances being tetrahydrocannabinol (THC), ethanol, and cocaine. Of the 147 patients, 127 (86%) were treated conservatively (Figs. 70-1 and 70-2). Only 20 patients (13%) underwent a spinal operative procedure. Thirteen of these patients underwent operations on the spine below T11, and nine had decompressive procedures (Fig. 70-3) with no neurologic improvement, except for one patient who improved from ASIA class C to D; the other four patients had signs of unstable fractures and underwent stabilization procedures (Fig. 70-4). Three of the decompressive procedures were done in a minimally invasive fashion (Fig. 70-5), via a 22 mm retractor tube, with no postoperative complications (i.e., CSF fistula or infection). Cervical operations were performed on six patients, mostly for stabilization (Figs. 70-6 and 70-7). One patient developed a cervical spinal cord infarct after a GSW to the thoracic spine (Fig. 70-8) and underwent a cervical decompressive laminectomy and fusion without significant neurologic improvement.

Figure 70-1  Gunshot wound to the thoracic spine, through the spinal canal, with complete neurologic deficit (paraplegia) below the level of injury. This patient was treated nonoperatively.

Figure 70-2  Gunshot wound to the cervical spine. The bullet went through the spinal canal, from posterior to anterior, and lodged in the vertebral body. The patient had a complete neurologic deficit and was treated conservatively.

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Figure 70-3  Top: Gunshot wound to L1 with incomplete neurologic deficit (American Spinal Injury Association class D injury) and bullet and bone fragments in the spinal canal. Bottom: An open decompressive lumbar laminectomy was performed without any immediate neurologic improvement.

Figure 70-4  Gunshot wound to L1 with complete neurologic deficit. A right-sided corpectomy was performed, followed by placement of pedicle screws bilaterally, one level above and below the lesion, and placement of a left-sided pedicle screw in the remainder of the L1 vertebral body.

70  •  Surgical Management of Gunshot Wounds to the Spine

Figure 70-5  Three patients with gunshot wounds below T11 (L3, L1, and L2, respectively) and mixed neurologic deficits (American Spinal Injury Association [ASIA] class C, A, and A, respectively). These patients underwent a minimally invasive laminectomy for canal decompression and bullet removal via a 22 mm tubular retractor. None of the patients had postoperative cerebrospinal fluid fistulas or infections. Only the incomplete patient improved, going from ASIA class C to class D.

Figure 70-6  Gunshot wound to the cervical spine with comminution of the C6 anterior and posterior elements and complete C4 neurologic deficit. A C6 corpectomy followed by anterior and posterior fixation was performed to optimize neck stability for maximal rehabilitation efforts.

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Figure 70-7  High-energy gunshot wound to the cervical spine. Anterior and posterior bony destruction over multiple levels was demonstrated on computed tomography. A long, posterior cervicothoracic fusion was performed.

Figure 70-8  Gunshot wound to the thoracic spine that presented with T4 paraplegia. Two days later, the patient developed quadriparesis. Magnetic resonance imaging showed extensive edema in the cervical spinal cord. A decompressive cervical laminectomy was performed, and the patient recovered most of his upper extremity strength and remained neurologically complete below T4.

Another patient had a GSW through the foramen transversarium with occlusion of the vertebral artery and retained fragments in the spinal canal, but some neurologic improvement was seen in the first few days (Fig. 70-9).

Summary GSWs to the spine represent an increasingly significant societal and clinical problem. Surgical intervention is clearly indicated in patients with segmental instability,

persistent CSF leak refractory to lumbar drainage, and in those with progressive neurologic deficit (rare). Decompressive procedures are still controversial, but they may offer some benefits in patients with incomplete neurologic deficit and compressive pathology, particularly below T11. Patients with complete lesions and compression in the cervical spine may recover one or two cervical segments after surgical decompression and may thus be considered surgical candidates. The potential benefits of operative intervention must be carefully weighed against the risks of CSF fistula, infection, and increased neurologic deficit in each patient.

70  •  Surgical Management of Gunshot Wounds to the Spine

Figure 70-9  Gunshot wound to the cervical spine through the right vertebral foramen, with complete occlusion of the vertebral artery and residual bullet and bone fragments in the canal. The patient exhibited a central cord syndrome with predominant right-sided weakness. A cervical laminectomy with canal decompression was performed, followed by a fusion. The patient continued to improve neurologically and was able to ambulate with   a cane.

References 1. Farmer JC, Vaccaro AR, Balderston RA, et al: The changing nature of admissions to a spinal cord injury center: violence on the rise. J Spinal Disord 11:400–403, 1998. 2. Roye WP Jr, Dunn EL, Moody JA: Cervical spinal cord injury: a public catastrophe. J Trauma 28:1260–1264, 1988. 3. Bishop M, Shoemaker WC, Avakian S, et al: Evaluation of a comprehensive algorithm for blunt and penetrating thoracic and abdominal trauma. Am Surg 57:737–746, 1991. 4. Kupcha PC, An HS, Cotler JM: Gunshot wounds to the cervical spine. Spine (Phila Pa 1976) 15:1058–1063, 1990. 5. Klimo P Jr, Ragel BT, Rosner M, et al: Can surgery improve neurological function in penetrating spinal injury? A review of the military and civilian literature and treatment recommendations for military neurosurgeons. Neurosurg Focus 28:E4, 2010. 6. Ragucci MV, Gittler MM, Balfanz-Vertiz K, et al: Societal risk factors associated with spinal cord injury secondary to gunshot wound. Arch Phys Med Rehabil 82:1720–1723, 2001. 7. Blair JA, Patzkowski JC, Schoenfeld AJ, et al: Are spine injuries sustained in battle truly different? Spine J 12(9):824–829, 2012. 8. Blair JA, Possley DR, Petfield JL, et al: Military penetrating spine injuries compared with blunt. Spine J 12(9):762–768, 2012.

9. Bono CM, Heary RF: Gunshot wounds to the spine. Spine J 4:230–240, 2004. 10. Kumar A, Wood GW 2nd, Whittle AP: Low-velocity gunshot injuries of the spine with abdominal viscus trauma. J Orthop Trauma 12(7):514–517, 1998. 11. Roffi RP, Waters RL, Adkins RH: Gunshot wounds to the spine associated with a perforated viscus. Spine (Phila Pa 1976) 14(8):808–811, 1989. 12. Wigle RL: Treatment of asymptomatic gunshot injuries to the spine. Am Surg 55:591–595, 1989. 13. Benzel EC, Hadden TA, Coleman JE: Civilian gunshot wounds to the spinal cord and cauda equina. Neurosurgery 20:281–285, 1987. 14. Cybulski GR, Stone JL, Kant R: Outcome of laminectomy for civilian gunshot injuries of the terminal spinal cord and cauda equina: review of 88 cases. Neurosurgery 24:392–397, 1989. 15. Waters RL, Adkins RH: The effects of removal of bullet fragments retained in the spinal canal: a collaborative study by the National Spinal Cord Injury Model Systems. Spine (Phila Pa 1976) 16:934– 939, 1991. 16. Cristante AF, de Souza FI, Barros Filho TE, et al: Lead poisoning by intradiscal firearm bullet: a case report. Spine (Phila Pa 1976) 35:E140–E143, 2010.

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Vertebroplasty and Kyphoplasty SOO YOUNG PARK and YONG-CHUL KIM

Overview Balloon kyphoplasty and vertebroplasty are minimally invasive options for treating painful vertebral compression fractures. These procedures can be performed on an outpatient basis; they can provide successful pain relief, along with a return to activities of daily living immediately after the procedures; and they can stabilize vertebral fractures. In addition, balloon kyphoplasty can reduce spinal deformity by restoring vertebral body height. The incidence of procedure-related complications such as cement leakage is low, especially in balloon kyphoplasty, whereas pain relief has been reported in more than 90% of patients. The medical cost of kyphoplasty is higher than that of vertebroplasty. Most patients (88%) who require vertebroplasty or kyphoplasty may also have facet joint pain adjacent to the corresponding affected vertebrae. Supplementary facet joint injections or medial branch blocks could, therefore, improve the level of pain relief in such cases. If the duration of nerve blocks is temporary, radiofrequency thermocoagulation of the corresponding medial branches will be required for long-term pain relief.

Treatment Objectives The treatment objectives of kyphoplasty or vertebroplasty are pain relief and early return to function. In cases of kyphoplasty, restoration of the anatomy could be achieved by reducing and stabilizing the fracture, restoring vertebral height, and diminishing the spinal deformity.

Indications Kyphoplasty or vertebroplasty is performed in patients who have recent vertebral fractures as a result of osteoporosis, angioma, myeloma, metastasis, and so on and who have pain refractory to conservative treatment, which includes bed rest, physical therapy, and medications. The best results are obtained when the vertebral collapse has occurred recently; that is, within 3 months of the patient’s seeking medical attention.1-3

Contraindications Contraindications to kyphoplasty and vertebroplasty may be absolute or relative.1-4 Absolute contraindications are as follows: 694

Coagulation disorders Local infection in the proposed site of access (osteomyelitis or spondylodiskitis) ■ Unstable fractures or neoplasms with involvement of the posterior vertebral wall (i.e., complex fractures with or without retropulsed fragments) and accompanying spinal canal compromise ■ Vertebra plana (complete vertebral body collapse) ■ ■

Relative contraindications to the procedure are as follows: Less than one third of the original vertebral body height remains. ■ Pedicles or articular facets are damaged. ■ Tumor invasion into the spinal canal makes any potential leakage of even a small amount of cement into the already compromised canal especially hazardous. ■

Complications Overall incidence of complications with the aforementioned procedures ranges from 0% to 9.8%.5-10 The most common complication is cement extravasation, which may be avoided with the following precautions11: Adequate imaging with high-quality digital fluoroscopy, adequate cement opacification with sterile barium, and injection of cement that is not too liquefied can all prevent leakage. ■ Filling the void with thick, toothpastelike cement under low injection pressure in kyphoplasty yields less cement leakage than filling the interstices of a fractured vertebra with thin, less viscous cement via a high-pressure injection, as is done in vertebroplasty. ■

Other rare complications are as follows: Pneumothorax and rib fracture during thoracic kyphoplasty ■ Pulmonary embolism ■ Bleeding or spinal epidural hematoma ■ Radiculopathy ■ Paraplegia ■ Infection ■ Cerebrospinal fluid leakage ■ Transient acute respiratory distress syndrome ■

Preoperative Preparation The physician should obtain a description of the symptoms from the patient, which may include complaints of motion

71  •  Vertebroplasty and Kyphoplasty

limitation and varying degrees of local pain with or without radiation around the trunk and farther anteriorly. Physical examination at the level of the recent fracture reveals corresponding tenderness upon deep palpation and pain provoked by percussion. The imaging diagnosis would include the following: Plain spine anteroposterior (AP) and lateral films ■ Computed tomography (CT) scan with or without threedimensional imaging to assess details of the bony architecture in cases of suspicion of a posterior cortical fracture (Fig. 71-1) ■ Magnetic resonance imaging (MRI) to detect signal change caused by bone edema at the level of a recent fracture (Fig. 71-2, A) ■

A

Bone scan to determine the most recent fracture in patients with multiple fractures (see Fig. 71-2, B)

■

Radiologic Anatomy for Kyphoplasty and Vertebroplasty Radiologic landmarks for kyphoplasty or vertebroplasty should be identified as follows (Fig. 71-3): Pedicles, to define the starting point of the bone access needle on each side ■ Spinous process, to gauge vertebral body rotation ■

B

Figure 71-1  Computed tomography scan with three-dimensional images of a vertebral body fracture from the right (A) and left (B). (Modified from Kim DH, Kim KH, Kim YC: Minimally invasive percutaneous spinal techniques. Philadelphia, 2011, Saunders Elsevier.)

A

B

Figure 71-2  A, T1-weighted sagittal magnetic resonance imaging shows a complete vertebral body collapse (vertebra plana) at T12 and L2. A few fracture fragments at T12 compress the spinal cord anteriorly. B, Bone scan image shows no radiotracer uptake at the T12 and L2 levels, indicating chronic, rather than acute, fractures at these levels. At the L3 lower vertebral body, a loss of high signal intensity is seen on the T1-weighted image, with high uptake on the bone scan image, indicating an acute pathologic process. Kyphoplasty or vertebroplasty at the T12 and L2 levels is contraindicated, whereas at L3, either procedure is indicated. (Modified from Kim DH, Kim KH, Kim YC: Minimally invasive percutaneous spinal techniques. Philadelphia, 2011, Saunders Elsevier.)

695

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SECTION J  •  Miscellaneous

A

B

C

Figure 71-3  Fluoroscopic images of the lumbar spine. A, On a true anteroposterior (AP) image, the pedicles (dotted circles) should be equidistant from both lateral margins of the corresponding vertebral bodies, and the spinous process should be located at the midline of the width of the vertebral body. B, On an oblique image, the pedicle (dotted circle) should be visualized at its widest and most circular aspects. C, On a true lateral view, the two pedicles should be superimposed. For assessment of the location of the needle tip and its correct trajectory, frequent checks of the AP and lateral views are essential.

Figure 71-4  The instruments used for kyphoplasty. (Modified from Kim DH, Kim KH, Kim YC: Minimally invasive percutaneous spinal techniques. Philadelphia, 2011, Elsevier.)

End plates, to enable planning of a posterior–anterior trajectory ■ Posterior cortical margin, to avoid the anterior margin of the spinal canal ■

Equipment for Vertebroplasty and Kyphoplasty Various devices have been introduced for vertebroplasty and kyphoplasty. All photos in this chapter were obtained from the kits supplied by Kyphon (Sunnyvale, CA; Fig. 71-4).

Procedure INSERTING TOOLS INTO THE FRACTURED VERTEBRAL BODY Three approaches have been introduced to access the vertebral body using a bone access needle: transpedicular, extrapedicular, or unipedicular-posterolateral (Fig. 71-5). The selection of approach depends on fracture configuration and the patient’s anatomy (Table 71-1).

Unipedicular Posterolateral Approach As a result of needle placement in the center of the vertebra, rather than in the anterior quarter, the unipedicular

Figure 71-5  Imaginary approach lines of various techniques for vertebroplasty and kyphoplasty. White arrow denotes transpedicular approach. Blue and red arrows denote extrapedicular and unipedicular posterolateral approaches, respectively. Arrow tips represent the final target points of each approach from where bone cement is injected. A yellow oval represents potential area of cavity made by the inflation of the balloon during kyphoplasty.

Table 71-1  Approach Methods for Percutaneous Vertebroplasty Approaches

Indications

Transpedicular

Most osteoporotic and osteolytic compression fractures Cancer invasion of the pedicle Pedicle screw fixation in place Compression fractures in upper and mid thoracic vertebrae Special cases in which a transpedicular or extrapedicular approach cannot be performed

Extrapedicular

Unipedicular posterolateral

71  •  Vertebroplasty and Kyphoplasty

posterolateral approach could promote leakage directly via the epidural veins to the epidural venous plexus along the anterior aspect of the spinal canal (Fig. 71-6). Also, this approach carries the possibility of transecting the segmental artery, or even injuring the exiting nerve root, because the needle trajectory potentially endangers the nerve root and segmental artery.12 This approach should only be performed by experienced physicians who have full understanding of radiologic anatomy and extensive experience in transpedicular and extrapedicular approaches.

Transpedicular Approach The transpedicular approach is usually performed in lumbar and lower thoracic vertebrae as follows: 1. To determine the skin entry site for the bone access needle, align the pedicles between the maximally compressed superior and inferior end plates for a true AP fluoroscopic image (Fig. 71-7, A, and 71-8). Next turn the C-arm obliquely, until the pedicle can be visualized at its widest and roundest points (see Fig. 71-7, B). With this view, the skin entry point is at the center of the target pedicle.

Figure 71-6  Imaginary approach line for safe unipedicular vertebroplasty. To prevent leakage of cement into the epidural space, the target point has to be at the anterior one fourth to one third and at the midline of the vertebral body. The skin entry point nearest to the midline will be the extension line from the anterior one fourth through the inner pedicle (red). The farthest skin entry point from the midline is the extension line from the anterior one third through the outer pedicle (blue). In most cases, the skin entry point is between 1.5 and 2.5 times the pedicular distance from the midline in the thoracic or lumbar vertebrae. Three vertical lines parallel the midline of the body, at one, two, and three pedicular distances (green). (Modified from Kim DH, Kim KH, Kim YC: Minimally invasive percutaneous spinal techniques. Philadelphia, 2011, Elsevier.)

A

B

2. After skin infiltration of local anesthetics, a 3-mm skin incision is made. Conscious sedation is the anesthesia of choice for kyphoplasty; we use 50 µg of fentanyl and 30 mg of ketorolac with or without 2 to 3 mg of midazolam intravenously. General anesthesia can be used for very anxious patients. For local anesthesia, an agent such as 2% lidocaine or 0.5% bupivacaine is used. 3. The bone access needle can be advanced through the center of the target pedicle with use of a tunnel vision technique (i.e., the needle is advanced parallel to the fluoroscopic beam) without concern for accidental pedicle and end plate damage (Fig. 71-9). 4. Verification of the needle trajectory is performed as follows: ■ Midpedicular level: When the bone access needle tip is presumed to be located at the midpoint of the pedicular diameter on the lateral view, its location on the AP view should be checked; here it should be central in the pedicle outline. If the tip is located too far laterally, the lateral cortical wall of the pedicle may be damaged, and ballooning of the bone tamp may not be possible. If the tip is located too far medially, the medial cortical wall of the pedicle may be damaged, thereby leading to spinal canal violation (Fig. 71-10). ■ At the level of the posterior surface of vertebral body in a lateral view: If the bone access needle reaches the posterior vertebral cortical margin on the lateral view, it should be just inside the medial border of the pedicle outline on the AP view and then is advanced slightly into the vertebral body. If the needle is placed too far laterally, it may damage the lateral cortical wall of the pedicle, and ballooning of the bone tamp may not be possible. If the needle is placed too far medially, it may result in accidental penetration of the medial cortical wall of the pedicle, thereby leading to spinal canal violation (Fig. 71-11).

Extrapedicular Approach The extrapedicular approach is commonly used in upper and mid thoracic vertebra. In contrast to the transpedicular route, the skin entry point in the extrapedicular approach is more lateral than the pedicle, and the trajectory of the needle is more medially directed. The approach is performed as follows: 1. The skin entry point is lateral to the pedicle, either through the thoracic transverse process or along the transverse process–rib junction (Fig. 71-12).

C

Figure 71-7  Placement of the bone access needle. A, Align the pedicles between the maximally compressed superior and inferior end plates in a true AP image. B, Turn the C-arm obliquely until the pedicle can be visualized at its widest and roundest. C, Lateral image of the vertebral body and pedicles shown for comparison. (Modified from Kim DH, Kim KH, Kim YC: Minimally invasive percutaneous spinal techniques. Philadelphia, 2011, Elsevier.)

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SECTION J  •  Miscellaneous

2. The bone access needle is advanced along the medial border of the rib, until the lateral border of the pedicle is reached on the AP image and the posterior vertebral body margin is reached on the lateral image. The tip should not pass medial to the lateral border of the pedicle on the AP image before the posterior aspect of the vertebral body is seen on the lateral image. 3. After correct needle placement has been confirmed on AP and lateral images, the bone access needle is advanced only about 5 mm beyond this position in kyphoplasty for the next steps of the procedure (Fig. 71-13), whereas in vertebroplasty, the needle is advanced about 5 mm before the anterior margin of vertebral body, and cement filling follows.

PLACING AND INFLATING THE BONE TAMP (BALLOON KYPHOPLASTY) Figure 71-8  Adjustment of C-arm for kyphoplasty or vertebroplasty in an anteroposterior projection. Both pedicles are located between the superior and inferior end plates.

A

The bone tamp is placed (see Fig. 71-13) and inflated (Fig. 71-14) as follows: 1. The bone access needle is exchanged for an Osteo Introducer needle (Medtronic, Memphis, TN) over a guide pin.

B

C

Figure 71-9  Trajectory of the transpedicular approach. A, Anteroposterior (AP) view. B, Lateral view. C, Axial representation. Symbols along the trajectory indicate the position of the bone access needle tip at various depths of insertion: circles show insertion point; squares show point at pedicle–vertebral body junction; triangles show midvertebral body. The needle tip should not pass medial to the medial border of the pedicle on the AP view until it is anterior to the posterior margin of the vertebral body on the lateral view. After penetration of the posterior margin of the vertebral body, the bone access needle is advanced only approximately 5 mm beyond this position. At that time, on the AP view, the tip should be located just medial to the medial border of the pedicle. (Modified from Kim DH, Kim KH, Kim YC: Minimally invasive percutaneous spinal techniques. Philadelphia, 2011, Elsevier.)

A

B

C

Figure 71-10  A, The bone access needle tip should be located at the midpoint of the pedicular diameter (blue line) on the lateral view. B and C, Its location on the anteroposterior view should be verified as central in the pedicle outline. If the tip is located too far laterally (1), the lateral cortical wall of the pedicle may be damaged, and ballooning of the bone tamp may not be possible. If the tip is located too far medially (2), the medial cortical wall of pedicle may be damaged, and thereby spinal canal violation may be anticipated (B and C). (Modified from Kim DH, Kim KH, Kim YC: Minimally invasive percutaneous spinal techniques. Philadelphia, 2011, Elsevier.)

71  •  Vertebroplasty and Kyphoplasty

A

B

C

Figure 71-11  If the bone access needle reaches the posterior vertebral cortical margin on the lateral view (red line), it should be just inside the medial border of the pedicle outline on the anteroposterior view and is then advanced slightly into the vertebral body (A). On the schematic drawing, the black needle shows correct needle placement, when the needle reaches the posterior vertebral cortical margin on the lateral view. The first needle shows a placement of the needle that is too lateral and may damage the lateral cortical wall of the pedicle, and ballooning of the bone tamp may not be possible. The second needle shows a placement that is too medial and that may result in an accidental penetration of the medial cortical wall of the pedicle, thereby violating the spinal canal (B and C). (Modified from Kim DH, Kim KH, Kim YC: Minimally invasive percutaneous spinal techniques. Philadelphia, 2011, Elsevier.)

A

B

C

Figure 71-12  The trajectory of the extrapedicular approach for needle or bone access needle placement. A, Anteroposterior view. B, Lateral view. C, Axial representation. Circles show insertion point; squares show point at pedicle–vertebral body junction; triangles show midvertebral body. (Modified from Kim DH, Kim KH, Kim YC: Minimally invasive percutaneous spinal techniques. Philadelphia, 2011, Elsevier.)

2. The Osteo Introducer needle is positioned near the posterior vertebral body margin, while the working instruments—the precision drill, bone tamp, and bonefiller device—are advanced anteriorly until they are approximately 5 mm from the anterior vertebral body border. Careful observation of the working instruments on a lateral view is very important to avoid accidental penetration of the anterior vertebral body border. 3. The inflatable bone tamp is inflated with liquid contrast media to 50 psi. The allowable balloon pressure in cancellous bone ranges from 70 to 300 psi, and the maximum allowable pressure is 300 psi. The pressure will typically increase until the bone yields, allowing the balloon to expand. As the bone shifts, the pressure in the balloon will gradually decrease.

1. Bone cement with a thick, pastelike consistency can be filled into the vertebral body cavity created by the inflatable bone tamp. As a result of the thicker consistency, the incidence of cement leakage in cases of kyphoplasty is significantly lower than that of vertebroplasty (Fig. 71-15). 2. Injection is continued until the void filling is achieved in kyphoplasty (Fig. 71-16). The incidence of cement leakage is relatively higher in vertebroplasty than in kyphoplasty. Filling is stopped immediately if any extravasation is noted into the surrounding veins, the spinal canal, or the disk space (Fig. 71-17). 3. After completing the injection, the Osteo Introducer needle is removed, and hemostasis is obtained by pressure. 4. The cement filler should be removed once the hardening time for the specific cement used has passed (Table 71-2).

MIXING THE CEMENT AND FILLING THE VOID The mixture of cement to be used (CMW1 bone cement, DePuy, Blackpool, UK) is 15 mL of powdered polymethylmethacrylate (PMMA), 8 to 9 mL of liquid PMMA, and 3 mL of barium sulfate as a guide. The factors related to the cement hardening time include the amount of barium sulfate, quantity of solvent, mixing time, and ambient temperature. Irrespective of the various hardening times for the multitude of cements available, the consistency must always remain constant.

Table 71-2  Sample Hardening Times for Polymethylmethacrylate (PMMA) Formulations* Formulation

Time (Min)

CMW1 Original CMW1 Radiopaque CMW2 CMW3

8 to 9 8 to 9 4.5 to 5 8.5 to 9.5

*Products listed are manufactured by DePuy, Blackpool, UK.

699

700

SECTION J  •  Miscellaneous

A

B

C Lateral border of spinous process

3 mm

D

E

G

H

F

Insert precision drill

I

Figure 71-13  Sequence of procedures for the insertion of the bone tamp. A through C: The bone access needle is exchanged for an Osteo Introducer over a guidewire. D through F: The Osteo Introducer is positioned near the posterior vertebral body margin, while the working instrument is advanced anteriorly, until they are approximately 3 mm from the anterior vertebral body border. G and H, The inflatable bone tamp is positioned after removal of bone filler. I, The inflatable bone tamp is inflated with liquid contrast medium to 50 psi. (Courtesy Medtronic, Memphis, TN.)

A

B

Figure 71-14  Inflating the bone tamp. Fluoroscopy shows the balloon filled with contrast media in lateral (A) and anteroposterior views (B). (Modified from Kim DH, Kim KH, Kim YC: Minimally invasive percutaneous spinal techniques. Philadelphia, 2011, Elsevier.)

71  •  Vertebroplasty and Kyphoplasty

A

B

Figure 71-15  The consistency of bone cement for vertebroplasty (left) and kyphoplasty (right). (Modified from Kim DH, Kim KH, Kim YC: Minimally invasive percutaneous spinal techniques. Philadelphia, 2011, Elsevier.)

A

B

C

D

Figure 71-16  Filling the void. Bone cement with a thick pastelike consistency can be filled into the vertebral body cavity created by the inflatable bone tamp. A, Injection is continued until the void filling is achieved using cement filler (B and C). It is stopped immediately if any leakage is noted into the surrounding veins, the spinal canal, or the disk space (D). (Courtesy Medtronic, Memphis, TN.)

A

B

C

Figure 71-17  Test with contrast medium for leakage into the venous system and epidural space. Before injection of cement, check for leakage into the venous system (A) or into the epidural space (B) on the lateral view. C, Schematic drawing of possible cement leakage if test procedure is omitted. (Modified from Kim DH, Kim KH, Kim YC: Minimally invasive percutaneous spinal techniques. Philadelphia, 2011, Elsevier.)

701

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SECTION J  •  Miscellaneous

Postoperative Management Absolute bed rest with regular monitoring of vital signs is required for 2 hours after the procedure for fixation of PMMA. ■ Most patients can be discharged on the day of surgery. ■ Progressive return to full activities and physical therapy is recommended. ■ Assistive devices, such as canes and walkers, may be useful for patients who have been unable to walk because of their painful vertebral fractures. ■ Postoperative bracing is not applied routinely. ■

A

Potential Adverse Results The potential adverse results of kyphoplasty are as follows: End plate rupture (Fig. 71-18) Uneven inflation of bone tamps (Fig. 71-19) 10 ■ Balloon rupture, which occurs in 20% ■ ■

B

Figure 71-18  A, Superior end plate rupture was identified on lateral fluoroscopy. B, Bone cement was seen to be injected only from the left side. (Modified from Kim DH, Kim KH, Kim YC: Minimally invasive percutaneous spinal techniques. Philadelphia, 2011, Elsevier.)

A

B

Figure 71-19  Uneven inflation of bilateral bone tamps. In many cases the balloons tend to inflate unevenly on the side of the fractured vertebra, which is the upper end plate in this case. Bone cement was seen to have leaked through the upper end plate in lateral (A) and AP (B) views. (Modified from Kim DH, Kim KH, Kim YC: Minimally invasive percutaneous spinal techniques. Philadelphia, 2011, Elsevier.)

71  •  Vertebroplasty and Kyphoplasty

References 1. Kim DH, Kim KH, Kim YC: Minimally invasive percutaneous spinal techniques. Philadelphia, 2011, Saunders Elsevier. 2. Masala S, Fiori R, Massari F, et al: Kyphoplasty: indications, contraindications and technique. Radiol Med 110:97–105, 2005. 3. Spivak JM, Johnson MG: Percutaneous treatment of vertebral body pathology. J Am Acad Orthop Surg 13:6–17, 2005. 4. Peh WCG, Gilula LA, Peck DD: Percutaneous vertebroplasty for severe osteoporotic vertebral body compression fractures. Radiology 223:121–126, 2002. 5. Coumans JV, Reinhardt MK, Lieberman IH: Kyphoplasty for vertebral compression fractures: 1-year clinical outcomes from a prospective study. J Neurosurg Spine 99:44–50, 2003. 6. Dudeney S, Lieberman IH, Reinhardt MK, et al: Kyphoplasty in the treatment of osteolytic vertebral compression fractures as a result of multiple myeloma. J Clin Oncol 20:2382–2387, 2002. 7. Garfin SR, Yuan HA, Reiley MA: New technologies in the spine: kyphoplasty and vertebroplasty for the treatment of painful

osteoporotic compression fractures. Spine (Phila Pa 1976) 26:1511– 1515, 2001. 8. Phillips FM, Ho E, Campbell-Hupp M, et al: Early radiographic and clinical results of balloon kyphoplasty for the treatment of osteoporotic vertebral compression fractures. Spine (Phila Pa 1976) 28:2260– 2267, 2003. 9. Theodorou DJ, Theodorou SJ, Duncan TD, et al: Percutaneous balloon kyphoplasty for the correction of spinal deformity in painful vertebral body compression fractures. Clin Imaging 26:1–5, 2002. 10. Lieberman IH, Dudeney S, Reinhardt MK, et al: Initial outcome and efficacy of kyphoplasty in the treatment of painful osteoporotic vertebral compression fractures. Spine (Phila Pa 1976) 26:1631–1638, 2001. 11. Phillips FM, Wetzel T, Lieberman I, et al: An in vivo comparison of the potential for extravertebral cement leak after vertebroplasty and kyphoplasty. Spine (Phila Pa 1976) 27:2173–2179, 2002. 12. Wong W, Mathis JM: Vertebroplasty and kyphoplasty: techniques for avoiding complications and pitfalls. Neurosurg Focus 18:E2, 2005.

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Bone Graft Harvesting Techniques JEFFREY S. HENN and CURTIS A. DICKMAN

Overview The success of many spinal procedures is determined by successful bone graft fusion. Although instrumentation can provide immediate rigid fixation, ultimately, bone fusion must occur to prevent long-term failure. Whether the person’s own bone is harvested (autograft) or cadaveric allograft is used, the goal is the formation of a living, bony arthrodesis.

Selecting a Bone Graft The type of bone graft used depends on the surgical procedure, the surgeon’s preference, and occasionally the patient’s preference. Autograft may be either cortical, cancellous, or mixed cortical and cancellous. Cortical bone is the strongest form of autograft and is typically used when strong structural support is required, such as fusion after anterior corpectomies.1 Compared with cancellous bone, cortical bone has fewer living cells and less surface area. Autologous cancellous bone provides only 60% of the compressive strength of cortical bone but has very high rates of fusion in appropriate cases.2 Cancellous bone provides the ideal combination of osteogenic, osteoinductive, and osteoconductive properties based on its composition of living cells and bone matrix proteins and its inherent architecture.1 Typically, pure cancellous bone is used for posterior spinal fusions, which do not require the graft to withstand compressive forces.1 Cortical-cancellous autografts are composed of both types of bone and offer the advantages of each. The grafts are stronger than cancellous bone, and they retain many of its advantages. A common example of cortical–cancellous bone is a tricortical iliac crest graft. Although autograft remains the gold standard for successful formation of long-term arthrodesis, there are associated drawbacks. Complications associated with graft harvest can range from additional postoperative pain to more significant problems. The quality and quantity of autograft are sometimes inadequate. One alternative is cadaveric allograft. Unlike autograft—which is live, nonreactive, and genetically identical to the host—allograft is nonliving bone. Compared with autograft, allograft becomes vascularized more slowly. The rate of bone fusion is also slower, and the risks of bone resorption, rejection, and infection are higher. However, the distinct advantage of allograft over autograft is the lack of complications associated with harvesting. Similarly, a relatively new category of 704

bone graft extenders may lead to successful fusion, despite not relying primarily on autograft or allograft.

Techniques of Bone Graft Harvest Regardless of the type of bone graft, the chances of successful arthrodesis can be improved with meticulous surgical technique and adequate preparation of the bone graft and surfaces for spinal fusion.3 Combination of this care and preparation with rigid internal fixation optimizes the likelihood of long-term fusion. In general, local trauma to tissue should be minimized to ensure maximum vascularity of the fusion site. Avoidance of monopolar coagulation and use of copious irrigation during drilling can minimize the risk of thermal injury to the bone. Periosteum and other soft tissue should be meticulously removed from the bone graft and fusion bed, because it can lead to a fibrous interface and nonunion. Typically, the fusion site should be decorticated to improve the chances of successful fusion. The bone graft should be shaped to fit precisely into the fusion site to maximize the surface area of bone-to-bone contact. In addition, space within the fusion bed should be eliminated, and all antiinflammatory medications should be avoided during the perioperative and postoperative period.

ANTERIOR ILIAC CREST GRAFTS Historically, bone graft harvested from the anterior iliac crest was commonly used for anterior cervical spine procedures that required cortical–cancellous bone. This particular indication is less common because of the recognition that fusion rates are high with allograft. However, anterior iliac crest bone may still have a role in anterior cervical fusions in select patients at high risk for nonfusion, and it is still used with some frequency for anterior lumbar fusion procedures. Anterior iliac crest bone is obtained through a linear incision made parallel to the iliac crest and directly over the harvest site. The bone should be harvested from at least 3 cm behind the anterior superior iliac spine to avoid disrupting the ilioinguinal ligament or creating an avulsion fracture (Fig. 72-1). A sandbag can be placed under the ipsilateral buttocks to assist with access to the anterolateral iliac spine. Dissection proceeds through the subcutaneous tissue to the fascial layer. After retractors have been placed, the fascia is opened directly over the iliac crest, and subperiosteal dissection is performed. A fascial cuff and periosteum

72  •  Bone Graft Harvesting Techniques

are left intact for secure closure. To expose a tricortical graft, medial and lateral subperiosteal dissection continues with a periosteal elevator, until adequate bone has been exposed. Dissection along the medial iliac crest must be done with great care. The dissection must remain subperiosteal to avoid inadvertent peritoneal entry or injury to the iliohypogastric, ilioinguinal, or lateral femoral cutaneous nerves (Fig. 72-2).4 Cauterization should be used sparingly to prevent the possibility of nerve injury. After the retractors have been deepened to provide excellent exposure to the tricortical graft, the bone may be harvested using either oscillating saws or osteotomes. If the graft will serve a weight-bearing function, oscillating saws are preferred, because osteotomes can cause microfractures that can weaken the graft. Some surgeons temporarily pack the medial and lateral exposure to avoid injury to the muscle or peritoneal cavity. After the graft has been harvested, bleeding is controlled with bone wax or Gelfoam soaked in thrombin. Drains are rarely needed, and the wound is closed in multiple layers; the periosteal layers and fascial layers are closed with interrupted sutures. Figure 72-1  Bone graft harvested from the anterolateral ilium should remain 2 to 3 cm behind the anterior superior iliac spine to avoid an avulsion fracture. Tricortical bone grafts can be harvested for (A) singlelevel interbody fusions or for (B) multisegment vertebral body reconstructions.

POSTERIOR ILIAC GRAFTS The posterior iliac region can be used to obtain tricortical grafts, cortical matchstick grafts, cortical-cancellous plates, or cancellous bone strips (Fig. 72-3). Bone can be obtained from the iliac crest or in a subcrestal fashion. When a posterior iliac crest tricortical graft is planned, the graft is harvested from the posterior superior iliac spine (PSIS) or lateral to the PSIS to avoid the sacroiliac joint and sciatic

Ilioinguinal nerve

Iliohypogastric nerve Ilioinguinal nerve

Circumflex iliac artery

Bone graft Lateral femoral cutaneous nerve

A

Lateral femoral cutaneous nerve

B

Figure 72-2  A, Fascial and periosteal incisions used for exposure of bone over the anterolateral iliac crest. B, The dissection should remain in a subperiosteal plane, and cautery should be avoided to prevent injury to the ilioinguinal, iliohypogastric, and lateral femoral cutaneous nerves.

705

706

SECTION J  •  Miscellaneous Superior cluneal nerves

Bone graft

Posterior sacroiliac ligaments

Superior gluteal artery and nerve Sciatic nerve

Figure 72-3  A variety of bone graft can be harvested from the posterior ilium. A, Tricortical strut graft. B, Cortical-cancellous plate. C, Cancellous bone strips.

notch.4-6 However, the graft should not be taken more than 8 cm from the iliac spine to avoid the risk of injury to the superior cluneal nerves, which can cause buttock numbness or painful neuromas (Fig. 72-4). Several variations of incision are used. Some surgeons prefer a vertical incision directly over the PSIS. Others prefer a curved skin incision beginning at the PSIS and extending superolaterally. Dissection proceeds through the subcutaneous tissue, and the fascia is opened directly over the iliac crest. Dissection continues medially and laterally in a subperiosteal fashion to avoid injury to the gluteal artery branches, which can cause brisk bleeding. Great care should also be used to avoid dissection in the region of the sciatic notch, where the main trunk of the superior gluteal artery, sciatic nerve, and ureter can be injured. Medial dissection involves stripping off part of the iliacus muscle. Care must be exerted to remain subperiosteal to avoid injury to the ilioinguinal nerve or pelvic contents. Subperiosteal dissection also avoids injury to the ureter, which lies within the retroperitoneal fat pad. Grafts are obtained using a combination of oscillating saw, osteotomes, and bone gouges or curettes. Hemostasis is obtained with bone wax or Gelfoam soaked in thrombin. Drainage is rarely necessary, and the wound is closed in layers; interrupted sutures are used to approximate the periosteal and fascial layers, and a layered closure is critical to avoid herniation of the abdominal contents. If tricortical bone is unnecessary, an alternative technique, known as the subcrestal exposure, can be used to harvest unicortical and cancellous bone. In this case, an incision is centered just lateral to the posterior iliac spine, and dissection proceeds along the posterior surface; the gluteal fascia is detached lateral to the PSIS so that an adequate cuff of connective tissue is left for closure. The

Figure 72-4  Graft taken from the posterior iliac crest should be kept above the line that intersects the posterior superior iliac spine. Care is taken to protect the sacral iliac ligaments medially, the sciatic nerve caudally, the gluteal vessels caudally and submuscularly, the superior cluneal nerves laterally, and the ureter anteriorly.

dissection avoids the sciatic notch, which can easily be palpated. When dissection is adequate, a Taylor retractor can be used to assist with exposure. A window of cortical bone can be removed using straight osteotomes. If additional cancellous bone is required, it can easily be obtained using bone gouges. The inner cortical table should not be breached. Cancellous bone and cortical-cancellous matchsticks are ideal for occipitocervical posterior fusions. After hemostasis has been obtained using bone wax or Gelfoam, the gluteal fascia must be reapproximated to the periosteum to avoid gait disturbances. Again, the wound is closed in layers; meticulous closure of the periosteum and fascial layer prevents abdominal herniation.

ALTERNATIVE AUTOLOGOUS SITES In most cases, the iliac crest is the preferred site for autologous bone graft, but bone can also be harvested from the rib, fibula, and calvarium. Ribs have a relatively thin cortex, are mechanically weak in resisting compressive loads, and provide a relatively small volume of bone. However, they are sometimes a useful alternative, if other sites cannot be used.7-9 Because of their limited mechanical strength, rib grafts should not be used to reconstruct major spinal deformities without the application of a rigid internal fixation device. To harvest a rib graft, a linear incision is made in the skin directly over the rib’s surface (Fig. 72-5). The outer surface of the rib is exposed by incising the overlying muscles and periosteum. Blunt dissection with a Doyen rib dissector is used to detach the intercostal muscles and parietal pleura from the undersurface. Care is taken to avoid injury to the neurovascular bundle, which lies just along the inferior surface of each rib. The ends of the rib grafts are dissected sharply using a rib cutter or oscillating saw. In most cases, we prefer the oscillating saw, because the rib cutter can

72  •  Bone Graft Harvesting Techniques

A

B

C

Figure 72-5  A, The incision exposes a rib along a curved segment. B, A Doyen periosteal elevator is used to dissect the neurovascular bundle and muscle attachment from the rib, remaining extrapleural. C, The rib is cut sharply with a cutting tool.

Figure 72-6  A, Incision to obtain a fibular strut graft. The incision is made parallel to the fibula to expose the middle-third segment of the fibula. B, A nonvascularized graft can be obtained by performing a subperiosteal dissection circumferentially around the desired segment. C, Vascularized graft may be obtained by preserving a muscular cuff around the fibular graft along with the nutrient vessels.

A

crush, splinter, and weaken the ends of the ribs. The remaining bone edges are smoothed and waxed to prevent pleural puncture and to avoid pneumothorax. After hemostasis is obtained, and the wound has been closed in multiple layers, a routine postoperative chest radiograph is obtained to rule out pneumothorax. Fibular grafts are obtained from the middle third of the fibular shafts (Fig. 72-6) to avoid injury to the peroneal

B

C

nerve at the proximal fibular head and to preserve ankle function distally.9-13 Overall, functional consequences are avoided. The incision parallels the fibula over the lateral surface of the middle of the leg. In most cases, a nonvascularized graft is obtained by performing a subperiosteal dissection circumferentially around the desired segment. Fibular graft provides strong, dense cortical bone that is ideal for reconstruction in areas under large loads or stress.

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However, because there is little cancellous bone, fusion may be relatively slow. Occasionally, a vascularized graft is preferred, in which case a muscular cuff is preserved around the fibular graft along with nutrient vessels. The muscles and fascia are dissected from the ends of the fibular surface, and a vascular vessel of the peroneal artery and vein is preserved. The bone is transected proximally and distally to the measured length with a Gigli or oscillating saw. After hemostasis is obtained, the wound is closed in routine fashion using multiple layers. In the case of vascularized grafts placed in the anterior cervical region, the vessels are usually anastomosed with the superior thyroid artery and vein or other accessible vessels. Posteriorly, the graft can be anastomosed to the occipital artery. Vascularized grafts have the advantage of being living tissue; hence they are incorporated rapidly. However, more surgical time and technical expertise is needed for harvesting and placement. Calvarial bone grafts are used for fusions in young children, because the iliac crest and fibula remain nonossified.9,14-17 Alternatives include a full-thickness graft, which can be obtained from the midline occipital bone, or splitthickness grafts, which can be obtained from the parietal bones (Fig. 72-7). In the case of a suboccipital graft, a linear incision is used to expose the suboccipital skull; one or two burr holes are used to expose the dura, and the atlantooccipital membrane is dissected along the edge of the foramen magnum. The bone is removed in standard fashion using a high-speed drill. In the case of split-thickness grafts, a bicoronal or C-shaped incision is made at the vertex to expose a

A

paramedian craniotomy. Midline bone is left intact over the superior sagittal sinus if bilateral craniectomies are needed. A reciprocating saw is used to split the diploic layers of the bone longitudinally, and the top half of each of the grafts is reattached to the skull with miniplates. The split-thickness graft can then be contoured to the desired shape for fusion.

ALLOGRAFT AND FUSION SUPPLEMENTS Although autograft remains the gold standard for arthrodesis, many procedures are performed using cadaveric allograft. For example, fibular allografts are routinely used for anterior cervical arthrodesis.18 Occasionally, fibular, tibial, or femoral strut grafts are used in the thoracolumbar spine. In the case of single-level diskectomies of the cervical spine, autografts and allografts have similar rates of fusion. For multilevel fusions or for fusions in patients who have a history of smoking, autografts have a slightly higher rate of fusion than allografts.19,20 Allografts are procured by bone banks using established standards. Typically, they are harvested in a sterile fashion, processed, and then freeze-dried or processed in a freshfrozen manner. Donors are routinely screened, and serology is tested to minimize the risk of infection. The risk of contracting the human immunodeficiency virus (HIV) through allograft transplantation has been estimated to be less than 1 in 1 million.21 To minimize the risk of immunogenetic reaction, allografts are treated with ethylene oxide, freezing, or freeze-drying.21 This bone must then be reconstituted in sterile saline before being shaped or cut. To optimize the

B

Figure 72-7  Calvarial bone grafts. A, Suboccipital, full-thickness rectangular bone graft is harvested. B, Split-thickness parietal calvarial graft is obtained. A full-thickness bone flap is removed and then divided with a reciprocating saw. The upper layer of the calvarial flap is reattached with miniplates.

72  •  Bone Graft Harvesting Techniques

chance of successful fusion, the hollow center of the allograft may be packed with autograft bone obtained during the surgical decompression. Occasionally, methylmethacrylate (MMA) is used in place of bone grafts or spinal fusion. However, MMA does not lead to bone fusion, because it is not osteoconductive, osteoinductive, or osteogenic. It does provide strength to resist compression, but it routinely fails under tension and must be anchored to the bone. It can also elicit a foreign-body reaction. Consequently, MMA is reserved for patients who are expected to place only minimal mechanical stress on their construct or in those whose life expectancy is short. Several developments have improved the rate of bone fusion, and numerous studies have shown that pulsed electrical or electromagnetic fields promote fusion, especially in long bones.22 Although fewer studies have evaluated the effects of electrical and electromagnetic stimulation in spinal fusion, they also appear to increase fusion rates in the spine.22 However, the technology is expensive, and patient selection is critical, because overall fusion rates are already relatively good. Other contemporary techniques to improve the rates of bone fusion rely on advances in molecular biology. The degree and strength of fusion are enhanced by a variety of osteoconductive proteins known as bone morphogenic proteins (BMPs), which can lead to higher rates of fusion with allograft; in addition, combinations of allograft and BMP have the potential to obviate the need for autologous bone graft.23-27 In fact, recent experience shows excellent fusion rates, even when BMP is used without autograft or allograft.

Conclusion Successful bone fusion is essential in cases of spinal fixation. The odds of having a successful fusion can be improved by handling the tissue gently, preparing the bone graft and fusion bed meticulously, and avoiding all antiinflammatory medication perioperatively and postoperatively. Autograft tends to be associated with a higher rate of fusion than allograft, but the benefits and risks of obtaining autograft must be considered. When it is necessary to harvest autograft, the risk of complications can be minimized by meticulous surgical technique and a thorough understanding of the regional anatomy. New developments in molecular biology are providing additional alternatives.

References 1. Yonemura KS: Bone grafts: types of harvesting and their complications. In Menezes AH, Sonntag VKH, editors: Principles of spinal surgery, New York, 1996, McGraw-Hill, pp 151–156. 2. Brantigan JW, Cunningham BW, Warden K, et al: Compression strength of donor bone for posterior lumbar interbody fusion. Spine (Phila Pa 1976) 18:1213–1221, 1993. 3. Dickman CA: Techniques of bone graft harvesting and spinal fusion. In Dickman CA, Spetzler RF, Sonntag VKH, editors: Surgery of the craniovertebral junction, New York, 1996, Thieme, pp 699–710.

4. Kurz LT, Garfin SR, Booth RE Jr: Harvesting autologous iliac bone grafts. A review of complications and techniques. Spine (Phila Pa 1976) 14:1324–1331, 1989. 5. Coventry MB, Tapper EM: Pelvic instability: a consequence of removing iliac bone for grafting. J Bone Joint Surg Am 54:83–101, 1972. 6. Lichtblau S: Dislocation of the sacro-iliac joint: a complication of bone-grafting. J Bone Joint Surg Am 44:193–198, 1962. 7. Habal MB: Different forms of bone grafts. In Habal MB, Reddi AH, editors: Bone grafts and bone substitutes, Philadelphia, 1992, WB Saunders, pp 6–8. 8. Prolo DJ, Rodrigo JJ: Contemporary bone graft physiology and surgery. Clin Orthop 200:322–342, 1985. 9. Sullivan JA: Bone grafting: sources and methods. In Weinstein SL, editor: The pediatric spine: principles and practice, New York, 1994, Raven, pp 1299–1310. 10. Conley FK, Britt RH, Hanberry JW, et al: Anterior fibular strut graft in neoplastic disease of the cervical spine. J Neurosurg 51:677–684, 1979. 11. Freidberg SR, Gumley GJ, Pfeifer BA, et al: Vascularized fibular graft to replace resected cervical vertebral bodies. Case report. J Neurosurg 71:283–286, 1989. 12. Rossier AB, Hussey RW, Kenzora JE: Anterior fibular interbody fusion in the treatment of cervical spinal cord injuries. Surg Neurol 7:55–60, 1977. 13. Whitecloud TS, LaRocca H: Fibular strut graft in reconstructive surgery of the cervical spine. Spine (Phila Pa 1976) 1:33–43, 1976. 14. Chadduck WM, Boop FA: Use of full-thickness calvarial bone grafts for cervical spinal fusions in pediatric patients. Pediatr Neurosurg 20:107– 112, 1994. 15. Duong DH, Chadduck WM: Reconstruction of the hypoplastic posterior arch of the atlas with calvarial bone grafts for posterior atlantoaxial fusion. Technical report. Neurosurgery 35:1168–1170, 1994. 16. Sagher O, Malik JM, Lee JH, et al: Fusion with occipital bone for atlantoaxial instability. Technical note. Neurosurgery 33:926–929, 1993. 17. Tanaka T, Ninchoji T, Uemura K, et al: Multilevel anterior cervical fusion using skull bone grafts. Case reports. J Neurosurg 76:298–302, 1992. 18. Cloward RB: Gas-sterilized cadaver bone grafts for spinal fusion operations: a simplified bone bank. Spine (Phila Pa 1976) 5:4–10, 1980. 19. Holmes R, Mooney V, Bucholz R, et al: A coralline hydroxyapatite bone graft substitute. Preliminary report. Clin Orthop Relat Res 188:252– 262, 1984. 20. Rish BL, McFadden JT, Penix JO: Anterior cervical fusion using homologous bone grafts: a comparative study. Surg Neurol 5:119–121, 1976. 21. Elder WJ, Adams M, Dickman CA: Bone harvest techniques, supplementation and alternatives. In Batjer HH, Loftus CM, Ondra SL, editors: Textbook of neurological surgery, Philadelphia, 2001, Lippincott Williams & Wilkins. 22. Oishi M, Onesti ST: Electrical bone graft stimulation for spinal fusion: a review. Neurosurgery 47:1041–1055, 2000. 23. Sandhu HS, Kanim LEA, Toth JM, et al: Experimental spinal fusion with recombinant human bone morphogenetic protein-2 without decortication of osseous elements. Spine (Phila Pa 1976) 22:1171– 1180, 1997. 24. Sheehan JP, Kallmes DF, Sheehan JM, et al: Molecular methods of enhancing lumbar spine fusion. Neurosurgery 39:548–554, 1996. 25. Urist MR: Bone transplants and implants. In Urist MR, editor: Fundamentals and clinical bone physiology, Philadelphia, 1980, JB Lippincott, pp 331–368. 26. Urist MR, Dawson E: Intertransverse process fusion with the aid of chemosterilized autolyzed antigen-extracted allogeneic (AAA) bone. Clin Orthop Relat Res 154:97–113, 1981. 27. Urist MR, Mikulski A, Lietze A: Solubilized and insolubilized bone morphogenetic protein. Proc Natl Acad Sci USA 76:1828–1832, 1979.

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Dural Tears VIKAS PATEL, SARAH E. HENRY, ELIZABETH S. ROBINSON, and MICHAEL FINN

Overview In spinal surgery, the occurrence of dural tears, both incidental and nonincidental, is not uncommon. Dural tears are more common with certain spinal procedures, such as revision laminectomy surgery, and they can be encountered incidentally, as with burst fractures and lamina fractures.1 Durotomies are also necessary for the resection of intrathecal lesions and for tethered cord releases. Although an effort has been made to study the frequency with which dural tears occur, there does not seem to be a consensus. In one review of the records, based on operative reports of 641 patients who underwent a decompression of the lumbar spine, 88 (14%) sustained an operative dural tear.2 Other studies have observed dural tear rates of 5.3% for open diskectomies, 17.4% for reoperation of herniated disks, 7.6% during primary lumbar surgery, and 15.9% for revision cases.3,4 Higher incidences may be associated with larger procedures and revision procedures, in ankylosing spondylitis, and with advanced age; the risk for complications in spinal surgery, including dural tear, increases in older patients.3-5 Although finding a durotomy intraoperatively can be a source of frustration and anxiety for the surgeon, it is extremely important to find and treat the tear efficiently. Fortunately, many effective techniques of treatment are available. In this chapter we will describe various methods for diagnosing dural tears, and we will discuss intraoperative and postoperative techniques available for treatment.

Anatomy Review The dura mater is the outermost of the three layers of the meninges that surround the brain and spinal cord and confine cerebrospinal fluid (CSF). The Latin dura mater literally means “tough mother” or “hard mother,” and this layer is so named because of its leathery exterior, and because it serves to protect the other two meningeal layers, the pia mater and the arachnoid mater. The dura is more prone to longitudinal tears, because most of the internal fibers run in a longitudinal direction. The dura extends distally to the S2 segment, envelops the arachnoid mater, and forms a sac filled with CSF (the thecal sac). The spinal cord lies within the subarachnoid space with its terminal portion, the conus medullaris, at the L1–L2 level.6 CSF fills the space over the spinal cord and is reabsorbed into venous sinus blood via arachnoid granulations. About 500 mL of CSF are made 710

per day, and CSF is turned over about three times daily; it flows from the lateral ventricles to the third and fourth ventricles, enters the basal cistern, and continues to the cortical and spinal subarachnoid spaces.7 A dural tear can range in size from a tiny hole invisible to the naked eye to a large defect that requires dural regeneration or patching. Any maneuver performed near the dura puts it at risk for damage. For example, tears can transpire directly during both soft and sharp dissection of soft tissues or during removal of bony material. Most commonly tears occur during dissection with a Kerrison rongeur, but they may also occur as a result of adhesion of dural matter to removed bone, postoperative contact of the dura with a remaining spicule of bone from surgery, or erosion of the dura in chronic stenosis.8 Further, puncture of the thecal sac can occur during medical procedures other than surgery, such as epidural injection or myelography.5 Often, a dural tear does not initially result in serious danger to the patient, but it can produce pain and discomfort until it is treated. Short-term symptoms of unrepaired dural tears may include a moderate to severe positional headache; nausea and vomiting; photophobia; and/or CSF drainage from the wound. There is also greater risk for deep infection. If left untreated or undiagnosed, long-term complications as a result of persistent dural tears and CSF leaks can occur, with the potential for significant morbidity. Specific complications include, but are not limited to, persistent CSF fistula, pseudomeningocele, nerve injury, arachnoiditis with subsequent chronic pain, and in rare cases meningitis. Also, intracranial bleeding and basilar herniation have been reported after dural tears as a result of the change in CSF pressure.

Clinical Diagnosis Frequently, a dural tear is recognized intraoperatively as a visible leak of CSF at the durotomy site. It may be a gush of fluid, or it may be as subtle as blood getting washed off of the dural surface from a pinhole leak. Excessive, clear output through a chest tube or subfascial drain can also be a sign of durotomy. A collapsed thecal sac or excessive epidural bleeding indirectly implies a dural tear intraoperatively.9 If detected, the dural tear should be repaired by the attending surgeon at the time of surgery. If not detected intraoperatively, imaging techniques can assist in diagnosing a dural tear. A magnetic resonance image (MRI), for example, can confirm a diagnosis of pseudomeningocele with the presumption of a dural tear.5

73  •  Dural Tears

Conventionally, a T2-weighted MRI is used to detect extraarachnoid fluid collections. MRI is preferred as a noninvasive imaging technique, however, the interpenetration of fluid and solid compositions of the spine with MRI can make the detection of dural leaks difficult.10 It is also not feasible to directly visualize dural tears smaller than 1 cm using MRI.11 Further, epidural hematoma after a laminectomy procedure is quite common and may be impossible to differentiate from CSF. In contrast, radionucleotide cisternography provides visualization of small leaks; radioactivity outside the subarachnoid space indicates a CSF leak. However, if there is no active leakage at the time of the test, or if the tear is smaller than the image resolution, identification of the leak via cisternography is impossible.12 Additionally, the injection is radioactive and therefore presents undue risk to the patient. Computed tomographic (CT) myelography is another frequently used imaging technique that can identify multiple CSF leaks, is sensitive, and illustrates the relationship of bony structures to extradural CSF collections. In many practices, CT myelography is the modality of choice if a dural tear requires a definitive diagnosis. However, the invasive nature of an injection may result in pial irritation, and the x-rays present a risk of ionizing radiation.10 Complications may also arise from a new CSF leak at the injection site or from infections that can originate at the dural puncture. Proteins are another option for confirming the existence of a dural tear: β-2 transferrin is a protein unique to CSF and inner-ear perilymph; and if in question, immunofixation electrophoresis is an option. The assay takes about 3 hours and requires one to two decontaminated drops of the fluid. Sensitivity of the assay is reported to be near 100%, and specificity is about 95%.13 The high concentration of another protein in CSF, β-trace protein, provides an alternative assay to β-2 transferrin. The β-trace protein assay takes about 20 minutes. A study of 176 samples found a sensitivity of 99% and a specificity of 100% for the β-trace protein assay.14 Unfortunately, many hospital labs do not offer these tests, and sample results may not be available for days.

Conservative and Nonsurgical Treatment of Dural Tears Conservative treatment of a patient should begin with a thorough evaluation. If the patient is suspected to have a CSF leak but is asymptomatic and does not have CSF leakage from the wound, no treatment is immediately necessary, although the patient should continue to be monitored. Postural headache is a common symptom of a dural tear and is believed to occur both because of meningeal irritation and increased CSF leakage as the lumbar fluid pressure increases in the upright position. Thus bed rest is often prescribed after lumbar durotomy. Caffeine is a vasoconstrictor and is therefore often prescribed because of its ability to provide relief to patients with postural headaches. Acetazolamide, a carbonic anhydrase inhibitor, may be used to reduce the normal volume of CSF produced, theoretically allowing the tear to more effortlessly seal itself. Resewing the superficial skin sutures under local anesthetics and with

antibiotic prophylaxis may seal the leak; however, this method has the potential to increase back pressure caused by the CSF.8 Alternatively, products such as Dermabond (Ethicon) can be used as a skin sealant. Overall, the goals of the aforementioned solutions are to reduce CSF leakage, relieve pain, and enable the tear to resolve on its own. However, more substantial, nonsurgical alternatives should be considered if symptoms fail to resolve after conservative treatment. Daily or continuous CSF drainage through a closed subarachnoid catheter in a separate dural site may reduce subarachnoid pressure and facilitate healing of the tear.15 In a study of 107 patients, 94% reported that CSF fistula or pseudomeningocele were cured or prevented by a lumbar subarachnoid drain. Complications were found to occur that included an infection rate of 5% (meningitis, wound infection, and diskitis); CSF overdrainage with nonpermanent neurologic deterioration, headache, nausea, and vomiting in 3% of patients; and temporary nerve root irritation in 14% of patients.16 Because of the risks of subarachnoid drain placement, some physicians recommend that subarachnoid drains should only be used if the leak is persistent and cannot be repaired operatively.2 When used, the lumbar drain is typically set at a height to encourage 10 to 15 mL/hour of drainage. Alternatively, the drain may be set at a height just below the level of the tear to ensure that low pressure is seen at the tear. For example, the drain can be opened at the cervicothoracic junction for cervical tears with the patient sitting in an inclined position. Overdrainage should be carefully guarded against, and frequent neurologic evaluations should be performed on any patient with a lumbar drain. Overdraining may mimic cerebral herniation, with altered mental status, cranial nerve deficits, respiratory anomalies, and papillary abnormalities. In such cases, the drain should be immediately clamped, and the patient should be placed in the Trendelenburg position. In the event of a lumbar tear, lumboperitoneal or ventriculoperitoneal shunting may be considered in refractory cases,17 however, the need for this is extremely rare. An epidural blood patch offers another nonoperative solution. In this approach, blood is withdrawn from the antecubital vein and injected, typically under fluoroscopic or CT guidance, into the epidural space near the fistulous tract.18 Blood-clotting factors form a patch over any holes in the dura to prevent further leakage of CSF while enabling normal healing. Complications of epidural blood patch have been reported that include vertigo, dizziness, ataxia, and tinnitus during injection, as well as a temporary increase in temperature, mild backache and/or stiffness, and transient or residual paresthesia, especially in the legs and toes.19,20 In a study of 118 patients, epidural blood patches successfully relieved headache in 89% of patients with severe headache after lumbar puncture. Of the remaining patients, a second epidural blood patch was performed on 11 patients, and it was successful in 91% for an overall success rate of 97.5%.19 A percutaneous fibrin glue injection is another nonoperative treatment for CSF leaks. A solution of cryoprecipitate is simultaneously injected with a calcium chloride and thrombin solution into the space overlying the CSF leak (Tisseel, Baxter Healthcare, Deerfield, IL; Fig. 73-1). Placement of the fibrin glue aggregate may be established using

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Figure 73-1  An injection of a percutaneous fibrin glue, such as Tisseel (Baxter Healthcare, Deerfield, IL), is another nonoperative treatment for cerebrospinal fluid leaks.

Figure 73-2  Running sutures secure a dural patch.

Figure 73-3  Running sutures mend a dural tear.

CT imaging. Using this procedure on six patients, a group of researchers successfully resolved CSF leaks in 50%; the three patients in whom leaks remained unresolved underwent surgery.21

or lateral tear, can be repaired using an onlay graft with or without a sealant.

Intraoperative Surgical Repair

Suture To suture the dura, small diameter, nonabsorbable sutures are typically used with a tapered needle. Suture materials include:

For tears found intraoperatively, or if nonoperative treatments are unsuccessful in postoperatively discovered tears, surgical treatment is advised. Techniques for surgical repair of dural tears vary based on the size, complexity, and accessibility of the tear. A simple, linear tear is typically repaired with a secure suture closure, using a running or an interrupted technique. A sealant may be added to reinforce the closure and eliminate leaks from the suture holes. A large tear can be patched with a dural substitute alone or in combination with sutures and/or a sealant (Figs. 73-2 and 73-3). A complex, unapproachable tear, such as an anterior

SURGICAL METHODS AND MATERIALS

Nurolon (Ethicon), a braided nylon Gore-Tex, a monofilament of expanded polytetrafluoroethylene (PTFE)9 ■ Prolene (Ethicon), a monofilament of polypropylene ■ Silk (Ethicon) ■ ■

Some surgeons prefer Gore-Tex, because the needle hole is smaller than the suture itself, which decreases the risk of

73  •  Dural Tears

suture hole leaks. Others prefer silk (Fig. 73-4), because fibrin and blood stick to the suture, which ultimately helps to seal the leaks. In a retrospective review, 338 dural tears were successfully repaired with silk sutures and a running, locking stitch; only 1.8% of patients developed a postoperative CSF leak that required surgical repair.4 Prior to attempting repair using sutures, the nerves should be carefully protected and manipulated back into the intradural space. This can be facilitated by allowing some of the CSF to leak out, decreasing intradural pressure. Some surgeons also advocate for irrigation of any hematoma out of the intradural space prior to closure to reduce nerve irritation and possibly reduce arachnoiditis. However, one risk in the dural closure suture process is injury to the nerve root, because it can be difficult for the surgeon to distinguish between the nerve tissue and the dura mater. Therefore, use of an operating microscope is encouraged to minimize this risk. After sutures are placed, a procoagulant such as Floseal (Baxter; Fig. 73-5) or a patch such as DuraGen (Integra LifeSciences, Cincinnati, OH; Fig. 73-6) can be placed over the suture line to help seal the leak.

Dural Substitutes The criteria for an ideal dural substitute varies, but it generally includes that the substitute should: Repair CSF leaks and produce a watertight closure Induce no inflammatory or immunogenic response ■ Cause no adhesion to the spinal cord, brain, meninges, or nerve roots ■ Not increase the risk of infection or bleeding ■ Have mechanical properties similar to native dura ■ Not swell excessively ■ Be easy to utilize, cost-effective, and readily available ■ Be nontoxic, noncarcinogenic, and inert ■ ■

Various types of allografts, autogenous dural substitutes, and synthetic or chemically modified tissues are used as dural substitutes. Some are assessed below. Allografts.  Cadaveric dura mater and fascia lata allografts were eliminated from use in dural tear repair because of the risk of infectious agents, including those that have been linked to Creutzfeldt-Jakob disease. As a result, AlloDerm (LifeCell, Bridgewater, NJ) was developed, an acellular human dermis allograft placed after removal of all of the epidermis and cells that could potentially lead to rejection. It should be noted, however, that each donor is tested for infectious agents to minimize the potential for infection. Advantages of AlloDerm include the following: It is immunologically inert. It does not produce adhesion formation or result in rejection. ■ Because the cellular ultrastructure remains, it enables vascular and cellular ingrowth. ■ It is easy to use. ■ ■

Figure 73-4  Silk sutures are often preferred because fibrin and blood stick to the suture, which helps seal the leaks.

Figure 73-5  After sutures are placed, a procoagulant such as Floseal (Baxter Healthcare, Deerfield, IL) can be placed over the suture line to help seal the leak.

Figure 73-6  A patch, such as DuraGen (Integra LifeSciences, Cincinnati, OH), can also be placed over a suture line to help prevent leaks.

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AlloDerm is convenient when an autograft harvest is impractical.22,23

■

A study used AlloDerm in 200 craniotomies for duraplasty; sutures secured the graft to the dura or cranium. At a minimum follow-up of 1 year, only 3.5% of patients required subsequent surgery, 1.5% developed postoperative CSF leaks, and 2% developed superficial wound infections.23 Autogenous Dural Substitutes.  Fat is a useful autogenous dural substitute, because it is impermeable to water and is believed to cause little scarring. It is recommended for dural tears that are difficult to access or those that cannot be repaired by standard suture techniques.24 Autogenous tissues are a good choice for a dural substitute because they 1) are nontoxic, 2) produce no immunologic reaction, and 3) carry no risk of infection to the patient. However, the addition of a second surgical site makes autografts unpopular. Also, it can be difficult if not impossible to suture the fat in a watertight fashion around the dural defect. A group of researchers used this procedure on 27 patients, using a large sheet of fat from the patient’s subcutaneous layer to cover both the dural tear and all of the exposed dura. Excess fat was tucked into the lateral recess to prevent peripheral CSF leaks, and the fat was tacked to the dura with sutures. Fibrin glue was then spread over the fat and covered with either Surgicel or Gelfoam. This procedure successfully repaired the dural tears in 96.3% of patients.25 Synthetic or Chemically Modified Materials.  Synthetic and chemically modified dural substitutes include expanded polytetrafluoroethylenes (ePTFEs), collagen matrices, and polyglactin derivative grafts. Given that synthetic dural substitutes can differ significantly, the advantages and disadvantages of each vary. In general, synthetic dural substitutes are often preferred, because they easily conform to the desired size and shape; are generally strong, pliable, and convenient; and are less susceptible to irregularities and/or necrosis. However, they can be expensive. In a study of 34 patients, ePTFE with continuous sutures was used to repair the dura mater. Mild CSF accumulation occurred postoperatively in 14.7% of patients, and 17.6% of patients underwent reoperations unrelated to the dural tears between 1 and 15 months after repair, and the strength of the ePTFE sheet was found to be preserved. A thin layer of granulation tissue had formed between the ePTFE sheet and the brain, but no adhesion between the sheet and scalp, subcutaneous tissue, or brain tissue was found.26 Another study reported a postsurgery CSF leak in 20% of patients when ePTFE and sutures were used alone; this rate decreased to 3% when fibrin glue was used in combination with ePTFE and sutures.27 In a study of 83 patients that used ePTFE as a dural substitute, the infection rate was 9.6%.28 Although successful with no immunogenic response and little adhesion to living tissues,26 a watertight closure with ePTFE can be difficult to obtain because of leaks through the suture holes in the ePTFE sheet.27 Examples of collagen matrices and collagen-derivative grafts include DuraGen, Durepair (TEI Biosciences, Boston, MA), and Dura-Guard (Synovis Surgical Innovations, St. Paul, MN). Each may be applied as an onlay or a suturable

graft and is often augmented with a dural sealant; porous collagen grafts with type I collagen fibers provide a matrix that supports neovascularization and fibroblast activity.29 Although each brand of collagen varies in regard to mechanical properties and the success of the repair, in general, collagen-based substitutes are used for four reasons: because they 1) promote fibroblast ingrowth, 2) form well to the application surface, 3) can be applied as an onlay, and 4) usually do not cause adhesion or an immunogenic response. Vicryl Collagen (Ethicon) is a resorbable mesh made of polyglactin 910, a copolymer of glycolide and L-lactide, coated with bovine collagen. In a study that used Vicryl Collagen as a dural substitute in 78 patients, 6.4% developed subcutaneous fluid collection. Four resolved without intervention, and one required a lumboperitoneal shunt. In addition, 5.1% of patients developed infections: two contracted aseptic meningitis, one had a superficial wound infection, and one experienced a severe extradural infection that required graft removal.30 The surgeons liked Vicryl Collagen because it is watertight and biocompatible, it causes minimal adhesion, and it resorbs within 2 months. However, quick resorption may not provide enough time for fibrous ingrowth, especially if an inflammatory reaction destroys the integrity of the barrier.30 Concerns regarding bovine spongiform encephalopathy (BSE), or “mad cow” disease, have led to the removal of Vicryl Collagen from the marketplace in many countries. In addition to the synthetic dural substitutes listed above, many other nonautologous products may be considered for use as dural substitutes: Duraform, a collagen matrix, and Ethisorb Dura Patch, an absorbable material comprising polyglactin 910 and polydioxanone (Codman & Shurtleff, Raynham, MA); DuraMatrix (Stryker, Kalamazoo, MI), a collagen matrix; and Durasis (Cook Biotech, West Lafayette, IN), a porcine small intestinal submucosa.

Dural Sealants Dural sealants are commonly used in dural repair to augment techniques using sutures and/or dural substitutes to create a watertight seal; they are not intended to replace sutures or dural substitutes. A sealant may be used to bond the dural edges, or one may be applied over a dural substitute and the native dura. The surgical area should be as dry as possible, and the CSF leak should be repaired before applying a sealant.9 Commonly used dural sealants include fibrin adhesives and polyethylene glycol (PEG) hydrogel. Human- or bovine-derived fibrin adhesives may be used to augment the repair of dural tears. Mixing a solution of fibrinogen and other clotting factors with calcium chloride and thrombin facilitates the conversion of fibrinogen to fibrin, which adheres to the native tissue. Fibrin sealants may be sprayed, spread in multiple layers, or applied in a single layer using a cannula. A comparison of these three application techniques in an in vitro histologic analysis and a pressure-resistance test found that the spray method was optimal.31 Fibrin dural sealants offer several advantages: they 1) are adhesive to tissue and help to form a watertight seal with a dural substitute or sutures; 2) promote coagulation and invoke minimal inflammation; 3) are pliable and easy to handle, and 4) are readily available.19,32 In addition, an animal model using fibrin glue found that epidural

73  •  Dural Tears

A

B

Figure 73-7  A and B, DuraSeal is an absorbable polyethylene glycol hydrogel sealant that is sprayed on or layered over sutures in dural repair.

scarring and fibrosis were diminished, and the coagulation cascade was promoted.33 A study of 20 patients that used sutures and fibrin glue found that 75% had no symptoms of a CSF leak after repair. One patient (5%) required reoperation because of a stitch loosening; however, there were no serious complications.34 Another study found no statistical difference in the postoperative CSF leak rate when fibrin glue was used to augment various dural repair techniques using sutures—and, at the discretion of the surgeon, a fascial or muscle patch (n = 278, 50.8%)—to repairs in which fibrin glue was not used (n = 269, or 49.2%).35 Concerns regarding fibrin sealants include timing: they take approximately 20 minutes to prepare, 3 to 5 minutes are required after application for optimal adherence, and 2 hours are needed for them to reach “full strength.” Further, they may inhibit bony fusion.35,36 Additionally, communicable disease transmission is a possible consequence of blood-based sealants. DuraSeal (Covidien, Mansfield, MA) is an absorbable PEG hydrogel sealant that is sprayed on or layered over sutures in dural repair (Fig. 73-7). Advantages include that it is biocompatible, nonbiologic (no risk of virus transmission), absorbable, flexible, and adherent to tissue. However, Food and Drug Administration (FDA) approval of DuraSeal cautioned that it should not be applied to confined bony structures where nerves are present, because hydrogel swelling of up to 50% in any direction could result in neural compression.37 DuraSeal was applied after sutures in 111 patients with dural tears who underwent cranial surgery; using one or two applications of the sealant as needed, this method was 100% effective in stopping CSF leaks intraoperatively. However, 4.5% of patients developed a postoperative CSF leak (one incisional and four pseudomeningoceles), and 7.2% of patients developed deep surgical site infections. Another report describes postoperative cervical cord compression induced by DuraSeal,38 and a third lists worsening quadriparesis of a patient after expansion of the hydrogel sealant.39 Although not sealants, Gelfoam and Surgicel have hemostatic properties and are often used with sutures or dural substitutes to increase the success of a dural repair (Fig. 73-8). In a study of 88 patients with dural tears, 97.7%

Figure 73-8  Surgicel is a compressed sponge with hemostatic properties. It is often used with sutures or dural substitutes to increase the success of a dural repair.

were successfully managed with Gelfoam and silk interlocking sutures and a closed-suction subfascial drain in intraoperative primary repair.2 Gelfoam has also been used successfully with fat grafts and fibrin glue.24

Other Dural Tear Surgical Solutions The benefits of using titanium nonpenetrating clips include 1) ease of application, especially in anatomically restricted areas; 2) their nonpenetrating nature, which theoretically minimizes postoperative CSF leaks; and 3) their compatibility with MRI scanning. A study using titanium nonpenetrating clips (Fig. 73-9) in the closure of spinal dura in 58 patients found that 13.8% of patients developed a postoperative CSF leak, and 10.3% developed infections (five superficial and one epidural).40 Concerning the rates of CSF leak and infection, the group’s initial experience with the clip system was that these complications might have been due to a learning curve. In another study of 26 patients who underwent 27 operations over a 20 month period, only one patient required reoperation 13 months after clip placement, and no significant complications were identified in the follow-up period, which ranged from 1 to 24 months.41

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SECTION J  •  Miscellaneous

inclined position. Patients and nurses should be informed that it is okay for the patient to roll from side to side, but the patient may not sit up or raise his or her head in bed. Mobilization should start gradually by first raising the head of the bed for 1 to 2 hours before allowing the patient to stand.

Summary Conservative treatment is the first step if a CSF leak is suspected and the patient is symptomatic after surgery or after a lumbar puncture. This is also the case when surgical repair is not possible. Bed rest, acetazolamide, resewing superficial skin sutures, or Dermabond may reduce CSF flow, relieve pain, and enable the dura to repair itself. ■ More substantial, nonoperative solutions include drainage through a closed subarachnoid catheter or an epidural blood patch. CT-guided percutaneous fibrin glue injection has been found to not have high rates of success. CSF drainage is more commonly used in surgical dural tear treatment to decrease the CSF pressure. ■ If a tear is noted intraoperatively, or if a patient remains symptomatic after nonsurgical solutions, surgical intervention is necessary. In surgical repair, small and easily accessible tears can be repaired with sutures and, as needed, a dural sealant. Sutures, often of Gore-Tex or silk, have been successful in repairing small, simple dural tears alone or with a dural sealant. ■ Fibrin-based sealants have been successfully used, but risk of viral contaminants must be eliminated prior to use. Caution should be taken regarding the maximum amount used, and fibrin-based sealants should be taken with PEG hydrogel sealants, because fibrin-based sealants swell. Cyanoacrylate polymer adhesives should not be used because of toxicity. ■ Large or inaccessible tears may be repaired with the onlay of a dural substitute that may be augmented with sutures and/or a dural sealant as needed. Cadaveric allografts should not be used because of the risk of infectious agents. AlloDerm (an allograft), fat (an autograft), ePTFE sheets, collagen matrices, and polyglactin-based products show promise. However, the techniques to use and the situations in which to best use them are as yet unproven. ■ Further analysis of surgical and nonsurgical treatment plans for dural tears will continue. Experience with dural repair techniques and materials have often been based on small numbers of patients with a high variability in the type and complexity of their tears. ■

Figure 73-9  A titanium nonpenetrating clip system.

Laser tissue welding for dural closure has also been considered for use alone and in combination with traditional suture techniques. Simply put, this method uses laser energy to connect tissues. A study in cadaveric dura mater compared dural closure using only sutures (n = 25) sutures and laser tissue welding (n = 25), or laser tissue welding alone (n = 25). The study found a statistically significant increase in leak pressure and tensile strength in the closures performed with sutures and laser tissue welding. Conversely, laser tissue welding alone provided an immediate leak-free closure that had poor tensile strength. However, using laser tissue welding alone can prove to be useful when space constraints make traditional dural tear suture techniques difficult.42

POSTOPERATIVE SURGICAL REPAIR Following any surgical repair, dural defects should ideally be deemed watertight to the Valsalva maneuver and the reverse Trendelenburg test. Also, it is absolutely imperative that the fascial closure is watertight to create an additional seal. The use of subfascial drains after dural surgical repair is controversial, because such drains may lead to the formation of a cerebellar herniation or durocutaneous fistula, if the dura should leak after repair. However, some physicians advocate using a subfascial drain, because it may allow the fascia and skin to heal. Other physicians consider factors such as the procedure performed, dural tear size, repair quality, tissue quality, and intraoperative blood loss to determine whether a subfascial drain should be used.5 If a drain is used, caution should be taken to prevent overdrainage, which could lead to headache, neurologic changes, subdural hematoma, or herniation.9 Chest tubes and wound VACs should not be placed on suction in the setting of dural tears, because the high pressure has the potential to further damage the torn tissue when the devices are removed. Postoperative bed rest is believed to reduce hydrostatic pressure on the repaired dura to enable faster healing4; however, recommendations for bed rest after surgical repair of a dural tear vary from zero days to early mobilization (24 hours) to several days.2,4,34 Physicians often recommend bed rest positions that will ultimately minimize pressure over the tear. For example, patients with lumbar tears are often advised to lie flat, whereas those suffering from cervical tears may experience less transmural pressure in an

References 1. Espiritu MT, Rhyne A, Darden BV: Dural tears in spine surgery. J Am Acad Orthop Surg 18:537–545, 2010. 2. Wang JC, Bohlman HH, Riew KD: Dural tears secondary to operations on the lumbar spine: management and results after a two-year minimum follow-up of eighty-eight patients. J Bone Joint Surg 80:1728–1732, 1998. 3. Stolke D, Sollmann WP, Seifert V: Intra- and postoperative complications in lumbar disc surgery. Spine (Phila Pa 1976) 14:56–59, 1989. 4. Khan MH, Rihn J, Steele G, et al: Postoperative management protocol for incidental dural tears during degenerative lumbar spine surgery:

73  •  Dural Tears a review of 3,183 consecutive degenerative lumbar cases. Spine (Phila Pa 1976) 31:2609–2613, 2006. 5. Cammisa FP, Jr, Girardi FP, Sangani PK, et al: Incidental durotomy in spine surgery. Spine (Phila Pa 1976) 25:2663–2667, 2000. 6. Modic MT, Masaryk TJ, Ross JS: Magnetic resonance imaging of the spine, Chicago, 1989, Year Book Medical Publishers, p 46. 7. Keenen TL, Antony J, Benson DR: Dural tears associated with lumbar burst fractures. J Orthop Trauma 4:243–245, 1990. 8. Hughes SA, Ozgur BM, German M, et al: Prolonged Jackson-Pratt drainage in the management of lumbar cerebrospinal fluid leaks. Surg Neurol 65:410–414, 2006. 9. Hanna AS, Nassr A, Harrop JS: Traumatic dural tears. In Patel VV, Brown C, Burger EL, editors: Spine trauma surgical techniques, New York, 2010, Springer-Verlag, pp 369–375. 10. Katramados A, Patel SC, Mitsias PD: Non-invasive magnetic resonance myelography in spontaneous intracranial hypotension. Cephalalgia 26:1160–1164, 2006. 11. Lee IS, Kim HJ, Lee JS, et al: Dural tears in spinal burst fractures: predictable MR imaging findings. Am J Neuroradiol 30:142–146, 2009. 12. Ali SA, Cesani F, Zuckermann JA, et al: Spinal-cerebrospinal fluid leak demonstrated by radiopharmaceutical cisternography. Clin Nucl Med 23:152–155, 1998. 13. Skedros DG, Cass SP, Hirsch BE, et al: Sources of error in use of beta-2 transferrin analysis for diagnosing perilymphatic and cerebral spinal fluid leaks. Arch Otolaryngol Head Neck Surg 109:861–864, 1993. 14. Risch L, Lisec I, Jutzi M, et al: Rapid, accurate and non-invasive detection of cerebrospinal fluid leakage using combined determination of beta-trace protein in secretion and serum. Clin Chim Acta 351:169– 176, 2005. 15. Kitchel SH, Eismont FJ, Green BA: Closed subarachnoid drainage for management of cerebrospinal fluid leakage after an operation on the spine. J Bone Joint Surg 71:984–987, 1989. 16. Shapiro SA, Scully T: Closed continuous drainage of cerebrospinal fluid via a lumbar subarachnoid catheter for treatment or prevention of cranial/spinal cerebrospinal fluid fistula. Neurosurgery 30:241– 245, 1992. 17. Aoki N: Lumboperitoneal shunt: clinical applications, complications, and comparison with ventriculoperitoneal shunt. Neurosurgery 26:998–1003, 1990. 18. Bosacco SJ, Gardner MJ, Guille JT: Evaluation and treatment of dural tears in lumbar spine surgery: a review. Clin Orthop Rel Res 389:238– 247, 2001. 19. Abouleish E, Vega S, Blendinger I, et al: Long-term follow-up of epidural blood patch. Anesth Analg 54:459–463, 1975. 20. Brodsky JB: Epidural blood patch: a safe, effective treatment for postlumbar-puncture headaches. Western J Med 129:85–87, 1978. 21. Patel MR, Louie W, Rachlin J: Postoperative cerebrospinal fluid leaks of the lumbosacral spine: management with percutaneous fibrin glue. Am J Neuroradiol 17:495–500, 1996. 22. Warren WL, Medary MB, Dureza CD, et al: Dural repair using acellular human dermis: experience with 200 cases: technique assessment. Neurosurgery 46:1391–1396, 2000. 23. Ophof R, Maltha JC, Von den Hoff JW, et al: Histologic evaluation of skin-derived and collagen-based substrates implanted in palatal wounds. Wound Repair Regen 12:528–538, 2004. 24. Black P: Cerebrospinal fluid leaks following spinal or posterior fossa surgery: use of fat grafts for prevention and repair. Neurosurg Focus 9:e4, 2000.

25. Black P: Cerebrospinal fluid leaks following spinal surgery: use of fat grafts for prevention and repair. J Neurosurg 96:250–252, 2002. 26. Yamagata S, Goto K, Oda Y, et al: Clinical experience with expanded polytetrafluoroethylene sheet used as an artificial dura mater. Neurol Med Chir (Tokyo) 33:582–585, 1993. 27. Nagata K, Kawamoto S, Sashida J, et al: Mesh-and-glue technique to prevent leakage of cerebrospinal fluid after implantation of expanded polytetrafluoroethylene dura substitute. Neurol Med Chir (Tokyo) 39:316–318, 1999. 28. Nakagawa S, Hayashi T, Anegawa S, et al: Postoperative infection after duraplasty with expanded polytetrafluoroethylene sheet. Neurol Med Chir (Tokyo) 43:120–124, 2003. 29. Narotam PK, van Dellen JR, Bhoola KD: A clinicopathological study of collagen sponge as a dural graft in neurosurgery. J Neurosurg 82:406–412, 1995. 30. Van Calenbergh F, Quintens E, Sciot R, et al: The use of Vicryl Collagen as a dura substitute: a clinical review of 78 surgical cases. Acta Neurochir (Wien) 139:120–123, 1997. 31. Sawamura Y, Asaoka K, Terasaka S, et al: Evaluation of application techniques of fibrin sealant to prevent cerebrospinal fluid leakage: a new device for the application of aerosolized fibrin glue. Neurosurgery 44:332–337, 1999. 32. Cain JE, Jr, Dryer RF, Barton BR: Evaluation of dural closure techniques: suture methods, fibrin adhesive sealant, and cyanoacrylate polymer. Spine (Phila Pa 1976) 13:720–725, 1988. 33. Vaquero J, Arias A, Oya S, et al: Effect of fibrin glue on postlaminectomy scar formation. Acta Neurochir (Wien) 120:159–163, 1993. 34. Hodges SD, Humphreys SC, Eck JC, et al: Management of incidental durotomy without mandatory bed rest: a retrospective review of 20 cases. Spine (Phila Pa 1976) 24:2062–2064, 1999. 35. Jankowitz BT, Atteberry DS, Gerszten PC, et al: Effect of fibrin glue on the prevention of persistent cerebral spinal fluid leakage after incidental durotomy during lumbar spinal surgery. Eur Spine J 18:1169– 1174, 2009. 36. Jarzem P, Harvey EJ, Shenker R, et al: The effect of fibrin sealant on spinal fusions using allograft in dogs. Spine (Phila Pa 1976) 21:1307– 1312, 1996. 37. U.S. Food and Drug Administration: Dural Sealant System P040034. 2009. Accessed 2011 November 20 at http://www.fda.gov/ MedicalDevices/ProductsandMedicalProcedures/ DeviceApprovalsandClearances/Recently-ApprovedDevices/ ucm078645.htm. 38. Thavarajah D, De Lacy P, Hussain R, et al: Postoperative cervical cord compression induced by hydrogel (DuraSeal): a possible complication. Spine (Phila Pa 1976) 35:25–26, 2010. 39. Blackburn SL, Smyth MD: Hydrogel-induced cervicomedullary compression after posterior fossa decompression for Chiari malformation. Case report. J Neurosurg 106:302–304, 2007. 40. Timothy J, Hanna SJ, Furtado N, et al: The use of titanium nonpenetrating clips to close the spinal dura. Br J Neurosurg 21:268–271, 2007. 41. Kaufman BA, Matthews AE, Zwienenberg-Lee M, et al: Spinal dural closure with nonpenetrating titanium clips in pediatric neurosurgery. J Neurosurg 6:359–363, 2010. 42. Foyt D, Johnson JP, Kirsch AJ, et al: Dural closure with laser tissue welding. Arch Otolaryngol Head Neck Surg 115:513–518, 1996.

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Index Page numbers followed by “f ” indicate figures and “t” indicate tables.

A

Abdomen, lumbar disk levels with respect to, 376f, 380f Abscess, epidural, 684 Accessory atlantoaxial ligament, 11 Accessory nerve (CN XI), 51f Adjacent-segment disease, after cervical artificial disk replacement, 194–195 Adolescent idiopathic scoliosis, 582–583 closure, 599 decortication/grafting, 599 derotation maneuver, 599 equipment, 592 freehand pedicle screw placement, 595–597 indications/contraindications, 589 Lenke curve types, 587 osteotomies, 595 positioning, 592 postoperative care, 600 reduction techniques, 598 surgical approach, 592–595 Airway compromise, in transoral approach to CVJ, 67 Alar ligaments, 48f paired, 10–11, 18 Alar screws, S2 in iliac fixation, 529–530 indications for, 521 patient positioning, 522 surgical technique, 522 Alignment cervical, following surgery, 161 impact of spinal column trauma, 564 lordotic, 556f sagittal, 562f in degenerative lumbar scoliosis, 615–616 Allografts in cervical corpectomy and fusion, 165–167 as dural substitute, 713–714 harvesting, 708–709 interbody, 228f in anterior lumbar fusion, 442 American Spinal Injury Association Impairment Scale, 634t Anchoring plate, in vertebral body reconstruction, 169f–172f Anderson and D’Alonzo classification, of odontoid fractures, 104f Anderson screw insertion technique, 217 Anesthesia for diskitis and osteomyelitis lumbar, 680 thoracic, 676 for PELD, 417–418 Aneurysmal bone cyst, 629f, 630 Aneurysms, spinal cord, 658 Angiogram nondigital subtraction, 655f vertebral, preoperative, 56 Ankylosing spondylitis, kyphotic deformity, osteotomy correction of, 662–670

Annuloplasty, CT-guided PETA, 305–306 Annulotomy, contralateral, 467f Annulus fibrosus, 123 Anterior approaches to flat back deformity, 607–608 to lumbar spine anterior column surgery, 386 for high-grade slip, 473–474 for scoliosis, 578–579 to lumbosacral junction, 489–493 midline transperitoneal approach, 490–491 retroperitoneal approach, 491–493 to thoracic spine for diskectomy, 284t for scoliosis, 578 to thoracolumbar spine, for scoliosis, 578 to TLJ, transpleural-transdiaphragmatic approach, 348–351 Anterior approaches to cervical spine for basilar invagination advantages and disadvantages, 71 transoral-transpalatopharyngeal approach, 70–71 CCJ high cervical retropharyngeal approach, 38–42 midline approach, 18–20 cervical diskectomy and fusion complications, 138, 153 operative technique, 131–137 endoscopic anatomic considerations, 153–154 controversies, 160 for CVJ rheumatoid arthritis, 89 foraminotomy (Jho), 139–151 indications and contraindications, 154 instruments and equipment, 154–155 surgical preparations and techniques, 155–160 for facet dislocation, 227 foraminoplasty (Jho), 147 instrumentation techniques anatomy review, 182 complications, 186 operative technique, 182–186 for kyphosis complications, 550–551 results, 549–550 surgical technique, 548–549 for ossification of PLL, 234–235 upper cervical spine, for instability after trauma, 114–117 Anterior approaches to CTJ low-cervical approach, 250, 275–277 posterior approach, 276–277 retropharyngeal and retromediastinal space, 250 stabilization techniques, surgical approaches, 274–275 superior mediastinum, 249–250 supraclavicular approach, 251 surgical anatomy, 243–245 thoracic inlet, 249

Anterior approaches to CTJ (Continued) thoracotomy, 276 transmanubrial-transclavicular approach, 251–252 transsternal-transmanubrial approach, 276 transsternal-transthoracic approach, 252–253 Anterior approaches to lumbar spine: retroperitoneal anatomy review, 375–377 contraindications, 378 dissection, 379–381 general indications, 377 for lumbar lesions anterior approach, 400–401 lateral approach, 399–400 operative technique, 378 patient positioning, 378–379 potential complications, 381 Anterior atlantodental interval (AADI), 13–14 Anterior iliac crest grafts, 704–705 Anterior longitudinal ligament, 127 Anterior lumbar interbody fusion advantages of, 450 complications, 458 in degenerative lumbar scoliosis, 618 indications and contraindications, 450–451 mini-open approach biologics, 457 diskectomy, 452–456 exposure, 451–452 interbody implants, 456 plating, 457 vascular dissection, 452 patient selection, 450 postoperative care, 458 Anterior release and fusion for scoliosis approach to segmental vessels, 574 closure, 576 compression between screws, 575 direct vertebral body derotation, 575 disk/vertebra removal, 573–574 equipment, 569 graft placement, 574 incision/exposure endoscopic access, 572 single and double thoracotomy (convex), 571–572 thoracolumbar access (T10-L4), 572–573 upper thoracic access (T1-T4), 571 internal thoracoplasty, 574 lateral decubitus positioning, 569–570 level of fusion, 569 outcomes, 576–577 pleural dissection, 573 preoperative and perioperative considerations, 569 prone positioning, 570–571 relative contraindications, 568–569 relative indications, 568 rib head removal, 574 rod derotation, 575 rod reduction/cantilever, 575

719

720

Index Anterior release and fusion for scoliosis (Continued) screw placement and staples, 574–575 in situ bending, 575–576 Anterior spinal artery, 646 Anterior tubercle, vertebral body, 121 Anterolateral approaches to thoracic spine for decompression and stabilization, 312–313 for diskectomy, 284t, 285 to thoracolumbar fractures, 366–369 Anterolateral transthoracic approaches to thoracic spine, 245–247 complications, 272–273 deep (intrapleural), 267–268 indications and contraindications, 268 operative technique, 268–271 postoperative care, 271 proximal approach, 271–272 superficial (extrapleural), 267 thoracolumbar junction approach, 272 Aorta bifurcations at L4-L5 disk level, 487f in L5-S1 disk space, 454f Apical ligament, 11, 18, 48f Approach surgeon, 391–392 Arnold ligament, 11 Arteriovenous malformations of spinal cord classification, 653 conus, 656, 658 extradural fistulas, 653–654, 657 extradural-intradural, 655, 658 genetics, 653 imaging, 656–657 intradural dorsal fistulas, 654, 657 intradural ventral fistulas, 654–655, 657–658 intramedullary, 655–656, 658 pathophysiology, 656 spinal cord aneurysms, 658 surgical considerations, 657 Arthrodesis concomitant with cervical laminoplasty, 209–210 occipital bolt or inside-out technique, 97 occipital condyle screw, 97–99 occipital plating, 97 occipitocervical wiring, 99–100 Arthroplasty: cervical disk complications and adverse outcomes, 193–195 equipment and operating room setup, 188–189 indications and contraindications, 187–188 operative technique, 189–192 patient positioning, 189 postoperative care, 193 potential disadvantages, 188 preoperative radiology, 188 Articular facet axial, 8f, 9–10 medial, resection of, 471f Artificial disk replacement, cervical, 187–195 Ascending lumbar vein, 377f Asterion, 52 Atlantoaxial complex, 15 Atlantoaxial fixation anterior, with facet screws, 116–117 posterior, 110 transarticular, 111 translaminar, 111–112

Atlantoaxial morphometry, skull base and, 11–14 Atlantoaxial subluxation, 77–78 rotatory, 78 Atlantooccipital joint, 51f, 53f Atlantooccipital joint axis angle, 13 Atlas (C1) anatomy, 5–7, 18f, 30 anterior arch, 61 anterior tubercle of, 43f arch removal, 65 ossification centers, 3f Autogenous dural substitutes, 714 Autografts for cervical corpectomy and fusion, 165–167 harvesting, 137 tricortical iliac crest, 166f Automated registration, 435–436 Axial lumbar interbody fusion anatomy, 506 approach, 509–510 complications, 511–512 indications and contraindications, 506–507 patient preparation and positioning, 507–509 screw placement, 510 technique of diskectomy, 510 two-level technique, 510 Axial rotation at C1-C2, 15 Axillary herniation, 420 Axis (C2) anatomy, 7–10, 19f, 30–31 Grauer type IIB injury, 104f Azygos vein, 300f, 328, 329f

B

Balloon kyphoplasty, 698–699 Barkow ligament, 11 Basilar invagination, 69–75 anterior surgical approaches, 70–71 endoscopic approaches, 74–75 indications for surgical treatment, 70 posterior approaches, 71–74 secondary to dens fracture, 82f Bending angle of Galveston rod, 538f Benign tumors aneurysmal bone cyst, 630 chondromas, 629–630 giant cell tumors, 628–629 hemangioma, 626–628 osteoid osteoma and osteoblastoma, 628 Bilateral Le Fort I maxillotomy, 31–33, 35f Bilateral Le Fort I osteotomy, 34 Biomechanical complications of occipitocervical fusion, 101 Biomechanics of CTJ anatomic considerations, 247–248 instrumentation, 248 of CVJ, occipitoatlantal complex, 14 of lumbosacral junction, 486 of sacrum, 514–515 Biopsy, for spinal metastases, 637 Bipolar forceps, 142 Blood supply to spinal cord, 124 Blunt finger dissection, anterior lumbar spine, 453f Bohlman’s triple-wire technique, interspinous wiring, 219–220 Bolt technique, occipital, 97

Bone access needle, 698f Bone exposure in LTA, 57 Bone graft harvesting allograft and fusion supplements, 708–709 alternative autologous sites, 706–708 anterior iliac crest grafts, 704–705 autograft, 137 bone graft selection, 704 posterior iliac grafts, 705–706 for posterior lumbar interbody fusion, 443f Bone grafts for cervical corpectomy and fusion, 165–167 intervertebral, 132f, 135 for laminoplasty, 238 for lumbar interbody fusion lateral approach, 466–467 posterior approach, 442 transforaminal approach, 446–447 in reconstruction of posterior arch, 208–209 in scoliosis surgery, 599 selection of, 704 supplementation in posterior osteotomy, 667f for vertebral replacement, 178 Bone morphogenetic protein (BMP) in anterior lumbar interbody fusion, 457 combined with allograft, 709 Bone tamp, placing and inflating, 698–699, 700f Bony structures of CCJ, 70f of CVJ atlas (C1), 5–7, 30 axis (C2), 7–10, 30–31 foramen magnum and occipital condyle, 4–5 hypoglossal canal, 54–55 from inside thoracic cavity, 327f of lumbosacral junction, 483–485 of OCJ, 93f of posterolateral lumbar spine, 382–383 Brachiocephalic trunk, 125f Brooks fusion, 114 Bryan disk end plate milling step for, 191f postoperative kyphosis of prosthesis, 194 Bullet migration, in spinal gunshot wounds, 688 Burst fractures, 389 L3, 390f–391f

C

C1-C2 trauma injuries atlantoaxial transarticular fixation, 111 atlantoaxial translaminar fixation, 111–112 atlantoaxial wiring techniques, 114 Halifax clamp fixation, 113–114 lateral mass-pars interarticularis screw fixation, 110–111 lateral mass-pedicle screw fixation, 111 posterior atlantoaxial fixation techniques, 110 posterior fixation and fusion of upper cervical spine, 114 upper cervical spine instability after, anterior approaches, 114–117 C2 pars/pedicle screw technique, for basilar invagination, 73

Index Cage grafts, for transforaminal lumbar interbody fusion, 446–447, 448f Cages in anterior cervical techniques, 185 carbon-fiber, 167, 173f intervertebral, at L5-S1, 472f ROI-A, 458f for vertebral restoration after cervical corpectomy, 165t, 167 Calcified disk herniation, 283f Calvarial bone grafts, 708 Cancellous bone strips, 706f Capillaries of spinal cord, 647 Capsular ligaments, 127 Carbon-fiber cages, 167, 173f C-arm gantry, zero-degree, in LTIF, 463f C-arm-guided percutaneous endoscopic thoracic diskectomy (PETD), 303–305 Carotid artery, 49f thrombosis, after cervical disk arthroplasty, 193 Carotid sheath, 121f, 124–126 Carotid triangle, 129f Caspar pins, 550f Caspar posts, 176f–177f Cauda equina, 384f Cavernous malformations of spinal cord clinical presentation, 650–651 epidemiology, 650 genetics, 650 imaging, 651 outcomes, 653 pathology, 651 surgical considerations, 651 surgical technique dorsally located lesions, 651–652 ventrally located lesions, 652–653 Cement, for kyphoplasty and vertebroplasty, 699, 701f Central arteries, 646–647 Cerebrospinal fluid (CSF) fistula, in spinal gunshot wounds, 687 leak complication of thoracic surgery, 273, 291 identification of, 711 Cervical corpectomy anatomy review, 162–164 complications, 179–181 indications and contraindications, 164 operative technique, 164–179 postoperative care, 179 Cervical disk arthroplasty complications and adverse outcomes, 193–195 equipment and operating room setup, 188–189 indications and contraindications, 187–188 operative technique, 189–192 patient positioning, 189 postoperative care, 193 potential disadvantages, 188 preoperative radiology, 188 Cervical diskectomy and fusion, anterior complications, 138 indications and contraindications, 131 operative technique, 131–137 Cervical diskitis and osteomyelitis approach, 673 débridement and decompression, 673 positioning, 673 reconstruction posterior instrumentation, 675 strut graft without anterior instrumentation, 674

Cervical kyphosis anterior approach complications, 550–551 results, 549–550 surgical technique, 548–549 clinical evaluation, 547–548 clinical presentation, 546–547 combined anteroposterior approach complications, 553 results, 553 surgical technique, 551–553 etiology, 546 posterior approach complications, 554 to osteotomy for ankylosing spondylitis, 663–668 results, 554 surgical technique, 553–554 surgical approaches, 548 Cervical laminoplasty advantages and disadvantages, 204 complications, 211 indications and contraindications, 203–204 operative technique, 204–210 postoperative care, 210–211 types of, 203 Cervical microforaminotomy diagnosis, 196 indications and contraindications, 196–197 Cervical pedicle screw fixation complications, 217 indications and contraindications, 214 operative technique, 214–216 postoperative management, 216–217 Cervical plating, 137 Cervical somites, 2 Cervical spine anterior instrumentation techniques anatomy review, 182 complications, 186 operative technique, 182–186 endoscopic approaches anatomic considerations, 153–154 controversies, 160 indications and contraindications, 154 instruments and equipment, 154–155 surgical preparations and techniques, 155–160 facet dislocation injuries clinical presentation, 222–223 initial management, 225–226 postoperative management, 229–230 radiographic evaluation, 223–225 surgical management, 226–227 surgical technique, 227–229 gunshot wound to, 689f, 691f–693f subaxial cervical triangles, 130 dorsal musculature, 128–130 fascia, 127–128 ligaments, 126–127 neurovascular structures, 124–126 posterior wiring, 219–221 surface anatomy, 120 ventral musculature, 128 vertebral column, 120–124 viscera, 126 upper anterior approaches, for instability after trauma, 114–117 lateral approaches, 50

Cervical spine (Continued) ligamentous complex surrounding, 47–48 posterior approaches, 47–50 for fixation and fusion, 114 technique for anterior approach to, 184 transmaxillary and transmandibular approaches anatomy, 30–31 complications, 36–37 indications and contraindications, 31–33 operative technique, 34–36 transoral approach anatomy, 17–20 indications and contraindications, 21–22 surgical technique, 22–29 Cervical spine disease, 79f Cervical triangles, 129f, 130 Cervicomedullary angle, 13 Cervicomedullary stenosis, 83f Cervicothoracic junction (CTJ) anterior approaches low-cervical, 250 retropharyngeal and retromediastinal space, 250 superior mediastinum, 249–250 supraclavicular, 251 thoracic inlet, 249 transmanubrial-transclavicular, 251–252 transsternal-transthoracic, 252–253 biomechanics, 247–248 posterolateral approaches anatomy, 254–258 costotransversectomy, 261–263 laminectomy, 258–259 lateral extracavitary parascapular extrapleural, 263–266 transpedicular, 259–261 surgical anatomy, 243–245 Chamberlain line, 12t Chance fractures, 389 Chemically modified materials, as dural substitutes, 714 Chest tubes, 369 Chin–brow angle, in ankylosing spondylitis, 663, 664f Chondromas, 629–630 Chondrosarcoma, 625 Chopin plate/Colorado II sacral plate, 522–524 indications for, 522–523 operative equipment, 523 patient positioning, 523–524 surgical technique, 524 Chordomas, 625–626, 627f Chromodiskography, 418 Chyle leak, 272 Chylothorax, 186 Circumflex iliac artery, 705f Clamp fixation, with Halifax clamps, 113–114 Clark stations, 13 Classification systems for lumbar fractures, 389 for sacral fractures, 497–500 of slips, 470 for spinal arteriovenous malformations, 654t for spinal fractures historic review, 365–366 Iowa system and algorithm, 366

721

722

Index Clivus anatomy, 20f superior view, 21f transmaxillary and transmandibular approaches anatomy, 30–31 complications, 36–37 indications and contraindications, 31–33 operative technique, 34–36 Clivus canal angle, 13 Closed reduction, in facet dislocation injury, 225–226 Cobb angle, 569f, 589 Collagen matrices, as dural substitutes, 714 Combined approaches anteroposterior for cervical kyphosis, 551–553 to CTJ, 281 to CVJ, 68f for rheumatoid arthritis, 89 Comminuted fractures, T-type sacral, 503f Common carotid artery, 124f Common iliac arteries, 487 Common iliac vein, 377f Compression fractures, 389 pathologic, 263f Computed tomography (CT) of atlas, 7f of axis vertebra, 9f of CVJ, 6f navigation based on, 436 percutaneous biopsy of chordoma guided by, 623f PETA guided by, 305–306 preoperative for CVJ rheumatoid arthritis, 81f for LTA, 56 showing rib resection, 265f Condylar fossa, 4–5 Continuous type of ossification of PLL, 233f Contralateral distraction, in transforaminal lumbar interbody fusion, 442–445 Conus arteriovenous malformations, 656, 658 Corpectomy cervical anatomy review, 162–164 complications, 179–181 indications and contraindications, 164 operative technique, 164–179 postoperative care, 179 en bloc, by posterior approach, 335–336 of fractured body, 367–368 in LECA, 330–331 in mini-TTA, 360–361 in TES, with anterior approach, 336–337 thoracic, 271 in thorascopic surgery, 297–298 Costal cartilage, splitting, 354 Costocervical trunk, 258f Costotransverse ligaments, 246f Costotransversectomy, 260f, 261–263 for disk herniation, 284t, 287–288 posterolateral approach to ventral spine via, 310–311 Costotransversectomy: thoracic spine, 331–334 exposure of vertebral bodies and spinal cord, 333–334 muscle dissection, 332 positioning and incision, 332 rib resection, 332–333 for thoracic primary and secondary tumors, 319–320 wound closure, 334

Cranial nerves exposure via LTA, 55 palsies, complication of CVJ transoral approach, 91 Cranial settling, 69 Craniocervical junction (CCJ) anatomy, 17–20 far-lateral approach, 51–52 high cervical retropharyngeal approach lateral approach, 42–44 medial (anterior) approach, 38–42 lateral approaches, 50 lateral retropharyngeal approach, 50–51 posterior approaches, anatomy, 47–50 surgical anatomy, 69 ventral pathology, 21 Craniovertebral junction (CVJ) biomechanics atlantoaxial complex, 15 occipitoatlantal complex, 14 bony anatomy, 54–55 cranial nerves, 55 embryology, 2–4 endoscopic approaches endonasal, 60, 63–64 transcervical, 62–63, 66–67 transoral, 61–62, 64–66 far-lateral transcondylar approach complications, 58 indications, 56 operative technique, 56–58 preoperative imaging, 56 muscle layers, 54 rheumatoid arthritis complications, 90–91 diagnosis and evaluation, 77–78 indications and relative contraindications, 78–79 postoperative care, 89–90 surgical approach, 79–89 surgical anatomy bony structures, 4–10 ligamentous and membranous structures, 10–11 neuroradiology, 11–14 ventral, 32f vertebral artery, 55 Cricoid cartilage, 121f Cricothyroid muscle, 244f Cruciate ligaments, 48f Cruciform ligament, 10 Crus of diaphragm identification of insertion point, 352 in mini-TTA, 356f

D

Débridement, in diskitis and osteomyelitis cervical, 673 lumbar, 681 Decompression bony, in midline open lateral diskectomy, 407 in diskitis and osteomyelitis cervical, 673 lumbar, 681 thoracic, 676–679 epidural, posterolateral transpedicular approach, 339–342 foraminal, 270 lateral extracavitary, 265f neural, in management of sacral fractures, 500t odontoid, 86f spinal canal, in mini-TTA, 360–361

Decompression (Continued) spinal cord, via anterior cervical foraminotomy, 147–149 transoral, MRI, 83f Decompression for lumbar lesions anterior approaches, 399–401 complications, 402–403 en bloc spondylectomy, 401–402 posterior approaches, 398–399 preoperative preparation, 397–398 reconstruction, 402 Decompression in thoracic trauma anatomy review, 309–310 complications, 313 indications and contraindications, 310 operative technique anterolateral, 312–313 posterior, 310–312 reconstruction, 313 Decompressive laminectomy complications, 201 indications and contraindications, 196–197 operative technique, 199–201 Decortication, in scoliosis surgery, 599 Deep vein thrombosis, prophylaxis for, 430 Degenerative disk disease, multilevel, corpectomy constructs in, 178f Degenerative lumbar scoliosis anterior and posterior approaches, 618 history and physical examination, 610–611 natural history, 610 nonoperative management, 612–613 operative care preoperative planning, 613–615 risks, 613 sagittal alignment, 615–616 staging, 616–617 radiologic evaluation, 611–612 Degenerative scoliosis, 584–585 Denis classification, of sacral fractures, 498 Dens, 8f anatomy, 7, 18, 47 C2 base of, 63f fracture, basilar invagination secondary to, 82f Derotation in scoliosis surgery, 599 vertebral body, 575 Developmental anomalies of CVJ, 3–4 Diagnostic imaging for dural tears, 710–711 MRI, for thoracic disk herniation, 283 for ossification of PLL, 233–234 of thoracic spine tumors, 316–317 Diaphragm detachment approach to TLJ, 352–353 from insertion to twelfth rib, 354–355 for thoracoscopic surgery, 296 Digastric muscle, 40f–43f, 129f Direct lateral interbody fusion (DLIF), 460f Disk herniation cervical recurrent, 151 treatment with PECD, 160 intervertebral, 227f lumbar extraforaminal, 421–423 far-lateral, 386f migrated, 419 nonmigrated, 418–419 in spinal gunshot wounds, 688 thoracic, 270–271. See also Thoracic microdiskectomy

Index Disk herniation (Continued) anatomic considerations, 282 decompressed central portion, 306f imaging, 283 prevalence and presentation, 282 surgical indications, 283–284 Disk space intervertebral, 134f–135f L5-S1, vessel bifurcations in, 454f removal of material from, 136f Diskectomy: cervical anterior approach, 190–191 instrumentation for, 184 for cervical corpectomy and fusion, 175–177 complications, 138 operative technique, 131–137 PECD preparation for, 156f safety zone for, 154f for posterior cervical microforaminotomy, 198 Diskectomy: lumbar complications, 423–424 indications and contraindications, 416 in lumbar interbody fusion anterior approach, 452–456 lateral approach, 466 posterior approach, 441 transforaminal approach, 446 operative technique anesthesia, 417–418 equipment, 416–417 operating room setup, 417 surgical anatomy interlaminar approach, 416 transforaminal approach, 412–415 surgical technique interlaminar PELD, 419–421 techniques to increase access for herniations, 421–423 transforaminal endoscopy, 418–419 Diskectomy: thoracic anterior approach, 284t anterolateral approach, 284t complications, 291–292 costotransversectomy, 287–288 lateral extracavitary approach, 288–289 in LECA, 330–331 PETD, C-arm-guided, 303–305 posterior approach, 284t posterolateral approach, 284t postoperative course, 291 retropleural approach, 285–287 in thorascopic surgery, 297 transfacet approach, 290–291 transpedicular approach, 289–290 transthoracic approach, 285 Diskitis and osteomyelitis cervical, 673–675 thoracic, 676–679 Docking of tubular retractor, 466 Dorsal approaches to spinal metastases, 637 Dorsal cavernous malformations of spinal cord, 651–652 Dorsal laminectomy, for thoracic diskectomy, 284t Dorsal musculature, 128–130 Dorsal sacral rami, 495f Dorsal triangle, 130 Double iliac screw fixation, with lumbar segmental fixation, 537–539

Downfracture, maxilla, bilateral Le Fort I osteotomy with, 34 Drains lumbar, 430 subarachnoid, 711 subfascial, after dural surgical repair, 716 Drill guide system, K-wires and, 105–106, 107f Drilling devices, for endoscopic surgery, 142 for lateral mass screw fixation, 218–219 DuraGen patch, 713f Dural arteriovenous fistulas, 58f Dural breech, 67 Dural opening, in intradural tumor resection, 640–641 Dural sealants, 714–715 Dural substitutes, 713–714 Dural tears anatomy review, 710 clinical diagnosis, 710–711 complication of thoracic surgery, 273 conservative and nonsurgical treatment, 711–712 fibrin glue for, 90 intraoperative repair, 712–716 postoperative repair, 716 Durotomy after lumbar microdiskectomy, 410 after surgery for lumbar stenosis, 430 Dysesthesia, 423–424

E

Eastern Cooperative Oncology Group Performance Score System, 634t Eggshell procedure, in closing wedge osteotomy, 670f Electromyographic monitoring in LTIF, 464–465 in transpedicular screw placement, 438 Embolization, preoperative, for thoracic tumors, 317–318 Embryology of CVJ developmental anomalies, 3–4 normal, 2–3 Emergency room management, of spinal gunshot wounds, 686–687 En block spondylectomy, for lumbar lesions, 401–402 Enchondroma, 629–630 End plates milling step, for Bryan disk, 191f preparation for cervical corpectomy, 177 for posterior lumbar interbody fusion, 441–442 for transforaminal lumbar interbody fusion, 446 rupture, 702f vertebral body, 120 Endonasal endoscopic approach for basilar invagination, 74–75 to CVJ, 60 preparation and positioning, 63 rationale, 63 surgical procedure, 63–64 Endoscopic access for scoliosis surgery, 572 Endoscopic anterior cervical foraminotomy (Jho) indications for, 140 postoperative management, 149 surgical results, 150 surgical tools and techniques, 140–142

Endoscopic approaches to basilar invagination advantages and disadvantages, 75 endonasal approach, 74–75 to CVJ endonasal, 60, 63–64 transcervical, 62–63, 66–67 transoral, 61–62, 64–66 for rheumatoid arthritis, 89 Endoscopic thoracic diskectomy, posterolateral, 301–306 End-to-end connectors, for CTJ stabilization, 278f Ependymoma, 643f Epidemiology of cavernous malformations of spinal cord, 650 of gunshot wounds to spine, 686 of hemangioblastoma, 648 of ossification of PLL, 232 Epidural abscess, 684 Epidural blood patch, 711 Epidural decompression, posterolateral transpedicular approach, 339–342 Epidural hematoma, 388 Epistropheus, 7 Erector spinae muscle group, 128, 255, 325, 327f, 329f Eustachian tubes, as landmarks in transoral approach to CVJ, 62 Evidence-based decision making, for spondylolisthesis reduction, 470 Ewing sarcoma, 624–625 Exercise, for flat back deformity, 604 Expandable cages, 165t, 167, 174f–175f, 178 after L3 corpectomy, 402f Expanded polytetrafluoroethylenes (ePTFEs), 714 Extended transoral procedures of CVJ, for rheumatoid arthritis, 88–89 Extradural arteriovenous fistulas, 653–654, 657 Extradural indications for LTA, 56 Extradural-intradural arteriovenous malformations, 655, 658 Extraforaminal disk herniation, 421 Extrapedicular approach, to kyphoplasty and vertebroplasty, 697–698 Extrapleural anatomy, 267 Extrapleural-retroperitoneal approach to TLJ diaphragm release from insertion to 12th rib, 354–355 with eleventh rib resection, 353–356 retroperitoneal space dissection, 353–354 vertebral body exposure, 355 wound closure, 355–356 Extrinsic ligaments of CVJ, 10

F

Facet capsule, 384f Facet dislocation injuries clinical presentation, 222–223 initial management, 225–226 postoperative management, 229–230 radiographic evaluation, 223–225 surgical management, 226–227 surgical technique, 227–229 Facet joint lumbar, angles of surface of, 478f vertebral body, 122–123

723

724

Index Facet screw fixation anterior atlantoaxial, 116–117 lumbar anatomy review, 477 closure, 480 contraindications, 478 indications, 477 operative technique, 478–480 Facet wiring technique, 220 Facetectomy, unilateral, in transforaminal lumbar interbody fusion, 442–445 Far-lateral approach to CCJ, 51–52 to lumbar microdiskectomy, transmuscular, 407–410 Far-lateral transcondylar approach (LTA) to CVJ anatomy, 54–55 complications, 58 indications, 56 operative technique, 56–58 preoperative imaging, 56 Fascia cervical, carotid sheath and, 124f investing layer, 127 pretracheal (visceral) layer, 127–128 prevertebral layer, 128 thoracodorsal, 333f Fascial sling, 40f Fibrin glue, 711–712 Fibular graft harvesting, 707–708 Finger sweep, posterior-to-anterior, 464f Fischgold-Metzger line, 13 Fistulas arteriovenous extradural, 653–654, 657 intradural dorsal, 654, 657 intradural ventral, 654–655, 657–658 CSF, in spinal gunshot wounds, 687 Flank approaches to lumbar spine, 377–380, 680f to lumbosacral junction, anterior retroperitoneal approach, 492–493 Flat back deformity anterior surgery, 607–608 clinical presentation, 602–603 conservative management, 604 etiology, 601–602 patient outcomes, 608 pedicle subtraction osteotomy, 606–607 radiographic workup and evaluation, 603–604 Smith-Peterson osteotomy, 604–606 Flexion-extension at C1-C2, 15 Fluoroscopy adjunct to lumbar spine surgery, 392 intraoperative in DLIF, 460f in endoscopic approach to cervical spine, 156f–157f in tubular hemilaminotomy, 429f in transpedicular screw placement, 434 Foramen magnum, 4–5, 19f, 95f Foraminal decompression, thoracic spine, 270 Foraminoplasty anterior cervical (Jho), 147 and oblique pediculotomy, 424f Foraminotomy in cervical laminoplasty, 209, 211f diskectomy and, 134–135 endoscopic anterior cervical (Jho) indications for, 140 postoperative management, 149 surgical results, 150 surgical tools and techniques, 140–142 Fracture-dislocations, 389

Fractures odontoid: screw fixation complications, 109 contraindications, 103 operative technique, 104–106 postoperative care, 106 pathologic compression fractures, 263f thoracolumbar classifications, 365–366 stabilization techniques, 366–372 Fractures: kyphoplasty and vertebroplasty bone tamp procedures, 698–699 cement mixture, 699, 701f complications, 694 extrapedicular approach, 697–698 indications and contraindications, 694 postoperative management, 702 preoperative preparation, 694–695 radiologic anatomy, 695–696 transpedicular approach, 697 unipedicular posterolateral approach, 696–697 Fractures: lumbar adjuncts to surgery, 392 classification, 389 evaluation for surgical approach, 391–392 indications for surgery, 391 intraoperative complications, 395 radiographic evaluation, 389–390 recovery and rehabilitation, 395 surgical approaches, 392–394 surgical procedure, 394–395 Fractures: sacral anatomy, 497 classification, 497–500 complications, 504–505 diagnosis, 497 outcomes, 503–504 surgical management, 500–502 Fragmentectomy, 419 Frankel grading system, for spinal metastases, 634t Freehand technique for pedicle screw placement, 595–597 for transpedicular screw fixation, 433–434 French door laminoplasty, 203, 204f, 210 Fungal infections of spine, 683 Fusion. See also Lumbar interbody fusion atlantoaxial, techniques, 114 cervical complications, 138 evolution of techniques, 168f operative technique, 131–137, 216 cervical corpectomy and anatomy review, 162–164 complications, 179–181 indications and contraindications, 164 operative technique, 164–179 postoperative care, 179 laminectomy and, for ossification of PLL, 234 long, to pelvis, 615 lumbar, low- and high-grade slip treated with, 470–472 occipitothoracic, 557f supplements, 708–709 T2 to pelvis, 617f Fusion bed preparation, for lateral mass screw fixation, 217

G

Gallie fusion, 114 Galveston technique, modified, 537 rod contouring, 537 Ganglion, C2, 53f

Gastrointestinal complications, in retroperitoneal approach to lumbar spine, 381 Gelfoam in dural tear repair, 715 in vertebral body reconstruction, 169f–172f Geniohyoid muscle, 244f Genitofemoral nerve injury, 403 Giant cell tumors, 628–629 Glossotomy for CVJ rheumatoid arthritis, 89 midline, mandibulotomy with, 34–36 Gluteal nerves, 534f, 536f Grafts bone. See Bone grafts complications, in cervical corpectomy and fusion, 180–181 lordotic interbody, 615–616 polyglactin, 714 strut. See Strut grafts Grauer type IIB injury of C2, 104f Greater auricular nerve, 44f Gunshot wounds to spine epidemiology, 686 indications for surgical intervention CSF fistula, 687 lead toxicity, 688 neurologic deficit, 688 spinal instability, 687–688 late complications, 688–689 Louisiana State University–New Orleans experience, 689–692 mechanisms of injury, 686 neurologic evaluation, 687 prehospital and emergency room management, 686–687 radiologic evaluation, 687

H

Halifax clamp fixation, craniocervical, 113–114 Hard palate splitting, 24f Harms cage, 167 Harrington rod distraction, 602f Harris measurements (Harris’s Rule of 12), 14 Head stabilization, in posterior approaches to CCJ, 48 Hemangioblastoma epidemiology, 648 genetics, 647–648 imaging, 648–649 outcomes, 650 pathology, 648 surgical considerations, 649 surgical technique, 649–650 Hemangioma, 626–628 Hematoma epidural, 388 postoperative, after surgery for lumbar stenosis, 430–431 Hemilaminectomy, for lumbar stenosis, 427 Hemilaminotomy, for lumbar stenosis tubular, 428–429 unilateral, 427 Hemipalatal flap, 36 Hemostasis, in intradural tumor resection, 643–644 Herniation. See Disk herniation Heterotopic ossification, after cervical disk arthroplasty, 194 High-grade slip anterior surgical technique, 473–474 fusion treatment, 470–472

Index Highly downmigrated herniations, 423 Hinge, lamina, 208f–209f Historical background, for sacral screw fixation, 513–514 Hoarseness, following cervical diskectomy, 138 Holder for endoscope, 141 Hyoid bone, 121f, 244f greater cornu of, 40f–43f Hyperlordosis, in lumbar spine, 556f Hypogastric plexus injury, 403 superior, arrangements of, 443f Hypoglossal canal, 4–5, 54–55, 95f Hypoglossal nerve (CN XII), 40f–43f, 125

I

Iliac crest grafts, anterior, 704–705 Iliac fixation alternative technique, 529–530 closure, 529 complications, 531 connection to construct, 529 equipment, 526 indications, 526 patient positioning and incision, 526–527 postoperative care, 530 screw insertion, 527–529 Iliac grafts, posterior, 705–706 Iliac rod (Galveston), 537f Iliocostalis muscle, 255, 327f, 349f Ilioinguinal nerve, 705f Iliolumbar vessels, 493f Iliosacral plating, posterior, 543 Image-guided navigation, in transpedicular screw placement, 434–438 In situ drilling, in odontoid fracture fixation, 107f Incisions for anterior cervical diskectomy and fusion, 132–133 for anterior release and fusion for scoliosis endoscopic access, 572 single and double thoracotomy, 571–572 thoracolumbar access (T10-L4), 572–573 upper thoracic access (T1-T4), 571 for cervical corpectomy, 175f for cervical disk arthroplasty, 189 for cervical laminoplasty, 205–207 on fourth rib, 338f L-shaped, for LECA, 329f for LTA, 57 for posterior approaches to lumbosacral junction, 494 for Scheuermann kyphosis, 558–559 for transmanubrial approach to CTJ, 251f T-shaped, for costotransversectomy, 333f Indices for atlantoaxial instability, 13–14 Indices for skull base and CVJ on anteroposterior/coronal view, 13 on lateral/sagittal view, 11–13 Infection after posterior lumbar surgery, 388 as complication of axial lumbar interbody fusion, 512 spinal indications and contraindications for surgical management, 672 operative technique, 672–684 in thoracotomy, 272 Inferior (recurrent) laryngeal nerve, 125 Infrahyoid muscle group, 128, 133f

Infraspinatus muscle, 326f Insertion points cannulated screw, for thoracoscopic surgery, 296–297 for lateral mass screw fixation, 217 pedicle screws for scoliosis surgery, 596f for thoracic vertebrae, 279f for transpedicular screw fixation, 433f Inside-out technique, for OCJ fixation, 97 Instability CVJ rheumatoid arthritis related, 80f occipitocervical anatomy of OCJ, 93–94 complications, 100–101 evolution of fixation techniques, 92 operative technique, 96–100 postoperative care, 100 spinal, 151 in spinal gunshot wounds, 687–688 Instrumentation anterior cervical, techniques, 182–186 for cervical endoscopic surgery, 155–160 CTJ, 248 for diskitis and osteomyelitis cervical, 675 thoracic, 679 for endoscopic anterior cervical foraminotomy, 140–142 in infected spine, 673 for laminoplasty for ossification of PLL, 238 for PELD, 416–417 for Scheuermann kyphosis, 559–560 segmental, in L3-L4 DLIF, 461f Interbody allografts, 228f in anterior lumbar fusion, 456 Interbody cage, 185f Interbody grafting, lordotic, 615–616 Intercostal musculature, 257 Intercostal vein, 359f Interlaminar approach to PELD, 416 chromodiskography, 419–421 fragmentectomy, 421 needle insertion, 420–421 Internal auditory canal, 95f Internal iliac arteries, 488 Internal jugular vein, 124f Intersegmental muscles, 382 Interspinous fusion, 114 Interspinous wiring, Bohlman’s triple-wire technique, 219–220 Intertransverse ligaments, 127, 385f Intervertebral disks herniation, 227f of subaxial cervical spine, 123 Intervertebral foramen (IVF), 412, 413f, 414 Intervertebral grafts, 132f, 135 Intradural arteriovenous fistulas dorsal, 654, 657 ventral, 654–655, 657–658 Intradural exposure, in LTA, 57–58 Intradural indications for LTA, 56 Intradural tumor resection approach to intradural-extramedullary tumor, 641–642 intramedullary tumor, 642–643 closure, 644 complications, 645 dural opening, 640–641 equipment, 639 exposure, 639–640 hemostasis, 643–644 indications and contraindications, 639 patient positioning, 639 postoperative care, 644–645

Intradural-extramedullary tumor, 641–642 Intramedullary arteriovenous malformations, 655–656, 658 Intramedullary tumor, 642–643 Intraoperative navigation isocentric fluoroscopic, 436 for lumbar fracture, 392 Intrapleural anatomy, 267–268 Intrinsic ligaments of CVJ, 10 Investing fascia, 124f Iowa algorithm for thoracolumbar fractures, 366 Isler classification of lumbosacral injuries, 500

J

Jackson intrasacral rod technique, 518–521 indications for, 519 patient positioning, 520 surgical technique, 520–521 Jho procedure: endoscopic anterior cervical foraminotomy indications for, 140 postoperative management, 149 surgical results, 150 surgical tools and techniques, 140–142 Jugular foramen, 5 Jugular tubercle, 55f Jugular vein external, 43f internal, 45f Junctional kyphosis, 556f, 562

K

Kerrison rongeurs, 135, 136f, 200f Kittner swabs, 134f Klaus height index, 13 Koenigsberg angle, 12t Kulkarni and Goel’s vertical atlantoaxial index, 13 Kyphoplasty for vertebral fractures cement mixture, 699, 701f complications, 694 extrapedicular approach, 697–698 indications and contraindications, 694 placing and inflating bone tamp, 698–699 postoperative management, 702 preoperative preparation, 694–695 radiologic anatomy, 695–696 transpedicular approach, 697 unipedicular posterolateral approach, 696–697 Kyphosis lumbosacral, 471f postlaminectomy, 201 swan-neck deformity, 280f thoracic, 486f degree of, 619f Kyphosis: cervical anterior approach complications, 550–551 results, 549–550 surgical technique, 548–549 clinical evaluation, 547–548 clinical presentation, 546–547 combined anteroposterior approach complications, 553 results, 553 surgical technique, 551–553 etiology, 546 posterior approach complications, 554 results, 554 surgical technique, 553–554 surgical approaches, 548

725

726

Index Kyphosis: posttraumatic thoracic correction of, 565–566 impact of spinal column trauma on alignment, 564 normal sagittal balance, 564 osteotomy-associated complications, 566–567 presenting symptoms, 564–565 Kyphosis: Scheuermann bone graft, 561 closure, 561 complications, 562 correction, 560–561 equipment and patient positioning, 558 exposure of vertebra, 559 incision and soft tissue dissection, 559 indications and contraindications, 558 instrumentation, 559–560 location of incision, 558–559 postoperative care, 561 retractor placement, 559 Kyphotic deformity of ankylosing spondylitis, 662–670 of thoracolumbar spine, pedicle subtraction osteotomy for, 668–670

L

Labioglossomandibulotomy, 28f Lag screws, in odontoid fracture fixation, 106, 108f–109f, 117f Lamina, vertebral body, 123 Laminectomy of C7, posterior cervical osteotomy with, 666f decompressive complications, 201 indications and contraindications, 196–197 operative technique, 199–201 dorsal, for thoracic diskectomy, 284t for lumbar fractures, 394f for lumbar lesions, 398 for ossification of PLL, 234 posterior approach to CTJ, 258–259 for posterior lumbar interbody fusion, 441–442 subtotal/total, for lumbar stenosis, 427 thoracic, 310f for primary and secondary tumors, 318–319 Laminofacet junction, creation of trough at, 207f–208f Laminoforaminotomy technique, 216f Laminoplasty cervical advantages and disadvantages, 204 complications, 211 indications and contraindications, 203–204 operative technique, 204–210 postoperative care, 210–211 types of, 203 for ossification of PLL bone graft and instrumentation, 238 incision and soft-tissue dissection, 237 indications and contraindications, 236 open-door technique, 236–238 techniques, 235–236 Laryngeal nerve, 40–41, 164 Lasers, Ho:YAG, 155f, 304f Lateral approaches to CCJ, surgical technique, 50 to thoracic diskectomy costotransversectomy, 287–288 retropleural, 285–287

Lateral extracavitary approach (LECA) corpectomy or diskectomy, 330–331 to CTJ, parascapular extrapleural, 263–266 muscle dissection, 329–330 neural foramen identification, 330 positioning and incision, 329 rib resection, 330 to thoracic decompression, 311 to thoracic diskectomy, 284t, 288–289 to thoracic tumors, 320–321 vertebral body reconstruction, 331 wound closure, 331 Lateral femoral cutaneous nerve, 705f Lateral lumbar interbody fusion complications, 467–468 contraindications, 459–460 extreme, 479f indications, 459 operative technique, 462–467 preoperative planning, 461–462 Lateral mass C1, 6–7 and C2 pars interarticularis, screw fixation, 110–111 and C2 pedicle, screw fixation, 111 vertebral body, 122 Lateral mass screw fixation C3-C7, technique for basilar invagination, 74 complications, 219 for CTJ stabilization, 278 indications, 217 operative technique drilling and screw placement, 218–219 insertion point and trajectory, 217 Lateral mass-lamina junction, creation of trough at, 207f Lateral retroperitoneal approach to lumbar fractures, 393 to lumbar lesions, 399–401 Lateral retropharyngeal approach to CCJ, 42–44, 50–51 Lateral transpedicular/extracavitary approach, to lumbar lesions, 398–399 Lateral transpsoas interbody fusion (LTIF) bailout strategies, 467–468 contraindications, 459–460 indications, 459 operative technique, 462–467 preoperative planning, 461–462 Latissimus dorsi muscle, 245f, 325, 327f, 345f Lauth ligament, 11 Le Fort I maxillotomy, bilateral, 31–33 Le Fort I osteotomy, with palatal split, 34 Lead toxicity, in spinal gunshot wounds, 688 Lenke curve types, 587 Lens cleanser for endoscope, 140–141 Levator scapulae muscle, 254, 326f Level for thoracic diskectomy, 291–292 Ligamenta flava, 127 removal, 445f Ligaments of atlas and axis, 18 of CCJ, 70f of CVJ, 10–11, 30–31 of lumbosacral spine and pelvis, 485f of rib articulation, 257 of subaxial cervical spine, 126–127 surrounding upper cervical spine, 47–48 Ligamentum nuchae, 127 Linea semicircularis, 483 LMNOP system, for spinal metastases, 635–636, 637t

Localized type of ossification of PLL, 233f Longissimus muscle, 255, 264f Longus colli muscle, 43f, 129f, 134 Longus muscle group, 128 Loosening of implant, in ilium, 531 Louisiana State University–New Orleans experience, spinal gunshot wounds, 689–692 Low-cervical approach to CTJ, 250, 275–277 Lower lumbar fractures, posterior approach, 393–394 Lower vertebral transcorporeal approach, anterior cervical foraminotomy (Jho), 145–147, 150 Low-grade slip, fusion treatment, 470–472 LTA. See Far-lateral transcondylar approach (LTA) to CVJ Lumbar diskectomy complications, 423–424 indications and contraindications, 416 operative technique anesthesia, 417–418 equipment, 416–417 operating room setup, 417 surgical anatomy interlaminar approach, 416 transforaminal approach, 412–415 surgical technique interlaminar PELD, 419–421 techniques to increase access for herniations, 421–423 transforaminal endoscopy, 418–419 Lumbar diskitis and osteomyelitis anterior reconstruction, 681 débridement and decompression, 681 exposure, 680–681 positioning and anesthesia, 680 posterior stabilization, 682 Lumbar facet screw fixation anatomy review, 477 closure, 480 contraindications, 478 direct screw placement, open technique, 478 indications, 477 open translaminar technique, 478–479 percutaneous translaminar facet fixation, 479–480 Lumbar fractures adjuncts to surgery, 392 classification, 389 indications for surgery, 391 intraoperative complications, 395 posterior approach to lower fractures, 393–394 to upper fractures, 392–393 radiographic evaluation, 389–390 recovery and rehabilitation, 395 surgical approach, 391–392 surgical procedure, 394–395 types, 389 Lumbar interbody fusion anterior approach advantages of, 450 complications, 458 mini-open approach, 451–458 patient selection, 450 axial approach anatomy, 506 complications, 511–512 indications and contraindications, 506–507 operative technique, 507–510 indications and contraindications, 440

Index Lumbar interbody fusion (Continued) lateral approach complications, 467–468 contraindications, 459–460 extreme, 479f indications, 459 operative technique, 462–467 preoperative planning, 461–462 posterior approach, 441–442 postoperative care, 448 transforaminal procedure, 442–448 Lumbar microdiskectomy anatomy, 405–406 history of, 404 indications, 404–405 midline open lateral approach, 406–407 minimally invasive tubular approach, 410 prospective studies, 404 transmuscular far-lateral approach, 407–410 Lumbar plexus injury, complication of LTIF, 467–468 passing through psoas muscle, 464f Lumbar scoliosis, degenerative anterior and posterior approaches, 618 history and physical examination, 610–611 natural history, 610 nonoperative management, 612–613 operative care preoperative planning, 613–615 risks, 613 sagittal alignment, 615–616 staging, 616–617 radiologic evaluation, 611–612 Lumbar spine approach to scoliosis, 578–579 gunshot wound to, 690f–691f Lenke curve types, 588f lordosis degree of, 612 preoperative radiographs, 616f restoration of, 606f pedicle subtraction osteotomy or kyphotic deformity, 669f transpedicular screw fixation pedicle anatomy, 432 screw insertion techniques, 432–438 Lumbar spine: anterior retroperitoneal approach anatomy review, 375–377 contraindications, 378 dissection, 379–381 general indications, 377 operative technique, 378 patient positioning, 378–379 potential complications, 381 Lumbar spine: osteomyelitis and tumors anterior approaches, 399–401 complications, 402–403 en bloc spondylectomy, 401–402 posterior approaches, 398–399 preoperative preparation, 397–398 reconstruction, 402 Lumbar spine: posterior and posterolateral approaches anatomy, 382–383 closure, 387–388 complications, 388 indications/contraindications, 384 operative technique, 385–387 patient positioning, 384–385 Lumbar stenosis avoidance of complications, 430–431 postoperative regimen, 430 subtotal/total laminectomy, 427

Lumbar stenosis (Continued) symptoms, 426–427 tubular hemilaminotomy, 428–429 unilateral hemilaminotomy/ hemilaminectomy, 427 wound closure, 429–430 Lumbopelvic fixation, 542f Lumbopelvic stabilization, posterior approach, 501–502 Lumbosacral injuries, Isler classification, 500 Lumbosacral junction anterior approach, 489–493 anterior vs. posterior pathology-guided approach, 489 biomechanics, 486 bony anatomy, 483–485 neural anatomy, 488–489 posterior approaches, 493–496 special considerations at, 387 surface anatomy, 483 vascular anatomy, 487–488 Lumbosacral kyphosis, 471f

M

Magerl screw insertion technique, 217 Magnetic resonance imaging (MRI) after transoral decompression, 83f evaluation of facet dislocation injury, 224–225 of lumbar fractures, 390 preoperative for CVJ rheumatoid arthritis, 82f for LTA, 56 Malignant tumors chondrosarcoma, 625 chordoma, 625–626 Ewing sarcoma, 624–625 multiple myeloma and plasmacytoma, 624 osteosarcoma, 625 Mandible positioning, in posterior approach to CCJ, 50 Mandible-splitting procedure, 27–28 Mandibular swing-transcervical, 36 Mandibulotomy median, for CVJ rheumatoid arthritis, 89 with midline glossotomy, 34–36 Mastoid process, 5f, 45f Maxillotomy bilateral Le Fort I, 31–33 open-door, for CVJ rheumatoid arthritis, 88–89 McGregor line, 12t McRae line, 12t Medial retropharyngeal approach to CCJ, 38–42 Mediastinal space, posterior, and neurovascular structure, 328–329 Metastatic disease of thoracic spine, 317 Metastatic tumors of spine clinical presentation, 633 evaluation, 633 management, 633–636 scoring systems for surgical decision making, 634–636 Methylmethacrylate, in place of bone graft, 709 Microdiskectomy lumbar anatomy, 405–406 indications, 404–405 midline open lateral approach, 406–407 minimally invasive tubular approach, 410

Microdiskectomy (Continued) transmuscular far-lateral approach, 407–410 thoracic anterolateral approaches, 285 complications, 291–292 lateral approaches, 285–289 posterolateral approaches, 289–291 postoperative course, 291 Microsurgical anterior cervical foraminotomy, 142–143 Midline open lateral diskectomy, lumbar, 406–407, 408f Midline posterior approach, to lumbosacral junction, 493–495 Midline transperitoneal approach, to lumbosacral junction, 490–491 Minimally invasive approaches cervical microforaminotomy and laminectomy, 197–198 direct lateral, to lumbar spine, 378, 380–381 posterior for lumbopelvic stabilization, 502 for thoracolumbar fractures, 370–372 tubular lumbar microdiskectomy, 410 Mini-open approach, to anterior lumbar interbody fusion, 451–458 Minithoracotomy-transdiaphragmatic approach (mini-TTA) bone grafting, 361 corpectomy and decompression of spinal canal, 360–361 diaphragmatic anatomy, 356–358 equipment and assistance, 363–364 positioning and technique, 358–359 prevertebral dissection and diaphragm detachment, 359–360 vs. thoracoabdominal approach, 361–363 vs. thoracoscopic surgery, 363 whole-lung ventilation, 363 Mixed type of ossification of PLL, 233f Modular cages, 165t, 167, 178 Multifidus muscle, 256 Multiple myeloma, 624 Muscle-splitting tubular dilators, 428f Myelograms, CT, preoperative, 82f

N

Navigation image-guided, in transpedicular screw placement, 434–438 intraoperative, for lumbar fracture, 392 Neck anterior, anatomic relationships, 175f cervical triangles, 130 dorsal musculature, 128–130 fascia, 127–128 ligaments, 126–127 neurovascular structures, 124–126, 163f pain, after laminoplasty, 211 surface anatomy, 120 ventral musculature, 128 vertebral column, 120–124 viscera, 126 Needle insertion angle, for PECD, 153, 159f Nerve palsy, C5, after microforaminotomy, 201 Nerve roots decompressed, 199f lumbar spine, 406 resection, laminectomy and, 338f S1, retraction, 472f sacrificing, at T2, 263f spinal cord, 123–124

727

728

Index Neural anatomy of lumbosacral junction, 488–489 Neural foramen identification of, 330 vertebral body, 121 Neuralgia, rib intercostal, 364 Neurologic complications of anterior cervical diskectomy and fusion, 138 of cervical corpectomy and fusion, 180 of LTA, 58 of occipitocervical fusion, 101 Neurologic deficit, in spinal gunshot wounds, 688 Neurologic evaluation, for spinal gunshot wounds, 687 Neurologic injury, in lumbar fractures, 391 Neuromonitoring adjunct to lumbar spine surgery, 392 in LTIF, 464–465 Neuromuscular scoliosis, 583 Neuroradiology, of CVJ, 11–14 Neurovascular anatomy of anterior sacrum, 516f of craniocervical complex, 31 posterior mediastinal space and, 328–329 of subaxial cervical spine, 124–126 Nonunion of fracture, odontoid, 109 Nucleotome probe, 304f Nucleus pulposus, 123

O

Obliquus capitis muscles, 69 Occipital condyles, 4–5, 52f–53f, 94f Occipital plating, 97 Occipital screw techniques occipital condyle screws, 97–99 posterior, for basilar invagination, 72 Occipital somites, 2 Occipital triangle, 129f Occipital-cervical fusion, for rheumatoid pannus, 85f Occipitoatlantal complex, 14 Occipitoatlantoaxial ligaments, 10 Occipitocervical junction (OCJ) instability anatomic complexities, 93–94 complications, 100–101 evolution of fixation techniques, 92 operative technique approach, 96–97 arthrodesis, 97–100 postoperative care, 100 Occipitocervical wiring, 99–100 Occipitothoracic fusion, 557f Occiput-C5 fusion, 90f Odontoid decompression, 86f Odontoid fractures: screw fixation complications, 109 contraindications, 103 operative technique incision and soft tissue dissection, 104–105 patient positioning, 104 placement of K-wire and drill guide system, 105–106 screw placement, 106 postoperative care, 106 technical variations, 109 Odontoid process. See Dens Odontoidectomy, transoral, 24–25, 27f Odontoid-specific ligaments, 10 Omohyoid muscle, 121f, 129f, 244f Open reduction internal fixation (ORIF), for lumbopelvic stabilization, 502

Open techniques for lumbar facet screw fixation, 478–479 for lumbopelvic stabilization, 501–502 Open-door laminoplasty, 203 for ossification of PLL, 236–238 Open-door maxillotomy, for CVJ rheumatoid arthritis, 88–89 Operating room setup for cervical disk arthroplasty, 188–189 for PELD, 417 for transoral robotic surgery, 65f Oral retractor systems, 71f Os avis, 3–4 Os odontoideum, 3–4 Ossiculum terminale persistens, 3–4 Ossification, heterotopic, 194f Ossification centers of atlas, 3f paired, 4f Ossification of PLL anterior approaches, 234–235 clinical presentation and natural course, 232–233 combined anterior and posterior approaches, 235 complications, 239 epidemiology, 232 laminectomy, 234 laminoplasty, 235–238 pathophysiology, 232 postoperative care, 238–239 radiographic findings, 233–234 Osteoblastoma, 628 Osteochondroma, 629–630 Osteoid osteoma, 628 Osteomyelitis and diskitis cervical, 673–675 lumbar, 680–682 thoracic, 676–679 Osteomyelitis of lumbar spine anterior approaches anterior retroperitoneal approach, 400–401 lateral retroperitoneal approach, 399–400 complications, 402–403 en bloc spondylectomy, 401–402 posterior approaches laminectomy, 398 lateral transpedicular/extracavitary approach, 398–399 preoperative preparation, 397–398 reconstruction, 402 Osteophytectomy in midline transperitoneal approach to lumbosacral junction, 490 in posterior cervical microforaminotomy, 198 Osteosarcoma, 625 Osteotomy for adolescent idiopathic scoliosis, 595 for cervical kyphosis, 552f for correction of kyphotic deformity of ankylosing spondylitis, 662–670 for degenerative lumbar scoliosis, 615 for flat back deformity pedicle subtraction technique, 606–607 Smith-Peterson technique, 604–606 Le Fort I, with palatal split, 34 for Scheuermann kyphosis, 560f for thoracic kyphosis, 565f, 566–567 trap-door, for placement of anterior cage, 261f Otolaryngologic complications, of cervical corpectomy and fusion, 180

P

Pain axial neck, after laminoplasty, 211 in flat back deformity, 602 neuropathic, in spinal gunshot wounds, 688–689 Palatal-splitting approach, 23 in endoscopic transoral approach to CVJ, 61f Le Fort I osteotomies with, 34 Pannus odontoid, rheumatoid arthritis related, 80f rheumatoid and basilar invagination, 88f with cervicomedullary stenosis, 83f Paramedian posterior approach to lumbosacral junction, 495–496 Parascapular region muscles, 254–256 Paraspinal muscles, 383f Parathyroid gland, 124f Paresis, postoperative, 670 Parietal pleura, 269f, 270, 301f Parotid gland, 44f–45f Pars interarticularis, C2, and C1 lateral mass: screw fixation, 110–111 Pathology-guided approach, to lumbosacral junction, 489 Pedicle screw fixation C1 lateral mass-C2 pedicle, 111 in C3-T2 construct, 230f cervical complications, 217 operative technique, 214–216 postoperative management, 216–217 transpedicular pedicle anatomy, 432 techniques of screw insertion, 432–438 Pedicle screws placement axial CT showing, 680f fluoroscopically assisted, 434 freehand, 595–597 in thoracolumbar fracture stabilization, 373f for transforaminal lumbar interbody fusion, 442 posterior approaches to CTJ, 278–279 S1 indications for, 515–516 patient positioning, 517 preoperative planning, 516 surgical approach, 517–518 surgical technique, 518 thoracic insertion points, 279f starting points, 312t Pedicle subtraction osteotomy for flat back deformity, 606–607 for kyphotic deformity of thoracolumbar spine, 668–670 for thoracic kyphosis, 566 Pedicles anatomy C2, 7–9 transverse angulation, 432 vertebral body, 121–122 cutting, in TES, 335 resection, for entrance to vertebral body, 341f Pediculotomy, 335f oblique, foraminoplasty and, 424f Pelvic incidence, 486, 487f, 611f Pelvic tilt, 486, 611f

Index Percutaneous endoscopic cervical diskectomy (PECD) intraoperative views, 158f needle insertion angle, 159f preparation for, 156f safety zone for, 153, 154f Percutaneous endoscopic lumbar diskectomy (PELD) complications, 423–424 indications and contraindications, 416 interlaminar approach, 416 operative technique anesthesia, 417–418 equipment, 416–417 patient positioning, 417 surgical technique increased access for herniations, 421–423 interlaminar, 419–421 transforaminal endoscopy, 418–419 transforaminal approach, 412–415 Percutaneous endoscopic thoracic annuloplasty (PETA), CT-guided, 305–306 Percutaneous endoscopic thoracic diskectomy (PETD), C-arm-guided, 303–305 Percutaneous sacroiliac fixation, 502 Percutaneous translaminar facet fixation, 479–480 Pharyngeal tubercle, 5f Pial arterial plexus, 646 Piriformis muscle, 489f, 534f Pituitary rongeurs, 136f Plates Chopin plate/Colorado II sacral plate, 522–524 designed for cervical laminoplasty, 210f, 212f placement in thorascopic surgery, 298–299 Plating anterior, after cervical corpectomy, 178–179 in anterior lumbar interbody fusion, 457 cervical, 137 contoured, in vertebral body reconstruction, 169f–172f occipital, 97–100 posterior iliosacral, 543 in reconstruction of posterior arch, 208–209 Platysma muscle, 38–40, 128, 133f Polyaxial screw-rod systems, 277 Polymethylmethacrylate (PMMA) sample hardening times, 699t in spinal reconstruction, 341–342 in vertebral body reconstruction, 165t, 167, 169f–172f, 178 Portal placement, for thoracoscopic surgery, 295–296 Posterior and posterolateral approaches to lumbar spine anatomy, 382–383 closure, 387–388 complications, 388 indications/contraindications, 384 operative technique, 385–387 anterior column surgery, 386 special considerations at L5-S1, 387 Wiltse’s approach, 386 patient positioning, 384–385 Posterior approaches to cervical spine atlantoaxial fixation, 110 for basilar invagination, 71–74 advantages and disadvantages, 74 C1 lateral mass screw technique, 72

Posterior approaches to cervical spine (Continued) C1-C2 transarticular screw technique, 72–73 C2 pars/pedicle screw technique, 73 C3-C7 lateral mass screw technique, 74 occipital screw technique, 72 translaminar screw technique, 73–74 CCJ anatomy, 47–48 positioning, 48 surgical technique, 48–50 CVJ, transoral, for rheumatoid arthritis, 89 endoscopic anatomic considerations, 153–154 controversies, 160 indications and contraindications, 154 instruments and equipment, 154–155 surgical preparations and techniques, 155–160 for facet dislocation, 227–229 for fixation and fusion of upper cervical spine, 114 for kyphosis complications, 554 results, 554 surgical technique, 553–554 microforaminotomy complications, 201 indications and contraindications, 196 operative technique, 197 osteotomy, for correction of kyphotic deformity in ankylosing spondylitis, 663–668 wiring of subaxial spine, 219–221 Posterior approaches to CTJ anteroposterior approach, 281 lateral mass screws, 278 pedicle screws, 278–279 posterior stabilization, 276–277 posterior-anterior-posterior approach, 281 translaminar screw, 279–281 Posterior approaches to lumbar spine fractures lower lumbar, 393–394 upper lumbar, 392–393 with anterior column stabilization, 393 high-grade slips, 474 lesions laminectomy, 398 lateral transpedicular/extracavitary approach, 398–399 scoliosis instrumentation, 579–581 lumbar decompression, 579 posterior-only approach, 581–582 Posterior approaches to lumbosacral junction complications, 496 incisions, 494 midline approach, 493–495 paramedian approach, 495–496 posterior positioning, 494 transverse approach, 496 Posterior approaches to thoracic spine for decompression and stabilization, 310–312 for diskectomy, 284t endoscopic procedures, 301–306 TES, 334–337 Posterior atlantodental interval (PADI), 14

Posterior element anatomy, 405–406 mass, compressing spinal cord, 343f resection in TES, 335, 336f for tumor, 342 Posterior iliac grafts, 705–706 Posterior ligamentous complex (PLC), integrity of, 365–366 Posterior longitudinal ligament (PLL), 127, 158f, 159 dissection along anterior dura, 342f opening after diskectomy, 185f ossification complications, 239 pathophysiology, 232 postoperative care, 238–239 radiographic findings, 233–234 surgical options, 234–238 removal for cervical corpectomy, 177–178 Posterior lumbar interbody fusion bone graft, 442 closure and postoperative care, 442 end plate preparation, 441–442 laminectomy, 441 traditional diskectomy, 441 Posterior sacrectomy, 533–536 Posterior spinal artery, 646 Posterior stabilization techniques lumbopelvic, 501–502 ORIF, 502 percutaneous sacroiliac fixation, 502 Posterior superior iliac spine, 528f Posterior thoracic cage, 256–258 Posterior tubercle, vertebral body, 121 Posterolateral approaches to CTJ anatomy muscles of scapular and parascapular region, 254–256 posterior thoracic cage, 256–258 costotransversectomy, 261–263 laminectomy, 258–266 lateral extracavitary parascapular extrapleural, 263–266 transpedicular approach, 259–261 Posterolateral approaches to thoracic spine, 247 for diskectomy, 284t endoscopic procedures, 301–306 transfacet approach, 290–291 transpedicular approach, 289–290 Posterolateral transpedicular approach for spondylectomy, 339–342 for thoracolumbar fractures, 369–370 Postlaminectomy cervical kyphosis, 546 Postoperative imaging of cervical disk arthroplasty, 193 of diskitis/osteomyelitis cervical, 676f thoracic, 679f Posttraumatic thoracic kyphosis correction of, 565–566 impact of spinal column trauma on alignment, 564 normal sagittal balance, 564 osteotomy-associated complications, 566–567 presenting symptoms, 564–565 Powers ratio, 14 Prehospital management, of spinal gunshot wounds, 686–687 Preoperative embolization, for thoracic tumors, 317–318

729

730

Index Preoperative imaging for cervical disk arthroplasty, 188 of cervical kyphosis, 555f of cervical spine, 212f for CVJ rheumatoid arthritis, 81f for LTA, 56 side-bending radiographs of type 5C curve, 594f of thoracic spine tumors, 316–317 Preoperative planning for cervical osteotomy for ankylosing spondylitis, 665f for degenerative lumbar scoliosis, 613–615 for kyphoplasty and vertebroplasty, 694–695 for lateral lumbar interbody fusion, 461–462 for LTIF, 461–462 for S1 pedicle screw technique, 516 for S2 alar screw technique, 522 Presacral vessel injury, as complication of axial lumbar interbody fusion, 512 Pretracheal fascia, 124f Prevertebral dissection, for thoracoscopic surgery, 296 Primary osseous lesions, thoracic, surgical decision making, 317 Primary tumors intradural, extramedullary, 640t, 641–642 intramedullary, 640t, 642–643 Probes, for PETD, 304f Procoagulants, 713f Prophylaxis, for deep vein thrombosis, 430 Prospective studies, lumbar microdiskectomy, 404 Prosthesis, Mobi-C disk, 192f Proximal thoracic spine approach, 271–272 Pseudarthrosis, 562 Psoas muscles, 351f, 353, 359–360, 462f, 489f Pudendal nerve, 488, 534f Pulmonary function decreased, in thoracic surgery, 272 in mini-TTA, 364t

Q

Quadratus lumborum muscle, 493f

R

Radicular arteries, 646 Radiofrequency probe, bipolar flexible, 304f Radiographic evaluation of degenerative lumbar scoliosis, 611–612 of facet dislocation injuries, 223–225 of flat back deformity, 603–604 of lumbar fractures, 389–390 for spinal gunshot wounds, 687 of thoracic spine tumors, 316–317 Radiologic landmarks, for kyphoplasty and vertebroplasty, 695–696 Radionucleotide cisternography, 711 Ranawat criterion, 13 Reconstruction after surgery for lumbar lesions, 402 after thoracic vertebrectomy, 313 in diskitis and osteomyelitis cervical, 674–675 lumbar, 681 thoracic, 676–679 posterior arch, 208–209 vertebral body, 169f–172f, 331 Reconstruction: sacral double iliac screw fixation, 537–539 modified Galveston technique, 537

Reconstruction: sacral (Continued) posterior iliosacral plating, 543 transiliac rod placement, 539–543 triangular frame technique, 539 Rectal injury, with axial lumbar interbody fusion, 511–512 Rectus abdominis muscle, 452f Rectus capitis posterior muscles, 70f Rectus sheath, anterior, 484f Recurrent laryngeal nerve, 125f Redlund-Johnell criterion, 13 Reduction maneuver, formal, for spondylolisthesis, 472–473 Reduction techniques, in scoliosis surgery, 598 Rehabilitation, after lumbar fracture surgery, 395 Retromediastinal space, 250, 257–258 Retroperitoneal approach to lumbar spine anterior approach anatomy review, 375–377 contraindications, 378 dissection, 379–381 general indications, 377 to lumbar lesions, 400–401 operative technique, 378 patient positioning, 378–379 potential complications, 381 lateral approach to fractures, 393 to lumbar lesions, 399–400 Retroperitoneal approach to lumbosacral junction anterior retroperitoneal flank approach, 492–493 anterior retroperitoneal midline approach, 491–492 Retroperitoneal space dissection, 353–354 Retropharyngeal approach to CCJ, high cervical lateral approach, 42–44 medial approach, 38–42 to cervical spine, 184 to pharyngotomy, 36 Retropharyngeal space, 250 Retropleural thoracic diskectomy, 284t, 285–287 Retroversion, pelvic, 612f Rheumatoid arthritis of CVJ complications, 90–91 diagnosis and evaluation atlantoaxial rotatory subluxation, 78 atlantoaxial subluxation, 77–78 indications and relative contraindications, 78–79 postoperative care, 89–90 surgical approach, 79–89 extended transoral procedures, 88–89 preoperative sagittal CT myelogram, 81f transoral, 85–87 Rhomboid muscles, 245f, 254, 264f, 325 Rib resection in costotransversectomy of thoracic spine, 332–333 eleventh rib, in extrapleural-retroperitoneal approach to TLJ, 353–356 in LECA, 330 tenth rib, in transpleuraltransdiaphragmatic approach to TLJ, 348–351 in transthoracic approach to midthoracic level, 344 Ribs articulation, vertebral body and, 256–257 exposure, in anterolateral transthoracic approach, 268–269 graft harvesting, 706–707 head, removal in scoliosis surgery, 574

Ribs (Continued) involvement in thoracic spine tumors, 337–339 osseoligamentous relationship with vertebra, 246f posterior thoracic cage, 326–328 Rigid working-channel scope, 303–305 Rod and wire construct, occipitocervical, 100f Rod technique, Jackson intrasacral, 518–521 Rods contouring in modified Galveston technique, 537 in scoliosis surgery, 598f insertion, in thoracolumbar fracture stabilization, 372 placement, for Scheuermann kyphosis, 560–561 reduction, in scoliosis surgery, 575 tapered, for CTJ stabilization, 278f Rongeurs, Kerrison, 135, 136f, 200f Rotatores muscle group, 256, 325–326 Roy-Camille screw insertion technique, 217 Roy-Camille subclassification, of sacral fractures, 498–500, 499f

S

S1 pedicle screws indications for, 515–516 operative equipment, 516 patient positioning, 517 preoperative planning, 516 surgical approach, 517–518 surgical technique, 518 S2 alar screws in iliac fixation, 529–530 indications for, 521 operative equipment, 521–522 preoperative planning, 522 surgical technique, 522 Sacral fractures anatomy, 497 approach to stabilization, 501 classification, 497–500 complications, 504–505 diagnosis, 497 posterior stabilization lumbopelvic, 501–502 ORIF, 502 percutaneous sacroiliac fixation, 502 surgical outcomes, 503–504 surgical timing, 500–501 Sacral plexus, 488 Sacral rami, dorsal, 495f Sacral screw fixation and plating anatomy, 514 Chopin plate/Colorado II sacral plate, 522–524 historical background, 513–514 Jackson intrasacral rod technique, 518–521 S1 pedicle screws, 515–518 S2 alar screws, 521–522 sacral biomechanics, 514–515 Sacral slope, 486 Sacral tumors proximal sacrum posterior sacrectomy, 533–536 ventral sacrectomy, 532–533 S3 and below, 532 sacral reconstruction double iliac screw fixation, 537–539 modified Galveston technique, 537 posterior iliosacral plating, 543 transiliac rod placement, 539–543 triangular frame, 539

Index Sacral vein, 377f Sacrectomy posterior, 533–536 ventral, 532–533 Sacroiliac joint, 483–485 percutaneous fixation, 502 Sacroiliac ligaments, posterior, 706f Sacrotuberous ligament, 508f Sacrum anatomy, 514 biomechanics, 514–515 key bony landmarks, 515f Safety zone for PECD, 153, 154f with respect to lumbar plexus, 381 triangular, in PELD, 413–415 Sagittal balance, normal, 564 Sagittal imbalance, 604f, 618f–619f Sagittal–vertical angle, in ankylosing spondylitis, 663, 664f Scalenus muscle group, 128, 129f Scapular region muscles, 254–256, 264f Scheuermann kyphosis bone graft, 561 closure, 561 complications, 562 correction, 560–561 equipment and patient positioning, 558 exposure of vertebra, 559 incision and soft tissue dissection, 559 indications and contraindication, 558 instrumentation, 559–560 location of incision, 558–559 postoperative care, 561 retractor placement, 559 Schmidt angle, 13 Schwannoma, 641f–642f, 644f Sciatic foramen, 488 Sciatic nerve, 534f, 536f Sclerotomes, axial, 2 Scoliosis anterior approaches, 578–579 degenerative, 584–585 lumbar, 603f neuromuscular, 583 posterior approach, 579–582 Scoliosis: adolescent idiopathic, 582–583 closure, 599 decortication/grafting, 599 derotation maneuver, 599 equipment, 592 freehand pedicle screw placement, 595–597 indications/contraindications, 589 Lenke curve types, 587 osteotomies, 595 positioning, 592 postoperative care, 600 reduction techniques, 598 surgical approach, 592–595 Scoliosis: anterior release and fusion approach to segmental vessels, 574 closure, 576 compression between screws, 575 direct vertebral body derotation, 575 disk/vertebra removal, 573–574 equipment, 569 graft placement, 574 incision/exposure endoscopic access, 572 single and double thoracotomy (convex), 571–572 thoracolumbar access (T10-L4), 572–573 upper thoracic access (T1-T4), 571 internal thoracoplasty, 574

Scoliosis: anterior release and fusion (Continued) lateral decubitus positioning, 569–570 level of fusion, 569 outcomes, 576–577 pleural dissection, 573 preoperative and perioperative considerations, 569 prone positioning, 570–571 relative contraindications, 568–569 relative indications, 568 rib head removal, 574 rod derotation, 575 rod reduction/cantilever, 575 screw placement and staples, 574–575 in situ bending, 575–576 Scoring systems, for spinal metastases, 634–636 Screw and rod constructs lateral mass, 229f occipitocervical, 99f Screw fixation. See also Facet screw fixation; Pedicle screw fixation C1-C2 lateral mass-pars interarticularis, 110–111 C1-C2 lateral mass-pedicle, 111 double iliac, with lumbar segmental fixation, 537–539 lateral mass complications, 219 operative technique, 217–219 occipital condyle, 97–99 Screw fixation: iliac alternative technique, 529–530 closure, 529 complications, 531 connection to construct, 529 equipment, 526 indications, 526 patient positioning and incision, 526–527 postoperative care, 530 screw insertion, 527–529 Screw fixation of fractures odontoid complications, 109 contraindications, 103 operative technique, 104–106 postoperative care, 106 thoracolumbar, placement of screw, 371–372 Screw fixation: sacral anatomy, 514 biomechanics, 514–515 Chopin plate/Colorado II sacral plate, 522–524 historical background, 513–514 Jackson intrasacral rod technique, 518–521 S1 pedicle screws, 515–518 S2 alar screws, 521–522 Sealants, dural, 714–715 Segmental artery injury, complication of LTIF, 467–468 Segmental fixation, lumbar, double iliac screw fixation with, 537–539 Segmental type of ossification of PLL, 233f Segmental vessels, 377f bilateral, ligation of, 347 in surgery for scoliosis, 574 Self-retaining retractors, 135f, 165f Semispinalis muscle, 245f, 256, 264f Semispinalis thoracis muscle, 325–326 Serratus posterior muscle, 255, 269f, 325, 349f Shoulder herniation, interlaminar PELD for, 420–421

Side-to-side domino connectors, for CTJ stabilization, 278f Silk sutures, 712–713 Sinuses, in OCJ, 94 Skull base, and atlantoaxial morphometry, 11–14 Smith-Peterson osteotomy for flat back deformity, 604–606 for thoracic kyphosis, 565–566 Soft palate splitting, 23, 24f–26f in endoscopic transoral approach to CVJ, 61f Soft tissue complications, of cervical corpectomy and fusion, 179–180 Somatosensory evoked potential (SSEP) monitoring, 56 Somites, occipital and cervical, 2 Spinal accessory nerve, 44f–45f Spinal canal anatomy, 405 decompression, in mini-TTA, 360–361 vertebral body, 122 Spinal column anterior, distraction of, 605f trauma, impact on alignment, 564 Spinal cord aneurysms, 658 blood supply, 124 decompressed, 308f decompression via anterior cervical foraminotomy, 147–149 dissection, in TES, 336f exposure, for costotransversectomy, 333–334 and nerve roots, 123 Spinal cord intradural tumors approach to intradural-extramedullary tumor, 641–642 intramedullary tumor, 642–643 closure, 644 complications, 645 dural opening, 640–641 hemostasis, 643–644 patient positioning and exposure, 639–640 postoperative care, 644–645 Spinal cord vascular lesions arteriovenous malformations, 653–658 cavernous malformations, 650–653 hemangioblastoma, 647–650 normal vascular anatomy, 646–647 Spinal deformity, adult, 583–584 Spinal endoscope, 416 Spinal fracture classifications historic review, 365–366 Iowa system and algorithm, 366 Spinal gunshot wounds epidemiology, 686 indications for surgical intervention CSF fistula, 687 lead toxicity, 688 neurologic deficit, 688 spinal instability, 687–688 late complications, 688–689 Louisiana State University–New Orleans experience, 689–692 mechanisms of injury, 686 neurologic evaluation, 687 prehospital and emergency room management, 686–687 radiologic evaluation, 687 Spinal infection diskitis and osteomyelitis cervical, 673–675 lumbar, 680–682 thoracic, 676–679

731

732

Index Spinal infection (Continued) epidural abscess, 684 indications for surgical management, 672 operative technique, 672–684 tuberculosis and fungal, 683 Spinal tumors benign, 626–630 evaluation, 622 malignant, 624–626 management, 622–624 presentation, 622 Spinalis muscle, 255 Spine Instability Neoplastic Score, 636t Spinopelvic inclination, 487f Spinous processes of C2, 49f, 94f C2 and C7, in laminoplasty, 206–207 splitting procedure, 203, 204f vertebral body, 123 Splayed facet complex, 223f Splenius muscles, 128, 245f, 255 Spondylectomy en bloc, for lumbar lesions, 401–402 single-stage posterolateral transpedicular approach, 339–342 total en bloc (TES), thoracic spine, 334–337 Spondylitis, rheumatoid, classification, 81f Spondylolisthesis reduction classification of slips, 470 evidence-based decision making, 470 formal reduction maneuver, 472–473 high-grade slip anterior surgical technique, 473–474 posterior surgical technique, 474 low- and high-grade slip, fusion for, 470–472 spondyloptosis, 474–475 Spondyloptosis, 474–475 Stabilization CTJ anterior approaches, 274–275 anteroposterior approach, 281 operative anatomy, 274 posterior approaches, 278–281 posterior-anterior-posterior approach, 281 occipitocervical, 85f posterior cervical for facet dislocation, 228–229 lateral mass screw fixation, 217–219 pedicle screw fixation, 214–217 wiring of subaxial spine, 219–221 posterior lumbar, in diskitis and osteomyelitis, 682 of sacral fractures, 500t, 501 in thoracic trauma anatomy review, 309–310 complications, 313 indications and contraindications, 310 operative technique, 310–313 of thoracolumbar fractures anterolateral approach, 366–369 posterior minimally invasive techniques, 370–372 posterolateral transpedicular approach, 369–370 Stabilization for lumbar lesions anterior approaches, 399–401 complications, 402–403 en bloc spondylectomy, 401–402 posterior approaches, 398–399 preoperative preparation, 397–398 reconstruction, 402

Staging of procedures for degenerative lumbar scoliosis, 616–617 for posterior stabilization, 684f for spinal tumors, 623f Stenosis cervicomedullary, 83f lumbar avoidance of complications, 430–431 operative techniques, 427–429 postoperative regimen, 430 symptoms, 426–427 wound closure, 429–430 with spondylotic bone spurs, 148f Sternocleidomastoid muscle, 31, 38, 39f, 42–44, 45f, 121f, 128, 162, 244f Sternohyoid muscle, 243 Sternothyroid muscle, 121f Sternotomy, in anterior approach to CTJ, 253f Strange–Vognsen and Lebech modified classification, of sacral fractures, 498–500, 499f Strut grafts, 100, 166f, 394f, 674, 678f, 681f, 706f Stylohyoid muscle, 129f Stylomastoid foramen, 5f Subarachnoid drains, 711 Subaxial cervical spine anterolateral approach, 674f cervical triangles, 130 dorsal musculature, 128–130 fascia, 127–128 ligaments, 126–127 neurovascular structures, 124–126 pedicle screw insertion, 215 posterior wiring complications, 220 operative technique, 219–220 surface anatomy, 120 ventral musculature, 128 vertebral column, 120–124 viscera, 126 Subfascial drains, after dural surgical repair, 716 Sublaminar wire, 581f Subluxation, atlantoaxial, 77–78 Submandibular gland, 38, 40, 41f Submandibular triangle, 129f, 130 Submental triangle, 129f, 130 Suboccipital triangle, 48, 49f, 52, 55f Subsidence, cage, 167 Superior hypogastric plexus, 489f Superior laryngeal nerve, 125 Superior mediastinum, 243 arterial structures, 249–250 fascial layers, 249 venous structures, 249 Superior pharyngeal constrictor muscle, 41f–42f Supraclavicular approach to CTJ, 251 Suprasternal approach to thoracic tumors, 322–323 Surface-matching registration, 435 Surgical tips, for endoscopic approach to cervical spine, 157–160 Surgicel, 715f Suspensory ligament of CVJ, 11 Suturing dural tears, 712–713 Sympathetic chain, 124f, 125 Synovial joints, posterior thoracic cage, 326–328 Synovitis, CVJ rheumatoid arthritis related, 80f Synthetic materials, as dural substitutes, 714

T

Tapered rods, for CTJ stabilization, 278f Tectorial membrane, 10–11, 18 Thoracic and thoracolumbar spine costotransversectomy, 331–334 lateral extracavitary approach, 329–331 muscular anatomy, 325–326, 327f posterior mediastinal space and neurovascular structure, 328–329 posterior thoracic cage, 326–328 spondylectomy and epidural decompression, 339–342 transcostovertebral approach, 331 Thoracic cage, posterior, 326–328 Thoracic cavity, 247f retromediastinal structures in, 328f–329f Thoracic diskitis and osteomyelitis anesthesia, 676 decompression and reconstruction, 676–679 localization, 676 patient positioning, 676 surgical approach, 676 Thoracic inlet, 249 Thoracic microdiskectomy anterolateral approaches, 285 complications, 291–292 lateral approaches, 285–289 posterolateral approaches, 289–291 postoperative course, 291 Thoracic spine anterior release for scoliosis, 578–579 anterolateral transthoracic approaches, 245–247 anatomic considerations, 267–268 complications, 272–273 operative technique, 268–271 proximal approach, 271–272 thoracolumbar junction approach, 272 decompression and stabilization techniques anatomy review, 309–310 complications, 313 indications and contraindications, 310 operative technique, 310–313 gunshot wound to, 689f, 692f kyphosis, 486f degree of, 619f Lenke curve types, 588f, 590f operative positioning for scoliosis surgery, 570f posterior endoscopic approach, 301–306 surgical technique, 302–306 posterolateral approaches, 247 surgical anatomy, 243–245 thoracoscopic approach complications, 299 surgical technique, 294–299 total en bloc spondylectomy, 334–337 Thoracic spine tumors clinical presentation and evaluation, 315–316 incidence, 315 lateral extracavitary approach, 320–321 metastatic disease, 317 preoperative embolization, 317–318 primary osseous lesions, 317 radiographic studies and preoperative diagnosis, 316–317 suprasternal approach, 322–323 thoracic laminectomy, 318–323 thoracotomy, 321–322 transpedicular approach and costotransversectomy, 319–320 Thoracoabdominal approach to lumbar spine

Index Thoracoabdominal approach (Continued) dissection, 379–380 general indications, 377 patient positioning, 378–379 to traumatized spine, 312–313 Thoracoabdominal approach to TLJ extrapleural-retroperitoneal approach, 353–356 minithoracotomy-transdiaphragmatic approach, 356–364 transpleural-retroperitoneal approach, 352–353 transpleural-transdiaphragmatic approach, 348–351 transthoracic approach to midthoracic level, 344–347 Thoracolumbar access for scoliosis surgery, 572–573 Thoracolumbar fascia, 329f Thoracolumbar fractures anterolateral approach, 366–369 classifications, 365–366 posterior minimally invasive techniques, 370–372 posterolateral transpedicular approach, 369–370 Thoracolumbar Injury Severity Score (TLISS), 365 Thoracolumbar junction (TLJ) extrapleural-retroperitoneal approach, 353–356 minithoracotomy-transdiaphragmatic approach, 356–364 transpleural-retroperitoneal approach, 352–353 transpleural-transdiaphragmatic approach, 348–351 transthoracic approach to midthoracic level, 344–347 Thoracolumbar spine approach to scoliosis, 578 kyphotic deformity, pedicle subtraction osteotomy for, 668–670 Lenke curve types, 590f Thoracoplasty, internal, 574 Thoracoscopic approach case illustration, 299–301 complications, 299 postoperative care, 299 surgical technique corpectomy, 297–298 instruments, 294–299 placement of portals, 295–296 plate or rod placement, 298–299 screw insertion, 296–297 Thoracotomy, 276 lateral transthoracic, 312 single and double (convex), for scoliosis, 571–572 transthoracic approach to thoracic tumors, 321–322 Three-column theory of spine (Denis), 365 Three-zone classification, of sacral fractures (Denis), 499f Thrombosis, carotid, after cervical disk arthroplasty, 193 Thyrohyoid muscle, 244f Thyroid cartilage, 121f Thyroid gland, 244f Timing of surgery, for sacral fractures, 500–501 Titanium mesh cages, 165t, 167, 173f, 178 in L2-L4 corpectomy site, 401f Titanium nonpenetrating clips, 715

Tokuhashi scoring system, for spinal metastases, 634, 635t Tomita scoring system, for spinal metastases, 634, 636t Total en bloc spondylectomy (TES): thoracic spine anterior reconstruction, 337 corpectomy with anterior approach, 336–337 indications, 334 surgical technique, 334–336 Toxicity, lead, in spinal gunshot wounds, 688 β-Trace protein assay, 711 Tracheoesophageal groove, 124f Traction, in management of facet dislocation injury, 226 Trajectory for axial lumbar interbody fusion, 508f entry point for lumbar herniations, 415f for kyphoplasty and vertebroplasty extrapedicular approach, 699f transpedicular approach, 698f for L5 pedicle screw, 437f for lateral mass screws, 217, 229f cervical, 279f safe route for needle into thoracic disk, 307f for screws in fracture stabilization, 368f Transarticular screw technique, C1-C2 for basilar invagination, 72–73 for trauma injuries, 111 Transcervical approach to CVJ, endoscopic, 62–63 preparation and positioning, 67 rationale, 66–67 surgical procedure, 67 Transcostovertebral approach to thoracic spine, 331 Transfacet approach to thoracic diskectomy, 284t, 290–291 Transforaminal approach to PELD, 412–415 for migrated herniations, 419 for nonmigrated herniations, 418–419 Transforaminal lumbar interbody fusion end plate preparation, 446 grafts, 446–447 pedicle screw placement, 442 rod-and-screw system assembly, 447–448 total diskectomy, 446 unilateral facetectomy, 442–445 Transiliac rod placement, 539–543, 543f Translaminar screw technique atlantoaxial, for trauma injuries, 111–112 for basilar invagination, 73–74 for CTJ stabilization, 279–281 lumbar facet screw fixation open, 478–479 percutaneous, 479–480 Transmandibular approach to clivus and upper cervical spine anatomy, 30–31 complications, 36–37 indications and contraindications, 31–33 operative technique, 34–36 Transmanubrial-transclavicular approach to CTJ, 251–252 Transmaxillary approach to clivus and upper cervical spine anatomy, 30–31 complications, 36–37 indications and contraindications, 31–33 operative technique, 34–36 Transmuscular far-lateral lumbar diskectomy, 407–410

Transoral approach to CCJ anatomy, 17–20 indications and relative contraindications, 21–22 preparation and positioning, 22 surgical procedure, 22–29 Transoral approach to CVJ endoscopic, 61–62 preparation and positioning, 64 rationale, 64 surgical procedure, 64–66 expanding maneuvers to, 32f plus mandibulotomy, 33f for rheumatoid arthritis, 85–87 anesthesia and equipment, 86–87 extended procedures, 88–89 patient positioning, 87 preoperative preparation, 86 surgical technique, 87 Transoral robotic surgery intraoperative radiograph during, 66f room setup for, 65f Transoral-transpalatopharyngeal approach, for basilar invagination, 70–71 Transpedicular approach to thoracic spine CTJ, 259–261 for kyphoplasty and vertebroplasty, 697 posterolateral, for thoracic spondylectomy, 339–342 for thoracic decompression, 310 for thoracic diskectomy, 284t, 289–290 for thoracic primary and secondary tumors, 319–320 Transpedicular screw fixation insertion techniques, 432–438 electromyographic monitoring, 438 fluoroscopically assisted, 434 freehand, 433–434 image-guided navigation-assisted, 434–438 pedicle anatomy, 432 Transpleural-retroperitoneal approach to TLJ, 352–353 Transpleural-transdiaphragmatic approach to TLJ closure, 350–351 diaphragm incision, 349–350 rib removal, 348 vertebral body exposure, 350 Transsternal-transmanubrial approach to CTJ, 276 Transsternal-transthoracic approach to CTJ, 252–253 Transthoracic approach to midthoracic level, 344–347 to thoracic diskectomy, 285 Transthoracic thoracotomy lateral, 312 for thoracic tumors, 321–322 Transuncal approach, anterior cervical foraminotomy (Jho), 143, 144f, 150 Transverse atlantal ligament, 18 Transverse ligament of C1, 9f, 47–48 Transverse occipital ligament, 11 Transverse posterior approach to lumbosacral junction, 496 Transverse process of C1, 6, 7f, 45f, 55, 94f of subaxial cervical spine, 121 Transverse sinus, 52f Transversospinalis muscle group, 128–130, 255–256, 325 Trap-door osteotomy, for placement of anterior cage, 261f Trapezius muscle, 129f, 245f, 254, 264f, 325

733

734

Index Trauma injuries to C1-C2 atlantoaxial transarticular fixation, 111 atlantoaxial translaminar fixation, 111–112 atlantoaxial wiring techniques, 114 Halifax clamp fixation, 113–114 lateral mass-pars interarticularis screw fixation, 110–111 lateral mass-pedicle screw fixation, 111 posterior atlantoaxial fixation techniques, 110 posterior fixation and fusion of upper cervical spine, 114 upper cervical spine instability after, anterior approaches, 114–117 Triangular frame reconstruction, sacral, 539 Triangular osteosynthesis, 504f Trough preparation, for cervical laminoplasty, 207–208 Tuberculosis of spine, 683 Tubular hemilaminotomy, for lumbar stenosis, 428–429 Tubular retractor system, 63 sequential dilation of, 465f Tumors, intradural approach to intradural-extramedullary tumor, 641–642 intramedullary tumor, 642–643 closure, 644 complications, 645 dural opening, 640–641 hemostasis, 643–644 patient positioning and exposure, 639–640 postoperative care, 644–645 Tumors of lumbar spine anterior approaches anterior retroperitoneal approach, 400–401 lateral retroperitoneal approach, 399–400 complications, 402–403 en bloc spondylectomy, 401–402 posterior approaches laminectomy, 398 lateral transpedicular/extracavitary approach, 398–399 preoperative preparation, 397–398 reconstruction, 402 Tumors of sacrum proximal sacrum posterior sacrectomy, 533–536 ventral sacrectomy, 532–533 S3 and below, 532 sacral reconstruction double iliac screw fixation, 537–539 modified Galveston technique, 537 posterior iliosacral plating, 543 transiliac rod placement, 539–543 triangular frame, 539 Tumors of spine benign, 626–630 evaluation, 622 malignant, 624–626 management, 622–624 presentation, 622 Tumors of thoracic spine clinical presentation, 315–316 embolization, preoperative, 317–318 incidence, 315 lateral extracavitary approach, 320–321 metastatic disease, 317 primary osseous lesions, 317 radiographic studies and preoperative diagnosis, 316–317

Tumors of thoracic spine (Continued) with rib involvement, stage operation of, 337–339 suprasternal approach, 322–323 thoracic laminectomy, 318–319 thoracotomy, 321–322 transpedicular approach and costotransversectomy, 319–320 Two-level technique, in axial lumbar interbody fusion, 510

U

Uncal process, vertebral body, 120–121 Uncovertebral junction, exposure of, 142 Unilateral hemilaminotomy/hemilaminectomy, for lumbar stenosis, 427 Unilateral Le Fort I osteotomy, with palatal split, 34 Unipedicular posterolateral approach, to kyphoplasty and vertebroplasty, 696–697 Up-angled curette, 429f Upper cervical spine anatomy, 17–20, 30–31 anterior approaches, for instability after trauma, 114–117 ligamentous complex surrounding, 47–48 posterior fixation and fusion of, 114 Upper lumbar fractures lateral retroperitoneal approach, 393 posterior approach, 392–393 with anterior column stabilization, 393 Upper vertebral transcorporeal approach, anterior cervical foraminotomy (Jho), 143–144, 145f, 150

V

Vagus nerve, 124f–125f Vascular anatomy of lumbosacral junction, 487–488 of spinal cord, 646–647 Vascular complications of cervical corpectomy and fusion, 180 of LTA, 58 of occipitocervical fusion, 101 Vascularized grafts, 708 Vena cava, bifurcations in L5-S1 disk space, 454f Venous bleeding, in posterior approach to CCJ, 49 Venous supply to CTJ, 243–244 to spinal cord, 647 Ventral approaches to spinal metastases, 637 Ventral cavernous malformations of spinal cord, 652–653 Ventral musculature, subaxial cervical spine, 128 Ventral sacrectomy, 532–533 Ventral triangle, 130 Vertebra exposure, for Scheuermann kyphosis, 559 muscles, anterior, 31 removal, in scoliosis surgery, 573–574 Vertebral angiogram, preoperative, for LTA, 56 Vertebral artery, 5–6, 20f, 45f, 49f, 53f corpectomy limited due to, 164f exposure via LTA, 55 in OCJ, 94, 95f at risk during screw insertion, 113f segments of, 125–126 in ventral approach to CVJ, 62f Vertebral body anterior and posterior tubercles, 121 collapse, 695f

Vertebral body (Continued) end plates, 120 facet joint, 122–123 fractured, inserting tools into, 696–698 lamina and spinous processes, 123 lateral mass, 122 neural foramen, 121 pedicles, 121–122 placement of screw through, 185f posterior ligamentous release of, 335–336 reconstruction, posterolateral transpedicular approach with, 369–370 replacement preparation, 178 resection posteroanteriorly, 339f restoration technologies, 164–167 bone grafts, 165–167 cages, 167, 173f, 175f PMMA reconstruction, 167, 169f–172f and rib articulation, 256–257 rib head contact with, 328f spinal canal, 122 transpedicular approach, 310f transverse process, 121 uncal process, 120–121 Vertebral body exposure for costotransversectomy, 333–334 extrapleural, 346 for extrapleural approach to TLJ, 355 transpleural, 344–346 Vertebral column, subaxial spine intervertebral disk space, 123 spinal cord, 123–124 vertebral body, 120–123 Vertebroplasty for vertebral fractures cement mixture, 699, 701f complications, 694 extrapedicular approach, 697–698 indications and contraindications, 694 postoperative management, 702 preoperative preparation, 694–695 radiologic anatomy, 695–696 transpedicular approach, 697 unipedicular posterolateral approach, 696–697 Vicryl Collagen, 714 Visceral structures of CTJ, 243 in relation to cervical corpectomy, 163 of subaxial cervical spine, 126 Viscerocarotid space, 243

W

Wackenheim clivus baseline, 12t Weinstein-Boriani-Biagini staging system, for spinal tumors, 623f Welcher basal angle, 11–12 Wiltse technique, posterolateral approach to lumbar spine, 386 Wiring atlantoaxial, 114 interspinous, Bohlman’s triple-wire technique, 219–220 K-wires, 105–106 in thorascopic surgery, 297f occipitocervical, 99–100 posterior, of subaxial spine, 219–221 Working channel endoscope, cervical, 154–155 Working zone, in PELD, 414f Wrong-level surgery, lumbar spine, 388

Z

Z-plasty, Hittori, 203, 204f

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