Spinal deformity a case based approach to managing and avoiding complications

Mummaneni, MD Joan O’Reilly Endowed Professor in Spinal Surgery, Vice Chairman, Department of Neurosurgery University of California, San Francisco, CA, USA Charles H.. Glassman, MD Dep

Spinal Deformity

Praveen V Mummaneni Paul Park

Charles H Crawford III Adam S Kanter

Steven D Glassman Editors

123

A Case-Based Approach

to Managing and Avoiding Complications

Spinal Deformity

Praveen V Mummaneni • Paul Park Charles H Crawford III • Adam S Kanter Steven D Glassman

ISBN 978-3-319-60082-6 ISBN 978-3-319-60083-3 (eBook)

DOI 10.1007/978-3-319-60083-3

Library of Congress Control Number: 2017951047

© The Editor(s) (if applicable) and The Author(s) 2018

This work is subject to copyright All rights are reserved by the Publisher, whether the whole or part of the material is concerned, specifically the rights of translation, reprinting, reuse of illustrations, recitation, broadcasting, reproduction on microfilms or in any other physical way, and transmission or information storage and retrieval, electronic adaptation, computer software,

or by similar or dissimilar methodology now known or hereafter developed.

The use of general descriptive names, registered names, trademarks, service marks, etc in this publication does not imply, even in the absence of a specific statement, that such names are exempt from the relevant protective laws and regulations and therefore free for general use The publisher, the authors and the editors are safe to assume that the advice and information in this book are believed to be true and accurate at the date of publication Neither the publisher nor the authors or the editors give a warranty, express or implied, with respect to the material contained herein or for any errors or omissions that may have been made The publisher remains neutral with regard to jurisdictional claims in published maps and institutional affiliations Printed on acid-free paper

This Springer imprint is published by Springer Nature

The registered company is Springer International Publishing AG

The registered company address is: Gewerbestrasse 11, 6330 Cham, Switzerland

Praveen V Mummaneni, MD

Joan O’Reilly Endowed Professor in

Spinal Surgery, Vice Chairman,

Department of Neurosurgery

University of California,

San Francisco, CA, USA

Charles H Crawford III, MD

University of Louisville,

Norton Leatherman Spine Center

Louisville, KY, USA

Steven D Glassman, MD

Department of Orthopedic Surgery

University of Louisville,

Norton Leatherman Spine Center

Louisville, KY, USA

Paul Park, MD Professor Director of Spinal Surgery, Department of Neurosurgery University of Michigan Ann Arbor, MI, USA Adam S Kanter, MD Chief, Division of Spine Surgery, Associate Professor of Neurological Surgery

University of Pittsburgh Medical Center Pittsburgh, PA, USA

their trust and understanding.

Charles H Crawford III, MD

With gratitude to the Leatherman spine fellows, who have made

me a better surgeon.

Steven D Glassman, MD

To my sons Jared and Jeremy, for teaching me that one man’s weakness can be another man’s strength, as fortitude comes in many forms.

Contents

1 A Historic Overview of Complications

in Spinal Deformity Surgery 1

Steven D Glassman

Part I Cervical

2 Occipitocervical Surgery Complication 7

Todd Vogel and Dean Chou

3 Transoral Odontoidectomy and C1-2 Posterior

Fusion Complication 17

Andrew K Chan, Michael S Virk, Andres J Aguirre,

and Praveen V Mummaneni

4 Mid-Cervical Kyphosis Surgery Complication 29

Dan Harwell and Frank La Marca

5 Cervical Kyphosis (Post- laminectomy) Surgery

Complication 35

Domagoj Coric and Tyler Atkins

6 Cervical Osteomyelitis and Kyphosis Complication 43

Priscilla S Pang, Jason J Chang, and Khoi D Than

7 Cervical Traumatic Deformity (Bilateral Facet

Dislocation) Complication 53

Young M Lee, Joseph Osorio, and Sanjay Dhall

8 Cervical Kyphosis (Neuromuscular) Surgery Complication 59

Salazar Jones and Charles Sansur

9 Cervicothoracic Kyphosis (Dropped Head Deformity)

Surgery Complication 67

Subaraman Ramchandran, Themistocles S Protopsaltis,

and Christopher P Ames

10 Iatrogenic Cervicothoracic Kyphosis Surgery

Complication 75

Frank Valone III, Lee A Tan, Vincent Traynellis,

and K Daniel Riew

Part II Thoracolumbar

11 Thoracic Scoliosis (AIS) Posterior Surgery Complication 93

Elizabeth W Hubbard and Daniel J Sucato

12 Scheuermann’s Kyphosis Surgery Complication 115

Abhishek Kumar, Dante Leven, Yuan Ren, and Baron Lonner

13 Thoracic Deformity (Pott’s Disease) Surgery Complication 123

Kin Cheung Mak and Kenneth M.C Cheung

14 Thoracolumbar Scoliosis (AIS) Posterior Surgery

Complication 137

Chewei Liu, Lee A Tan, Kathy M Blanke,

and Lawrence G Lenke

15 Congenital Thoracolumbar Deformity Complication 145

Thomas Kosztowski, Rafael De la Garza Ramos,

C Rory Goodwin, and Daniel M Sciubba

16 Thoracolumbar Deformity (Trauma)

Surgery Complication 155

Robert F Heary and M Omar Iqbal

17 Thoracic Deformity (Tumor) Surgery Complications 167

William C Newman and Nduka M Amankulor

18 Thoracic/Lumbar Deformity (Tumor)

MIS Surgery Complication 173

Todd Vogel, Junichi Ohya, and Dean Chou

19 Lumbar Deformity (Vascular) Surgery Complication 181

Gurpreet S Gandhoke, Adam S Kanter,

and David O Okonkwo

20 Lumbar Scoliosis (Degenerative)

Posterior Surgery Complication 185

Travis Loidolt, Jeffrey L Gum, and Charles H Crawford III

21 Lumbar (Degenerative) Scoliosis: Complication

in Anterior/Posterior Surgery 199

Martin C Eichler, Ryan Mayer, and S Samuel Bederman

22 Thoracolumbar Deformity MIS (Palsy)

Surgery Complication 211

Neel Anand, Jason E Cohen, and Ryan B Cohen

23 Lumbar Scoliosis (Degenerative) and MIS (Lateral)

Surgery Complications 219

Yusef I Mosley and Juan S Uribe

24 Lumbar Scoliosis (Degenerative) MIS Surgery

(PSO/TLIF) Complication 225

Peng-Yuan Chang and Michael Y Wang

25 Lumbar Scoliosis (Degenerative) MIS Surgery (PJK) Complication 233

Jacob R Joseph and Paul Park

26 Lumbar Deformity MIS Lateral (Visceral) Surgery Complication 239

Kourosh Tavanaiepour and Adam S Kanter

27 Thoracolumbar Deformity: MIS ACR Complications 245

Gregory M Mundis Jr and Pooria Hosseini

28 Lumbar Deformity (Infection) Surgery Complication 259

Sasha Vaziri and Daniel J Hoh

29 Sagittal Plane Deformity Surgery:

Pedicle Subtraction Osteotomy (PSO) Complication 269

Hongda Bao, Sravisht Iyer, and Frank J Schwab

30 Sagittal Plane Deformity Surgery (VCR) Complication 281

John C Quinn, Avery L Buchholz, Justin S Smith, and Christopher I Shaffrey

31 Lumbar Deformity Spondylolisthesis (Moderate–High Grade) Complication 291

Randall B Graham, Sohaib Hashmi, Joseph P Maslak, and Tyler R Koski

32 Pediatric Moderate-/High-Grade Spondylolisthesis Surgery Complication 301

34 Sacral Insufficiency Fracture Surgery Complication 321

Michael LaBagnara, Durga R Sure, Christopher I Shaffrey, and Justin S Smith

35 Sacral Tumor Surgery Complications 329

Peter S Rose

Index 343

Andres J Aguirre, MD Department of Neurological Surgery, University of

California, San Francisco, San Francisco, CA, USA

Nduka M Amankulor, MD Department of Neurological Surgery,

University of Pittsburgh Medical Center, Pittsburgh, PA, USA

Christopher P Ames, MD Department of Neurological Surgery, University

of California, San Francisco, USA

Neel Anand, MD Department of Surgery, Cedars-Sinai Spine Center, Los

Angeles, CA, USA

Tyler Atkins, MD Department of Neurosurgery, Carolinas Medical Center,

Charlotte, NC, USA

Hongda Bao, MD, PhD Hospital for Special Surgery, Weil-Cornell School

of Medicine, New York, NY, USA

S Samuel Bederman, MD, PhD, FRCSC Restore Orthopedics and Spine

Center, Orange, CA, USA

Sigurd H Berven, MD Department of Orthopaedic Surgery, University of

California – San Francisco (UCSF), San Francisco, CA, USA

Kathy M Blanke, RN Department of Orthopedics, The Spine Hospital,

NewYork Presbyterian, New York, NY, USA

Avery L Buchholz, MD, MPH Department of Neurological Surgery,

University of Virginia, Charlottesville, VA, USA

Andrew K Chan, MD Department of Neurological Surgery, University of

California, San Francisco, San Francisco, CA, USA

Jason J Chang, MD Department of Neurological Surgery, Oregon Health

& Science University, Portland, OR, USA

Peng-Yuan Chang, MD Neuroregeneration Center, Department of

Neurosurgery, Neurological Institute, Taipei Veterans General Hospital, Taipei, Taiwan

Departments of Neurosurgery & Rehabilitation Medicine, University of Miami Miller School of Medicine, Lois Pope Life Center, Miami, FL, USA

Contributors

Kenneth M.C Cheung, MD, FRCS, FHKAM(Orth) Department of

Orthopaedics & Traumatology, The University of Hong Kong, Hong Kong,

SAR, China

Dean Chou, MD Department of Neurological Surgery, University of

California, San Francisco, San Francisco, CA, USA

Jason E Cohen, BS Albert Einstein College of Medicine, Bronx, NY, USA

Ryan B Cohen, BS Boston University School of Medicine, Boston, MA,

USA

Domagoj Coric, MD Department of Neurosurgery, Carolinas Medical

Center/Carolina Neurosurgery and Spine Association, Charlotte, NC, USA

Charles H Crawford III, MD University of Louisville, Norton Leatherman

Spine Center, Louisville, KY, USA

Rafael De la Garza Ramos, MD Department of Neurosurgery, Johns

Hopkins University School of Medicine, Baltimore, MD, USA

Sanjay Dhall, MD Department of Neurological Surgery, University of

California, San Francisco, San Francisco, CA, USA

Martin C Eichler, MD Department of Orthopaedics and Traumatology,

Kantonsspital St Gallen, St Gallen, Switzerland

Gurpreet S Gandhoke, MD, MCH Department of Neurological Surgery,

University of Pittsburgh Medical Center, Pittsburgh, PA, USA

Steven D Glassman, MD Department of Orthopedic Surgery, University of

Louisville, Norton Leatherman Spine Center, Louisville, KY, USA

C Rory Goodwin, MD, PhD Department of Neurosurgery, Johns Hopkins

University School of Medicine, Baltimore, MD, USA

Department of Neurosurgery, Duke University Medical Center, Durham, NC,

USA

Randall B Graham, MD Northwestern University Feinberg School of

Medicine, Department of Neurological Surgery, Chicago, IL, USA

Jeffrey L Gum, MD Norton Leatherman Spine Center, Louisville, KY,

USA

Yazeed M Gussous, MD Department of Orthopaedic Surgery, Ohio State

University, Columbus, OH, USA

Dan Harwell, MD Department of Neurosurgery, University of Michigan,

Ann Arbor, MI, USA

Sohaib Hashmi, MD Department of Orthopaedic Surgery, Northwestern

University Feinberg School of Medicine, Chicago, IL, USA

Robert F Heary, MD Department of Neurological Surgery, University

Hospital, Rutgers University, Newark, NJ, USA

Daniel J Hoh, MD Department of Neurological Surgery, University of

Florida, Gainesville, FL, USA

Pooria Hosseini, MD San Diego Spine Foundation, San Diego, CA, USA Elizabeth W Hubbard, MD Department of Orthopaedic Surgery, University

of Kentucky and Shriner’s Hospital for Children Lexington, Lexington, KY, USA

Sravisht Iyer, MD Hospital for Special Surgery, Weil-Cornell School of

Medicine, New York, NY, USA

Salazar Jones, MD Department of Neurosurgery, University of Maryland,

Baltimore, MD, USA

Jacob R Joseph, MD Department of Neurosurgery, University of Michigan,

Ann Arbor, MI, USA

Adam S Kanter, MD Chief, Division of Spine Surgery, Associate Professor

of Neurological Surgery, University of Pittsburgh Medical Center, Pittsburgh,

PA, USA

Michael P Kelly, MD, MCSI Washington University, School of Medicine,

Department of Orthopedic Surgery, Saint Louis, MO, USA

Tyler R Koski, MD Northwestern University Feinberg School of Medicine,

Department of Neurological Surgery, Chicago, IL, USA

Thomas Kosztowski, MD Department of Neurosurgery, Johns Hopkins

University School of Medicine, Baltimore, MD, USA

Abhishek Kumar, MD, FRCSC Department of Orthopedic Surgery,

Louisiana State University, New Orleans, LA, USA

Michael LaBagnara, MD Department of Neurosurgery, University of

Virginia, Charlottesville, VA, USA

Frank La Marca, MD Department of Neurosurgery, University of Michigan,

Ann Arbor, MI, USA

Young M Lee, MD Department of Neurological Surgery, University of

California, San Francisco, San Francisco, CA, USA

Lawrence G Lenke, MD Department of Orthopedics, The Spine Hospital,

NewYork Presbyterian/Allen, New York, NY, USA

Dante Leven, DO, PT Orthopedic Surgery, Mount Sinai Hospital, New

York, NY, USA

Chewei Liu, MD Department of Orthopedics, Cathay General Hospital,

Taipei, Taiwan

Travis Loidolt, DO Bone and Joint Hospital at St Anthony, Oklahoma City,

OK, USA

Baron Lonner, MD Orthopedic Surgery, Mount Sinai Medical Center, New

York, NY, USA

Kin Cheung Mak, MBBS, FRCS, FHKAM (Orth) Department of

Orthopaedics and Traumatology, The University of Hong Kong, Hong Kong,

SAR, China

Joseph P Maslak, MD Department of Orthopaedic Surgery, Northwestern

University Feinberg School of Medicine, Chicago, IL, USA

Ryan Mayer, MD Department of Orthopaedic Surgery, University of

Kentucky, Lexington, KY, USA

Yusef I Mosley, MD Department of Neurological Surgery, University of

South Florida, Tampa, FL, USA

Praveen V Mummaneni, MD Joan O’Reilly Endowed Professor in Spinal

Surgery, Vice Chairman, Department of Neurosurgery, University of California,

San Francisco, CA, USA

Gregory M Mundis Jr., MD Scripps Clinic Torrey Pines, La Jolla, CA,

USA

William C Newman, MD Department of Neurological Surgery, University

of Pittsburgh Medical Center, Pittsburgh, PA, USA

Junichi Ohya, MD Department of Neurological Surgery, University of

California, San Francisco, San Francisco, CA, USA

David O Okonkwo, MD, PhD Department of Neurological Surgery,

UPMC Presbyterian, Pittsburgh, PA, USA

M Omar Iqbal, MD Department of Neurological Surgery, Rutgers

University, Newark, NJ, USA

Joseph Osorio, MD, PhD Department of Neurological Surgery, University

of California, San Francisco, San Francisco, CA, USA

Priscilla S Pang, MD, MS Department of Neurological Surgery, Oregon

Health & Science University, Portland, OR, USA

Paul Park, MD, Professor, Director of Spinal Surgery, Department of

Neurosurgery, University of Michigan, Ann Arbor, MI, USA

Themistocles S Protopsaltis, MD Department of Orthopedic Surgery,

NYU Langone Medical Center, New York, NY, USA

John C Quinn, MD Department of Neurological Surgery, University of

Virginia, Charlottesville, VA, USA

Subaraman Ramchandran, MBBS, MS (Orth) Department of Orthopedic

Surgery, NYU Langone Medical Center’s Hospital for Joint Diseases, New

York, NY, USA

Yuan Ren, PhD Orthopedic Surgery, Mount Sinai Medical Center, New

York, NY, USA

K Daniel Riew, MD Department of Orthopedic Surgery, The Spine

Hospital, NewYork-Presbyterian/The Allen Hospital, New York, NY, USA

Peter S Rose, MD Orthopedic Surgery, Mayo Clinic, Rochester, MN, USA

Charles Sansur, MD Department of Neurosurgery, University of Maryland,

Baltimore, MD, USA

Frank J Schwab, MD Hospital for Special Surgery, Weil-Cornell School of

Medicine, New York, NY, USA

Daniel M Sciubba, MD Department of Neurosurgery, Johns Hopkins

University School of Medicine, Baltimore, MD, USAThe Johns Hopkins Hospital, Baltimore, MD, USA

Christopher I Shaffrey, MD Department of Neurological Surgery,

University of Virginia, Charlottesville, VA, USA

Justin S Smith, MD, PhD Department of Neurological Surgery, University

of Virginia, Charlottesville, VA, USA

Daniel J Sucato, MD Texas Scottish Rite Hospital, Department of

Orthopaedic Surgery, University of Texas at Southwestern Medical Center, Dallas, TX, USA

Durga R Sure , MBBS Department of Neurosurgery, University of Virginia,

Charlottesville, VA, USADepartment of Neurosurgery, Essentia Health Duluth, Duluth, MN, USA

Lee Tan, MD The Spine Hospital, Columbia University Medical Center, New

York, NY, USA

Kourosh Tavanaiepour, DO Division of Spine Surgery, Department of

Neurological Surgery, UPMC Presbyterian, Pittsburgh, PA, USA

Khoi D Than, MD Department of Neurological Surgery, Oregon Health &

Science University, Portland, OR, USA

Alexander A Theologis, MD Department of Orthopaedic Surgery,

University of California – San Francisco (UCSF), San Francisco, CA, USA

Vincent Traynellis, MD Department of Neurosurgery, Rush University

Medical Center, Chicago, IL, USA

Juan S Uribe, MD Department of Neurological Surgery, University of

South Florida, Tampa, FL, USA

Frank Valone III, MD Spine Institute, California Pacific Orthopaedics, San

Francisco, CA, USA

Sasha Vaziri, MD Department of Neurological Surgery, University of

Florida, Gainesville, FL, USA

Michael S Virk, MD, PhD Department of Neurological Surgery, University

of California, San Francisco, San Francisco, CA, USA

Todd Vogel, MD Department of Neurological Surgery, University of

California, San Francisco, San Francisco, CA, USA

Michael Y Wang, MD FACS Departments of Neurosurgery & Rehabilitation

Medicine, University of Miami Miller School of Medicine, Miami, FL, USA

Steven D Glassman

Surgical treatment of spinal deformity has

advanced dramatically over the past 25 years

Surgeons have developed a more

comprehen-sive three-dimensional understanding of spinal

deformity, and surgical strategies and tools

tar-geting multidimensional deformity correction

have paralleled our conceptual progress With

these new and frequently more aggressive

surgi-cal techniques have come anticipated and

unan-ticipated challenges We have encountered, and

in some cases generated, a new set of

complica-tions In the chapters that follow, the authors

present a case-based approach designed to

explore the prevention and treatment of

compli-cations associated with modern spinal deformity

surgery

Twenty-five years ago, the success of spinal

deformity surgery was somewhat limited by a

focus on the coronal plane, the absence of modern

neuromonitoring techniques, and a reticence to

undertake major surgical procedures in older

patients Patients over 65 years old were often

con-sidered too old for any fusion procedure, much

less a significant deformity correction Attitudes

toward surgery in older patients have since

changed dramatically, leading among other things

to a rapid expansion in adult spinal deformity gery [2] Underlying this change is a re- equilibration of societal standards defining expectations for quality of life in the elderly Translating these attitudes to medical decision- making has been facilitated by the increased focus

sur-on health-related quality of life (HRQOL) sures as the final pathway for evaluation of medi-cal and surgical interventions To some extent, this move away from occurrence of complications as the primary determinant of what should be consid-ered an acceptable procedure has, at least tempo-rarily, changed the dynamic in surgical decision-making

mea-As patients have sought out more aggressive surgical treatment, and surgeons have seemingly become less risk adverse, the profile of complica-tions in spinal deformity surgery has changed This trend is epitomized by the dramatic increase

in three-column osteotomies performed over the past 5–10 years [6] Aggressive osteotomies afford the ability to correct complex and rigid deformities While potentially avoiding compli-cations of sagittal malalignment or under correc-tion, they introduce risks of excessive blood loss

or neurologic injury not frequently encountered with older less aggressive deformity correction procedures

Prior to the advent of Harrington rod mentation, spinal deformity surgery entailed pro-longed periods of casting and bed rest and was effectively limited to a pediatric population

instru-S.D Glassman (*)

Department of Orthopedic Surgery,

University of Louisville, Norton Leatherman

Spine Center, Louisville, KY 40202, USA

e-mail: sdg12345@aol.com

1

Subsequently, improved fixation techniques lead

to more aggressive surgical treatment as well as a

wider target population including adults with

spi-nal deformity Anterior surgery also became

increasingly common, as it afforded improved

deformity correction and better fusion rates

At the time of my residency training in the late

1980s, concerns regarding complications with

deformity surgery focused on the more

aggres-sive corrections obtained with segmental

instru-mentation, particularly given more rudimentary

neuromonitoring capabilities with

somatosen-sory evoked potentials (SSEPs) and wake-up test

While segmental instrumentation provided

improved control as compared to the Harrington

rod fixation, three-dimensional control of

osteot-omies was suboptimal and presented a

substan-tial risk The use of thoracic pedicle screws was

just being introduced, and there was tremendous

controversy about whether screw misplacement

might result in high rates of catastrophic

neuro-logic injury

Anterior procedures were often necessary as

posterior hook rod instrumentation generated less

powerful correction and limited control of

rota-tional deformity [3, 4] Concerns regarding

ante-rior surgery included the risk for neurologic

injury with ligation of multiple segmental

ves-sels One of our initial research studies at the

Norton Leatherman Spine Center was a review of

complications in 447 patients undergoing

ante-rior procedures for spinal deformity correction

[8] That study demonstrated a fairly high

com-plication rate in neuromuscular deformity, but

acceptable risk related to other major surgical

interventions, and no cases of neurologic injury

Another area of frequent controversy through

the 1990s was the timing of combined anterior/

posterior deformity correction procedures

Multiple studies examined the relative risks of

same-day versus staged surgery [1 12, 13] No

clear consensus was reached; however, the

dis-cussion waned as the predominance of posterior-

only surgery seemed to obviate the issue

Interestingly, this question may have reemerged,

as staging of three-column osteotomies has

become a popular option within posterior-only

correction strategies

Impaired pulmonary function has always been

a concern in spinal deformity patients, although the specific manifestations of this problem have changed over time Before spinal deformities were routinely treated in childhood, very large curves resulted in significant pulmonary compro-mise, particularly in juvenile and congenital deformity patients We seldom see this today Subsequently, non-segmental correction strate-gies often included supplemental thoracoplasty Thoracoplasty improved the cosmetic result but

at a cost in terms of diminished pulmonary tion An adverse effect on pulmonary function also led deformity surgeons away from the con-cept of anterior thoracic instrumentation strate-gies [7 10] Both thoracoplasty and anterior thoracic instrumentation are infrequent in the era

func-of segmental pedicle screw fixation

More recently, the discussion has shifted beyond simply avoiding iatrogenic pulmonary compromise, as was seen with thoracoplasty or anterior thoracic instrumentation One of our major accomplishments in the past 10 years is the proactive management of pulmonary function in the high-risk setting of early-onset scoliosis (EOS) and other chest wall deformities [5 11] Despite the tremendous success of new and more aggressive treatment strategies for EOS, these procedures have also introduced a new set of complications

To some degree, new and unanticipated plications may be the price of progress, and only time will define the true impact of these compli-cations With the advent of thoracic pedicle screws, many surgeons predicted an epidemic of neurologic complications, but while occasional problems were observed, that epidemic never really developed In a similar vein, there are now concerns that minimally invasive approaches for deformity treatment could have unique complica-tions and may not always achieve radiographic and clinical goals While early studies have not supported these concerns [14], those surgeons using MIS techniques should understand the lim-itations of current MIS techniques, be aware of algorithms that may support appropriate patient selection [9], and understand the complication profile of these techniques

com-Certainly avoiding complications is an

impor-tant aspirational goal; however, the willingness

and ability to manage complications are an

inher-ent part of spinal deformity surgery In the

chap-ters that follow, a group of outstanding spine

deformity surgeons share their experience and

insight with both common and not so common

complications This is a critical preparation for

any modern spinal deformity practitioner

References

1 Acaroglu ER, Schwab FJ, Farcy JP Simultaneous

anterior and posterior approaches for correction of

late deformity due to thoracolumbar fractures Eur

Spine J 1996;5(1):56–62.

2 Bess S, Line B, Fu KM, McCarthy I, Lafage V, Schwab

F, Shaffrey C, Ames C, Akbarnia B, Jo HK, Kelly M,

Burton D, Hart R, Klineberg E, Kebaish K, Hostin

R, Mundis G, Mummaneni P, Smith JS International

Spine Study Group: the health impact of

symptom-atic adult spinal deformity: comparison of deformity

types to United States population norms and chronic

diseases Spine 2016;41(3):224–33.

3 Bradford DS, Ahmed KB, Moe JH, Winter RB,

Lonstein JE The surgical management of patients

with Scheuermann’s disease A review of twenty-four

cases managed by combined anterior and posterior

spine fusion J Bone Joint Surg 1980;62-A:705–12.

4 Byrd JA, Scoles PV, Winter RB, Bradford DS,

Lonstein JE, Moe JH Adult idiopathic scoliosis

treated by anterior and posterior spinal fusion J Bone

Joint Surg 1987;69-A:843–50.

5 Farley FA, Li Y, Jong N, Powell CC, Speers MS,

Childers DM, Caird MS Congenital scoliosis SRS-22

outcomes in children treated with observation,

sur-gery and VEPTR Spine 2014;39(22):1868–74.

6 Kim YJ, Bridwell KH, Lenke LG, Cheh G, Baldus

C Results of lumbar pedicle subtraction osteotomies

for fixed sagittal imbalance A minimum 5 year low- up study Spine 2007;32(20):2189–97.

7 Lenke LG, Newton PO, Marks MC, Blanke KM, Sides

B, Kim YJ, Bridwell KH Prospective pulmonary tion comparison of open versus endoscopic anterior fusion combined with posterior fusion in adolescent idiopathic scoliosis Spine 1976;29(18):2055–60.

8 McDonnell MF, Glassman SD, Dimar JR, Puno

RM, Johnson JR Perioperative complications of anterior procedures on the spine J Bone Joint Surg 1996;78-A(6):839–47.

9 Mummaneni PV, Shaffrey CI, Lenke LG, Park P, Wang MY, La Marca F, Smith JS, Mundis GM Jr, Okonkwo DO, Moal B, Fessler RG, Anand N, Uribe

JS, Kanter AS, Akbarnia B, Fu KM Minimally sive surgery section of the International Spine Study Group The minimally invasive spinal deformity sur- gery algorithm: a reproducible rational framework for decision making in minimally invasive spinal defor- mity surgery Neurosurg Focus 2014;36(5):E6 doi: 1 0.3171/2014.3.FOCUS1413

10 Newton PO, Perry A, Bastrom TP, Lenke LG, Betz

RR, Clements D, D’Andrea L Predictors of change in postoperative pulmonary function in adolescent idio- pathic scoliosis: a prospective study of 254 patients Spine 1976;32(17):1875–82.

11 Phillips JH, Knapp DR, Herrera-Soto J Mortality and morbidity in early-onset scoliosis surgery Spine 2013;38(4):324–7.

12 Shufflebarger HL, Grimm JO, Bui V, Thomson

JD Anterior and posterior spinal fusion Staged sus same-day surgery Spine 1991;16:930–3.

ver-13 Spivak JM, Neuwirth MG, Giordano CP, Bloom

N The perioperative course of combined anterior and posterior spinal fusion Spine 1994;19:520–3.

14 Uribe JS, Deukmedjian AR, Mummaneni PV, Fu KM, Mundis GM Jr, Okonkwo DO, Kanter AS, Eastlack

R, Wang MY, Anand N, Fessler RG, La Marca F, Park P, Lafage V, Deviren V, Bess S, Shaffrey CI, International Spine Study Group Complications in adult spinal deformity surgery: an analysis of mini- mally invasive, hybrid, and open surgical techniques Neurosurg Focus 2014;36(5):E15.

Part I Cervical

© The Author(s) 2018

P Mummaneni et al (eds.), Spinal Deformity, DOI 10.1007/978-3-319-60083-3_2

Occipitocervical Surgery Complication

Todd Vogel and Dean Chou

T Vogel • D Chou (*)

Department of Neurological Surgery, University of

California, San Francisco, 505 Paranassus Ave, Room

779 M, San Francisco, CA 94143-0112, USA

e-mail: choud@neurosurg.ucsf.edu

2

Introduction

The occipitocervical junction is an area of

criti-cal transition from the skull base to the spinal

column Multiple individual segments make up

this transitional location These include the

skull base with the occipital condyle (C0), atlas

(C1), and axis (C2) Cervical segments C3 to C7

make up the subaxial spine that may play a role

in surgery Understanding their anatomy is

important to successful surgical planning and

execution The spinal segments are held together

by thick bands of ligaments that give them some

mobility while restricting excessive movement

These osseous structures provide protection for

the spinal cord as it passes through the spinal

canal Inflammatory disease processes,

infec-tion, tumor invasion, congenital disorders, and

trauma can lead to failure of these osseous

structures Ligaments are crucial in maintaining

the alignment of the osseous structures and can

be disrupted by inflammatory, infectious,

con-genital, and traumatic means leading to

instabil-ity Additionally, the vertebral artery passes

through the osseous structures before ing the atlanto-occipital membrane to form the basilar artery A thorough understanding of the anatomy provides the surgeon with guidance and complication avoidance when operating at the occipitocervical junction

penetrat-The occipital condyles are kidney-shaped structures that lie on the ventrolateral aspect of the foramen magnum [1] They articulate with the superior articular facets of the atlas This joint allows for the flexion and extension and slight side-to-side rocking of the head in the coronal plane [2] There is no rotational move-ment associated with the atlanto-occipital joint The inferior articulating surface of C1 is con-cave to allow articulation with the shoulders of C2 The ventral arch of C1 serves as a bridge between the lateral masses This bridge serves

as a dorsal articulating surface with the toid or the peg-like structure ascending superi-orly from the body of C2 The dorsal arch of C1 has a rudimentary spinous process, but there is

odon-no significant dorsal protrusion The dorsal arch

is round at midline but laterally flattens as it attaches to the lateral masses The superior sur-face of the lateral dorsal arch forms a groove,

the sulcus arteriosus, on which the vertebral

arteries run bilaterally [2]

The axis, or C2, is a unique osseous ture The odontoid, a peg-like structure project-ing rostrally from the body of C2, forms a synovial joint with the atlas This is the main

struc-joint for rotational movement at the

occipitocer-vical junction Additionally, C1 articulates with

C2 just lateral to the odontoid and on top of the

body of C2 The C2 inferior articular process

forms an articulation with the superior C3

artic-ulation surface and assumes a more typical

ori-entation similar to the subaxial cervical spine

lateral masses

Ligaments act to restrict excessive motion

between these osseous structures while

permit-ting flexion, extension, lateral bending, and

rota-tion at the occipitocervical juncrota-tion [3] Three

ligaments span the divide between the odontoid

and the skull base The cruciate, or cruciform,

ligament is the strongest and most important

liga-ment at the occipitocervical junction It has four

arms that meet over the dorsal aspect of the

odon-toid The superior limb inserts on the skull; the

inferior limb inserts on the dorsal body of C2;

and the transverse ligament attaches on the bony

tubercles of the C1 lateral masses The apical

ligament spans the interval from the odontoid tip

to the basion The alar ligaments are symmetric

structures spanning the odontoid tip to the medial

edges of bilateral occipital condyles These

liga-ments restrict excessive rotation and lateral

bend-ing to the contralateral side Additional support

to these ligaments comes from the anterior

longi-tudinal ligament that extends from the

atlantoax-ial complex to the basion The posterior

longitudinal ligament continues as the tectorial

membrane, which runs from the dorsal surface of

the odontoid to insert on the ventral surface of the

foramen magnum

Vascular anatomy of the occipitocervical

region is of utmost importance to avoid pitfalls

The major vessels at play include the vertebral

arteries and internal carotid arteries The

verte-bral arteries are at risk for injury along their

nor-mal course if implants are misplaced The left

vertebral artery is dominant in approximately

60–75% of cases [4 5] The right vertebral

artery may be hypoplastic in 10% of cases, and

the left will be hypoplastic in 5% of cases [6]

The vertebral artery is divided into four

sec-tions V1 represents the first vertebral segment

from the origin off the subclavian artery to

where the vertebral artery enters the first

fora-men transversarium The vertebral artery enters C6 in nearly 90% of the cases [7] The V2 seg-ment courses through the transverse foramen in the cervical spine until it exits C3 V3 exists from the C3 transverse foramen to the atlanto-occipital membrane In this segment, the verte-bral artery exits the C3 foramen and takes a sharp turn at the superior articular facet of C2, exiting at 45° from the C2 foramen It then enters the C1 transverse foramen and travels horizontally along the superior aspects of the C1

ring, along the sulcus arteriosus It then enters

the atlanto-occipital membrane approximately

15 mm off midline [8] V4 is the intradural tion of the artery until it forms the basilar artery There is a 2.7% incidence of a tortuous or anomalous vertebral artery in the V2 portion and 5.4% incidence of an anomalous course in the V3 portion [9 10] The internal carotid artery is also at play when placing lateral mass screws at C1 The internal carotid artery runs just lateral to the C1 lateral masses along the ventral aspect of the spinal column, so care must

por-be taken to avoid excessive ventral and lateral placement of C1 lateral mass screws

Indications for occipital fusion can be broken into two subcategories: spinal instability and cord compression causing myelopathy Spinal instability parameters were traditionally estab-lished from trauma literature and case reports using radiographic methods to determine occipi-tocervical dislocation These included the basion- axial interval, the basion-dental interval, Power’s ratio, and the atlanto-occipital interval (Table 2.1) [11] The basion-axial interval is measured from the basion to the rostral extension of posterior axial line This measurement best measures ante-rior or posterior dislocations Normal values on X-rays are less than 12 mm for adults Basion- dental interval measures the distance from the basion to the closest point on the tip of the dens

on X-rays This best measures distracted atlanto- occipital dislocations Again, it is less than

12 mm for adults The atlanto-occipital interval is the measure of the distance between the condyle and the C1 superior articular surface It should measure less than 2 mm in adults and less than

5 mm in pediatric patients on X-rays Power’s

ratio cannot be used with foramen magnum

frac-tures or atlas fracfrac-tures [12] The ratio is calculated

by dividing the distance from the basion to

poste-rior arch of C1 by the distance from anteposte-rior arch

of the C1 to the opisthion Adults should be <1

and pediatrics <0.9 using this method MRI now

gives us the opportunity to screen for

ligamen-tous injuries Short tau inversion recovery (STIR)

sequences are most helpful in demonstrating a

transverse ligament injury [13]

There are many potential fractures that may

lead to occipitocervical fusion These include

occipital condyle fractures, and there are types I,

II, and III Type III fractures involve an avulsion

of the condyle from the skull base These are

typically treated with external immobilization,

but occipitocervical fusion has been used in cases

with associated cervical fractures or significant

ligamentous injuries C1 fractures typically occur

following an axial loading mechanism The

man-agement of C1 fractures depends upon the

integ-rity of the transverse portion of the cruciate

ligament These were traditionally evaluated with

an open mouth odontoid view using the rule of

Spence, in which the cruciate ligament is

consid-ered disrupted if the total overhang of both C1

lateral masses on C2 is greater than 7 mm [14]

Additionally, the cruciate ligament may be

dis-rupted if the atlantodental interval is greater than

3 mm in adults and 4 mm in pediatrics [4 12, 15]

MRI has replaced plain radiographs as a more

sensitive means for assessing for ligamentous

injury that may be unstable It should be noted

that there are a variety of combinations of C1 and

C2 fractures that may lead to consideration for an

occipitocervical fusion

Instability can occur in certain patient tions Rheumatoid arthritis affects a little less than 1% of the Caucasian adult population in the United States It is characterized by destruction of the synovial joints In the cervical spine, this results in translational followed by vertical subluxation of C1 on C2 [16] It is in these latter cases that occipi-tocervical fusion or C1–C2 fusion may be consid-ered Additionally, there may be compression of the spinal cord by an inflammatory pannus leading

popula-to signs of myelopathy in addition popula-to instability of this joint Basilar invagination can occur as part of the vertical subluxation Screening for this can be done with a multitude of radiographic studies including the Clark station, McRae line, Chamberlain line, McGregor line, Redlund-Johnell criterion, Ranawat criterion, Fischgold-Metzger line, and Wackenheim line [17–23] (Table 2.2) Riew et al evaluated the sensitivity and specificity of these screening measurements [24] The Wackenheim line and Clark station were most sensitive (fewest false negatives) at 88% and 83%, respectively The Redlund-Johnell criterion

is the most specific measurement (fewest false positives) at 76% The Fischgold-Metzger line has

a negative predictive value of 100% Riew et al recommended a combination of these tests to screen for basilar invagination that included the Clark station, the Redlund-Johnell criterion, and the Ranawat criterion

There are many congenital disorders associated with atlanto-occipital instability and/or compres-sion of the spinal cord at the craniovertebral junc-tion The most common of these is in Down’s syndrome in which there is an incidence of atlanto-axial subluxation in about 20% of patients [25]

Table 2.1 Radiographic parameters for determining atlanto-occipital dislocation

Basion-axial interval (BAI) From the basion to the rostral extension of posterior axial

line This best measures anterior or posterior dislocations

Adults < 12 mm Basion- dental interval (BDI) From the basion to the closest point on the tip of the

dens This best measures distracted atlanto-occipital dislocations

Adults < 12 mm

Atlanto- occipital interval The measure of between the condyle and the C1 superior

articular surface

Adults < 2 mm Pediatrics < 5 mm Power’s ratio (cannot be used

with foramen magnum fractures

or atlas fractures)

The ratio is calculated by dividing the distance from the basion to posterior arch of C1 by the distance from anterior arch of the C1 to the opisthion

Adults < 1 Pediatrics < 0.9

Mucopolysaccharidoses (Morquio and Lesch-

Nyhan syndromes) have an incidence of

atlanto-axial subluxation as high as 50% [26] Morquio

syndrome in particular is found to have os

odontoi-deum and ligamentous laxity Additional disorders

include Klippel-Feil syndrome, achondroplasia,

osteogenesis imperfecta, Goldenhar syndrome, and

Conradi syndrome

Myelopathy in the upper cervical spine as a

result of cord compression can come from

mul-tiple pathologies Rheumatoid arthritis with

pan-nus formation may lead to spinal cord

compression and possible instability as discussed

above While this may be decompressed and

fix-ated with C1–C2 fusion, occasional extension to

the occiput may be required given anatomy

con-straints Infection, tumor, and degenerative

pro-cesses may also lead to spinal cord compression

requiring decompression and fusion

Case Presentation

A 48-year-old male with a history of Down’s

syn-drome presented 5 years after undergoing

occipi-tocervical fusion to C6 for myelopathy on exam

and ligamentous laxity on dynamic films There

were no documented complications at the time of

surgery At presentation he was noted to be ing purulent material the superior aspect of his incision Further inspection demonstrated exposed implants The family who had accompanied him stated he had been treated multiple times over the previous year for drainage from this area and an inability to heal to his wound He was also noted

leak-to have progressive loss of hand function and was

no longer able to use utensils to feed himself He was unable to participate in individual motor test-ing but was antigravity on exam He was noted to

be myelopathic with Hoffman’s sign and clonus bilaterally His incision was well healed except at the superior aspect of the incision where his occipital plate was visible and he was draining frank pus

Imaging work-up included MRI and CT of the cervical spine Sagittal T2-signal MRI (Fig 2.1) demonstrated severe stenosis at C1 with myeloma-lacia of the spinal cord Sagittal contrasted T1 MRI demonstrated no spinal epidural abscess (Fig 2.2)

CT demonstrated where the cervical plate had eroded through the skin (Fig 2.3), migration of the screws into the foramen at C2/C3 (Fig 2.4), migra-tion of the screws in the bilateral transverse foramen

at C4 (Fig 2.5), and pseudarthrosis of the implants with respect to the lateral mass screws at multiple levels on sagittal CT reconstructions (Fig 2.6)

Table 2.2 Radiographic criteria used to establish basilar invagination in degenerative spine conditions

Clark station Dividing the C2 body into three equal parts Ventral arch of C1 travels into the

region of the middle station, then basilar invagination is suspected McRae line A line drawn from the basion to the opisthion Odontoid tip above this line

Chamberlain line A line drawn from the hard palate to the

opisthion Odontoid tip >6 mm above this lineMcGregor line A line drawn from the hard palate to the caudal

base of the occiput Odontoid tip >8 mm above this line in men, odontoid tip greater than

9.6 mm above this line in women Redlund-Johnell criterion A line drawn from the hard palate to the

opisthion (McGregor line) A second line is drawn from the midpoint of the caudal margin

of C2

Basilar invagination if measurement is less than 34 mm in males and less than 29 mm in females

Ranawat criterion The distance between the center of the second

cervical pedicle and line between the transverse axis of the atlas is measured along the axis of the odontoid process

Measurement less than 15 mm in males and less than 13 mm in females

Fischgold-Metzger line Line drawn between two digastric grooves on

anteroposterior radiographs

Normal if odontoid tip is >10 mm below this line, abnormal if odontoid tip is above this line Wackenheim line Line drawn along the clivus extending

inferiorly into the upper cervical spine

Odontoid tip transects this line

However, it did show solid fusion of the

occipital-cervical junction near the midline on sagittal CT

reconstructions (Fig 2.7) After consultation with

infectious disease and a neurovascular specialist, it

was determined the best course of action would be

to remove the implants

The patient was taken to surgery and

posi-tioned prone with his head secured in a

Mayfield head holder His old incision was

opened and normal anatomy at the racic junction identified Dissection was then carried cephalad exposing the old implants This was removed without significant inci-dence We had contacted our cerebrovascular surgeon prior to the case and assured his avail-ability prior to starting removal of hardware in case a vertebral artery injury had occurred from the screw migration There was noted to be no

cervicotho-Fig 2.1 T2 sagittal MRI image demonstrating

myeloma-lacia from spinal stenosis at C1

Fig 2.2 Sagittal contrasted T1 MRI demonstrating no

gross spinal epidural abscess causing spinal cord

com-pression in a patient with a chronically infected implants

and wound

Fig 2.3 Axial CT demonstrating where the cervical plate

had eroded through the skin

Fig 2.4 Axial CT demonstrating where screws placed at

C2/C3 had migrated into the neuroforamen

CSF leak on multiple Valsalva maneuvers The

C1 posterior arch was dissected free from the

dura and removed with Kerrison’s The

patient’s wound was then closed by plastic

sur-gery with a vertical mattress suture at the skin

Multiple cultures were sent, and methicillin-

resistant Staphylococcus aureus was cultured

Infectious disease started the patient on a 6-week course of vancomycin The patient’s hand function returned over the next few days, and he began eating with utensils

Complication Avoidance

One of the keys to operating at the cal junction is a firm understanding of the anat-omy In particular, vascular injury can lead to deadly outcomes Dissection around the lateral mass of C2 and the arch of C1 requires extreme caution Blunt dissection may be carried out with

occipitocervi-a combinoccipitocervi-ation of Penfield dissectors occipitocervi-and stasis maintained with bipolar cautery and/or thrombin Gelfoam powder and a cottonoid When exposing the posterior ring of the atlas, lateral dis-section should be limited to 15 mm lateral to the midline [27] Furthermore, since the vertebral artery typically runs along the superior aspect of C1 posterior ring, dissection along the inferior aspect is safest There is often significant bleeding from the epidural venous plexus surrounding the C2 nerve root, and this is best controlled with thrombin-soaked Gelfoam slurry and a cottonoid.Instrumentation placement puts the vertebral artery at risk at multiple locations One of the

hemo-Fig 2.5 Axial CT demonstrating C4 lateral mass screws

placed into the bilateral transverse foramen

Fig 2.6 Sagittal CT demonstrating pseudarthrosis of the

hardware with haloing around the screw and bony

interface

Fig 2.7 Sagittal CT demonstrating solid fusion at

occipi-tocervical junction

keys to complication avoidance is obtaining

pre-operative imaging to assess the course of the

ver-tebral artery to understand where it may vary

from normal anatomy In regard to normal

anat-omy, the use of anatomical landmarks can aid in

the safe placement of instrumentation During

placement of C1 lateral mass screws, both the

vertebral and carotid arteries are at risk The

ver-tebral artery can be avoided by using an

anatomi-cal starting point, that is, midpoint of the lateral

mass where it meets the posterior arch The screw

is then directed 10–15° medially to avoid the

ver-tebral artery which courses laterally The carotid

artery rests on the lateral edges of the anterior

border of the C1 lateral mass The anterior arch

may be bluntly perforated or the screw placed

just short of the anterior arch to avoid injury to

the carotid artery Typical screw length is

30–36 mm, which leaves the head of the screw

dorsal to the C1 arch in order to connect the rod

into the C1 screw The course of the vertebral

artery can be variable at C2 Understanding the

preoperative imaging to plan instrumentation is

critical to screw selection C2 pedicle screws may

be placed by utilizing a starting point slightly

superior and medial to the center of the lateral

mass It is aimed 10 to 25° medially and 15°

cephalad [28] Typical screw length is 22–26 mm

A high-riding vertebral artery within the body of

the C2 is prohibitive to placement of a long C2

pars screw Alternatives include the short C2 pars

screw or translaminar screws [29] We prefer the

Magerl technique for placement of lateral mass

screws in the subaxial spine to avoid vertebral

artery injury [8] The starting point is 1 mm

medial and caudal from the midpoint of the

lat-eral mass and is directed latlat-eral and cephalad

around 30°, respectively

If a vertebral artery is injured, three steps

are key to prevention of further injury First is

control of the active hemorrhage; second is

prevention of acute neurological injury from

ischemia; and third is prevention of

postopera-tive complications such as thromboembolism

or pseudoaneurysm Primary control of an

active hemorrhage can be obtained by primary

repair, bypass surgery, or sacrifice [30]

Hemostasis should be obtained with pressure applied by thrombin-soaked Gelfoam pledgets and cottonoids One should avoid using inject-able thrombin particulate combinations because these may embolize into the vessel and cause a stroke For primary repair, exposure of the vertebral artery above and below the injured segment may entail opening the transverse foramen a level above and below The vessel can then be repaired directly by 7–0 or 8–0 Prolene If direct repair is not an option, the vessel can be sacrificed or bypassed A vessel should be sacrificed if there is good retrograde flow Endovascular coiling is an option to stop bleeding in an injured vertebral artery or if there is a pseudoaneurysm following an injury [31] If a vertebral artery has been injured, extreme caution must be taken in instrument-ing the contralateral side as a bilateral verte-bral artery injury is potentially fatal [32] Postoperatively a conventional angiogram or

CT angiogram should be obtained to determine the extent of injury and an antiplatelet medica-tion considered for prevention of further thromboembolism and stroke

In the case above, the occipital plate eroded through the skin following surgery and led to chronic and recurrent surgical site infections The occipital plate was placed too superiorly and dor-sally on the skull at the index surgery, thus becoming more prominent than the external occipital protuberance The occipital plate should

be placed approximately 1 cm below the external occipital protuberance The midline of the skull base provides the thickest bone for fixation of the occipital plate Bicortical purchase should be attempted with screw fixation This is accom-plished by drilling in 2 mm increments and pal-pating with a ball tip probe for loss of resistance demonstrating perforation of the inner cortex of the skull During screw preparation, a CSF leak may occur while drilling through the skull This can be filled with thrombin-soaked Gelfoam fol-lowed by placement of the screw It should be noted the skull thins quickly away from midline Extensive contouring of rods to match a patient’s anatomy is helpful in avoiding screw pullout

postoperatively This is most common in the

sub-axial spine where a construct levered into the

subaxial lateral mass screws after being secured

to the occipital plate and C1 or C2 screws may

lead to screw pullout and pseudarthrosis [33]

Finally, occipitocervical fusions are high risk for

pseudarthrosis [34] Generous arthrodesis

prepa-ration and use of autograft and allograft as needed

should be utilized We typically brace patients for

12 weeks postoperatively and follow them at

rou-tine intervals with cervical flexion/extension

films once the collar is discontinued to watch for

signs of pseudarthrosis

Summary Points

• The occipitocervical junction is an area of

critical transition from the skull base to the

spinal column

• The use of multiple imaging modalities is

helpful in making a sound diagnosis for either

instability or spinal cord compression

• A thorough understanding of the bony,

vascu-lar, and ligamentous anatomy is crucial for

safe placement of implants

• An understanding of common complications,

avoidance techniques, and repairs should

complications arise is necessary

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Introduction

Atlantoaxial subluxation (AAS) refers to a loss

of stability between the atlas (C1) and axis (C2)

and may result from a number of factors [1]

Causes can be subdivided into five categories:

congenital (hypoplasia, Marfan or Down’s

syn-dromes, aplasia of the odontoid process),

trau-matic (fractures and/or ligamentous disruption),

inflammatory (rheumatoid arthritis), infectious

(osteomyelitis or retropharyngeal abscess), and

neoplastic (metastatic and primary lesions) [2]

Relevant Anatomy

The principal motion at the C1–C2 joint is axial

rotation The C1 ring is unique in that there is no

vertebral body or spinous process The widest

cervical vertebra is composed of an anterior and

posterior arch On the anterior arch lies an

ante-rior tubercle which serves as the attachment site

of the anterior longitudinal ligament and the

lon-gus colli muscle On the superolateral aspect of the posterior arch lies the vertebral artery in a groove named the sulcus arteriosus In about 15% of individuals, this groove is roofed and termed the arcuate foramen On its superior sur-face, C1 has a concave articular surface that artic-ulates with the occipital condyles

The C2 vertebral body consists of a body, toid process, pedicles, pars interarticularis, lamina, and a large, bifid spinous process There are multi-ple articulating surfaces The unique feature lies in its C2 odontoid process which projects superiorly and has multiple ligamentous attachments to C1 and the occiput The odontoid process receives its blood supply from two sources The tip of the pro-cess is supplied by the apical branch of the hypo-glossal artery (anterior circulation), whereas the base receives its blood supply from the branches of the vertebral artery (VA; posterior circulation)

odon-The VA, as it ascends in the cervical spine, exits the C2 transverse foramen and takes a 45° lateral projection before entering the C1 transverse fora-men (V3 vertical portion) The VA then turns medially and travels along the C1 sulcus arteriosus (V3 horizontal portion) before turning anteriorly and piercing the atlanto-occipital membrane

There are numerous ligaments that maintain stabilization of the atlantoaxial complex The cruciate ligament consists of three components (superior, inferior, and transverse) The trans-verse component, otherwise known as the trans-verse atlantal ligament (TAL), maintains stability

of the atlantoaxial complex by affixing the

odon-© The Author(s) 2018

P Mummaneni et al (eds.), Spinal Deformity, DOI 10.1007/978-3-319-60083-3_3

Transoral Odontoidectomy and C1-2 Posterior Fusion Complication

Andrew K Chan, Michael S Virk, Andres J Aguirre, and Praveen V Mummaneni

A.K Chan • M.S Virk • A.J Aguirre

Department of Neurological Surgery,

University of California, San Francisco,

San Francisco, CA 94143, USA

P.V Mummaneni (*)

Department of Neurosurgery,

University of California, San Francisco,

San Francisco, CA 94143, USA

e-mail: Praveen.mummaneni@ucsf.edu

3

toid to the anterior ring of the C1 preventing

AAS If the TAL is compromised, the paired alar

ligaments (occipital alar and atlanto-alar) provide

support in preventing alantoaxial subluxation

The apical ligament, which attaches the tip of the

odontoid process with the basion, does not

pro-vide any significant stability in preventing

sub-luxation [3] The tectorial membrane, the

accessory atlantoaxial ligament, and the

atlanto-dental ligament may offer minor stabilization of

the alantoaxial complex

Typical Presentation

Presenting Symptoms/Signs

Presentation varies depending on the type and

etiology of AAS Patients presenting with

rota-tory AAS rarely have a neurologic deficit but

present with headache, neck pain, torticollis,

reduced range of motion, and a classic cock-

robin head position (20° lateral tilt to one side,

20° rotation to the other side, and slight flexion)

[4] In children presenting with AAS with an

upper respiratory tract infection (URI),

inflam-mation from the URI may cause injury to the

TAL or facet capsules, resulting in AAS, a

condi-tion known as Grisel syndrome [5]

Patients presenting with anterior AAS may

present with a neurologic deficit (33%) [6]

Those presenting with anterior AAS or AAS

due to a neoplastic or inflammatory process may

present with sequelae of a compressive or erosive

tumor/pannus with local or referred pain (67%

and 27%, respectively) and signs of cervical

myelopathy including hyperreflexia (67%),

spas-ticity (27%), weakness (27%), and sensory

dis-turbance (20%) [7] Local pain can arise from

compression of the C2 nerve root and results in

upper cervical or suboccipital pain Referred pain

may be experienced in the mastoid, occipital,

temporal, or frontal regions

In AAS, patients may also present with

pos-tural dizziness, dysarthria, or diplopia associated

with vertebrobasilar insufficiency if the VA is

compressed [8]

Imaging

AAS is most commonly diagnosed on cervical spine plain radiographs On AP plain radiographs, rotatory subluxation is visualized as a frontal pro-jection of C2 with a simultaneous oblique projec-tion of C1 [9] The lateral mass that is subluxed anteriorly appears as a larger, more medialized lat-eral mass on the AP projection The spinous pro-cess of C2 may appear tilted to one direction and rotated to the contralateral direction AAS may be particularly obvious on dynamic films, where the magnitude of AAS is increased on neck flexion.Two measurements provide information on atlantoaxial joint stability: the anterior atlantoden-tal interval (ADI) and the posterior atlantodental interval (PADI) The ADI, or the distance between the posterior aspect of the anterior C1 arch and the anterior aspect of the odontoid process, if >3 mm (or >4 mm in the pediatric population, >6 mm in the rheumatoid population), suggests disruption of TAL though it does not correlate with the risk of neurologic injury or the presence of clinically sig-nificant symptoms The ADI may be elevated with anterior AAS due to disruption of the TAL The PADI, or the distance between the posterior aspect

of the odontoid process and the anterior aspect of the posterior arch of C1 (i.e., the amount of room available for the spinal cord), predicts neurologic recovery following surgery Patients with pre-op PADI < 1 cm showed no neurologic recovery [10].Further information may be gleaned on the integrity of the TAL On an open-mouthed odon-toid X-ray, the rule of Spence suggests that the TAL may be disrupted if the total overhang of both C1 lateral masses on C2 is greater than 7 mm [11].Computed tomographic imaging is useful to fully characterize fracture types and locations It may demonstrate rotation or subluxation of the atlas Magnetic resonance imaging is the gold standard to evaluate the competence of the TAL, the effects of subluxation, the extent of a pannus, and the extent of upper cervical spinal cord com-pression MRI findings of high gradient-echo sig-nal within the TAL, loss of continuity of the TAL,

or blood at the insertion site of the TAL on C1 may suggest TAL disruption Provoked magnetic

resonance imaging films may be done with the

head flexed to fully appreciate the extent of the

C1–C2 subluxation

For patients suspected of having a foramen

transversarium abnormality on CT or MRI, the

ver-tebral artery can be further assessed with CT or MR

angiogram and/or digital subtraction angiography

Classification

There are three types of AAS: rotatory, anterior,

and posterior AAS was first classified by Greenberg

in 1968 as reducible and irreducible [12] Rotatory

subluxation is further classified by the presence of

injury to the TAL, facet capsules, and the amount

of anterior displacement in a classification scheme

by Fielding and Hawkins [4] (Table 3.1)

A more recent classification scheme proposed

by Wang provides treatment recommendations

based on the type of AAS [1] (Table 3.2).

Types of Pathology (Table 3.3 )

Treatment Options

Treatment options are dependent on both types of

subluxation and pathology Rotatory subluxation,

if treated within the first few months, is generally

reducible by traction alone If the subluxation has been present >1 month, traction is less successful [13] If traction is successful in reducing the AAS, then the surgeon can do a posterior fusion [4] Irreducible rotatory AAS or rotatory AAS that has failed reduction and immobilization should be treated with staged traction and surgi-cal fixation A staged anterior transoral odontoid-ectomy and atlantoaxial joint osteotomy to release the C1–C2 complex possibly followed by skull traction and then a second stage C1–C2 posterior fusion are also the options [13] The construct may require extension if additional pathology is present

In the unique case of Grisel syndrome, otics should be administered for the causative pathogen prior to traction and immobilization for 6–8 weeks [14] The type of immobilization is directed by Fielding and Hawkins classification with Type 1 injuries requiring a soft collar, a Type 2 injury requiring a Philadelphia collar or SOMI, and Type 3 or 4 injuries requiring possible halo immobilization Surgical reduction and fixa-tion is reserved for those that fail traction and immobilization

antibi-Anterior subluxation treatment is dependent

on the integrity of the TAL and type of TAL injury In the rare Type 1 TAL injury, there is an anatomic disruption from tear of the TAL itself

In this case, the TAL is unlikely to heal, and these injuries require surgical stabilization [15] In the more common Type 2 injury, there is a physio-logic disruption of the TAL at its attachment point to C1 (e.g., as may occur with C1 lateral mass fractures) Reduction and immobilization, with a halo, is associated with a 74% chance of TAL healing and should be attempted prior to surgical stabilization Thus, in anterior AAS, traction reduction and immobilization should be utilized for Type 2 TAL injuries Surgical fusion

is considered for all Type 1 TAL injuries, Type 2 TAL injuries that remain unstable after 3 months

of immobilization, and those with irreducible injuries C1–C2 posterior fusion alone is usually sufficient if the C1 arch is intact or in the case of unilateral ring or anterior C1 arch fractures However, fractures at multiple sites on the C1 ring or on the posterior arch may require an occipital to cervical fusion

Table 3.1 Fielding and Hawkins classification of

rota-tory atlantoaxial subluxation

Type

Description AD

(mm) CommentTAL a Facet injury

I Intact Bilateral ≤3 Dens acts

as pivot

II Injured Unilateral 3.1–5 Intact joint

acts as pivot III Injured Bilateral >5 Rare Very

unstable

IV Incompetence of the odontoid

with posterior displacement

Rare Very unstable From Greenberg [ 5 ], Table 28–18, with kind permission

from Thieme Medical Publishers, Inc.

aTAL transverse atlantal ligament, AD anterior

displace-ment of C1 on C2

Surgical Options

Current common options for fixation of the

atlan-toaxial complex include posterior clamps,

poste-rior wiring techniques, C1–C2 transarticular

screw fixation, posterior C1 lateral mass screw

with C2 pars or pedicular screw fixation,

occipi-tocervical fixation, and anterior C1 lateral mass

to C2 fixation [16–19]

Current options for decompression of the C1–

C2 complex include posterior laminectomies and

anterior transoral surgery [20, 21]

Several complications can result for any of

these techniques, and we will explore one case

that illustrates the potential for morbidity

Pertinent History and Physical

Exam Findings

The patient is a 67-year-old male transferred in

from an outside hospital He was bacteremic with

methicillin-sensitive Staphylococcus aureus and

started on empiric antibiotics prior to arrival Opiates, amphetamines, and cocaine were present

on his urine toxicology screen He reported sive right flexion and rotation of his neck over sev-eral months His neck was stiff, and he was unable

progres-to rotate progres-to the left or extend his neck He reported a recent fall with loss of consciousness and noted sub-sequent neck pain and left-sided arm and leg weak-ness greater than the right side On exam, the patient’s head was rotated and laterally flexed to the right, placing his right cheek on his right shoulder (Fig 3.1c) His left arm strength exam was as fol-lows: deltoid 0/5, biceps and triceps 3/5, and grip 4/5 His right arm was 4−/5 in the deltoid and oth-erwise 4/5 throughout His left leg was 3/5 in the iliopsoas and otherwise 4−/5 throughout His right leg was 4+/5 throughout His sensation was intact to all modalities He had a positive Babinski sign bilat-erally but no other pathological reflexes The initial

CT scan demonstrated C1–C2 subluxation with Type 2 dens fracture and retroflexion, causing sig-nificant mass effect on the spinal cord at the cervi-comedullary junction (Fig 3.1c) A CT angiogram revealed right vertebral artery occlusion at the site

of the C2 fracture (throughout the V3 segment of this vessel), so he was started on aspirin (Fig 3.1f)

An MRI further demonstrated an embolic infarct in the right inferolateral cerebellum He was placed in

a halo vest while being treated for bacteremia and vertebral artery dissection as well as being moni-tored for withdrawal in an intensive care unit set-ting Operative treatment was deferred for 1 week until the patient was optimized medically as requested by the neurology and ICU team in light of his recent stroke During this time, his left arm and leg weakness progressed in spite of halo immobili-zation to the extent that he was unable to grip with his left hand and his left leg was 2/5 proximally and 3/5 distally

Table 3.2 Wang classification of AAS

Type Description Diagnosis Treatment

I Instability Reducible in dynamic X-rays Posterior fusion alone

II Reducible Reducible with skeletal traction under general anesthesia Posterior fusion alone III Irreducible Irreducible with skeletal traction under general anesthesia Transoral decompression

+ posterior fusion

IV Bony dislocations Dislocations with bony anomalies that are visualized

by reconstructive computed tomography scan

Transoral decompression (± posterior fusion) From Yang et al [ 1 ], Table 2

Table 3.3 Types of pathology

Congenital (hypoplasia, Marfan or Down’s syndromes,

aplasia of the odontoid process, or os odontoideum)

Congenital hypoplasia of the odontoid process, also

known as Morquio syndrome, or odontoid process

fracture, may result in anterior AAS despite a normal

ADI on plain films

Traumatic (fractures and/or ligamentous disruption)

Trauma can cause disruption of the TAL

Inflammatory (rheumatoid arthritis)

Inflammatory states may result in weakened

attachment points of the TAL

Infection

Osteomyelitis or retropharyngeal abscess may result in

osseous or ligamentous disruption

Neoplastic (metastatic and primary lesions)

occlusion of the right

vertebral artery at the

level of its entrance into

the C2 transverse

foramen (g) Sagittal

T2-weighted MRI

demonstrating cervical

cord compression and

cord signal change (h)

Axial T2-weighted MRI

at the level of maximal

compression due to the

posterior displaced

odontoid process

Radiographic Images

A non-contrast CT scan and subsequent CT

angiogram (Fig 3.1) of the cervical spine revealed

a Type 2 dens fracture through a presumed prior

site of erosive rheumatoid-related pannus as well

as subluxation of C1 on C2 (Fig 3.1c) Underlying

erosions throughout the dens, C2 vertebral body

and right lateral mass of C1 were also visualized

suggesting a concomitant C2 osteomyelitis

(Fig 3.1d, e) The fractured odontoid was

retro-verted posteriorly and leftward with associated

invagination and canal narrowing The fracture

line extended to the right foramen transversarium

There was multilevel degenerative change with

anterolisthesis of C3 on 4 and C4 on 5 and C7 on

T1 The CT angiogram was significant for a

non-dominant right vertebral artery occlusion that

occurs abruptly at the C2 fracture line and

contin-ues throughout the V3 vertebral artery segment

(Fig 3.1f) There was reconstitution of the vessel

via retrograde flow in the proximal V4 segment

The right posterior-inferior cerebellar artery

(PICA) likely filled via collaterals

An MRI further demonstrated the severe cord

compression posterior to C2 (Fig 3.1g, h)

Edema extended from the top of the medulla

through the bottom of C3 level in the spinal cord

There was disruption of the anterior and posterior longitudinal ligaments, cruciate ligaments, TAL, and apical and odontoid ligaments as well as injury to the origin of the ligamentum flavum Fluid within the right occipital condyle-C1 artic-ulation indicated capsular injury or infection There was extensive prevertebral swelling and edema throughout the neck musculature

The MRI of his brain was also significant for

an embolic infarct in the right inferolateral cerebellum

Surgery Performed

The patient was initially placed in a four-pin halo for traction and then immobilization to restore alignment from occiput-C1–C2 While placing the pins, the patient sustained two skull fractures

at two different sites through the inner cortical table (Fig 3.2) No intracranial bleeds occurred due to these fractures Traction was then aban-doned due to his osteoporotic skull fractures.The halo pins were repositioned and he was secured in a halo vest to permit mobilization Surgery was delayed for 1 week due to evidence

of a new posterior fossa stroke from the vertebral artery dissection

Fig 3.2 Complications of halo pin placement (a) Demonstrates a skull fracture due to pin placement with an 8-lbs

torque wrench (b) Demonstrates inner table violation due to pin placement

The surgical plan was to perform a two-stage surgery in order to stabilize the occiput-C1–C2 junction and then to decompress the spinal cord For stage 1, an occiput to C6 posterior spinal fusion was planned as he had stenosis, listhesis, and osteoporosis in the upper and mid-cervical spine, and the patient was placed prone and the crown of the halo was locked into the Mayfield clamp A C1 lateral mass screw and a C2 pars screw were placed on the left, but this was not possible on the right given the fractures and bony erosion A C2 laminectomy was performed, and a partial C1 inferior laminectomy was performed (Fig 3.3a, b).

The patient was removed from the halo after stage 1 and returned to the ICU for recovery The patient remained stable during that interval and

on day 3 was taken back to the OR for a tomy and an anterior, transoral odontoidectomy

tracheos-An endoscope (0° and 30°) was introduced through the mouth and used for visualization throughout the case A midline incision was made from the nasopharynx to 3 cm inferiorly, and the mucosa and longus muscles were divided with Bovie cautery The ring of C1 was identified superiorly, and fluoroscopy was used to confirm the location The anterior arch was drilled to

2 mm beyond the lateral margin of the odontoid bilaterally The dura was circumferentially dis-sected away from the fractured odontoid frag-ment; however, the dura was adherent and eroded

by the odontoid pathology, and a large dural rent was encountered upon removal of the dens The dura at the margins of this dural tear was mark-edly attenuated with poor structural integrity Cerebrospinal fluid was leaking in a pulsatile fashion, and the anterior spinal cord was visual-ized (Fig 3.3c) The dura was subsequently repaired, as described below, and the patient was taken back to the ICU for recovery

Fig 3.3 Postoperative (a) lateral and (b) AP plain films

demonstrating excellent correction of the subluxation

with an occiput to cervical 6 fusion (c) T2-weighted

sag-ittal MRI reveals high-intensity fluid in continuity with the thecal sac consistent with a CSF leak

Detailed Description

of the Complications

The initial complication in the management of

this case occurred while placing the patient in

skull pins to fit him in a halo vest Two of the four

pins were placed in the frontal skull, while the

remaining two were placed in the

temporopari-etal skull On follow-up CT scan, it was noted

that the left temporoparietal pin had fractured

through the osteoporotic skull inner table;

how-ever, no intracranial bleed occurred (Fig 3.2a)

Both temporoparietal pins were removed and

relocated to a more posterior location in the

pari-etal bone where the osteoporotic skull appeared

to be marginally thicker on CT imaging However,

again, one of the two pins (right parietal)

frac-tured through the inner table of the skull

(Fig 3.2b) There was no intracranial bleed

asso-ciated with this fracture either All pins were

placed with the manufacturer provided torque

wrench and tightened to the manufacturer

speci-fied 8 inch-lbs All surgeons must be mindful of

this potential problem in osteoporotic patients

The second complication occurred during the

stage 2 procedure while decompressing the

ven-tral spinal cord by resecting the fractured and

possibly osteomyelitic odontoid fragment After

drilling down the anterior arch of C1 with

suffi-cient margins to establish a resection corridor, the

free-floating fractured odontoid was encountered

firmly adherent to the ventral dura The dura was

gently and meticulously dissected away from the

bony fragment using Rhoton microinstruments

under endoscopic visualization In spite of

metic-ulously freeing the fragment from the adherent

dura with microinstruments, we found that CSF

started to leak from posterior to the dens We

noted the dura here was eroded and very thin

The dens was slowly resected, and there was a

5×5 mm dural tear surrounded by thinned dura

with wispy, shredded margins Cerebrospinal

fluid was leaking in a pulsatile fashion, and the

ventral cord was visualized through the defect

There was not sufficient redundancy nor integrity

in the dural margins to attempt primary suture

repair An alternative approach was elected as

described below

Complication Management

Skull Fracture with Halo Pins

The anterior pins should be placed 1 cm above the lateral one third of the orbit This should be anterior and medial to the temporalis and lateral

to the supraorbital nerve The posterior pins should be placed opposite the frontal pins so that opposing forces are exerted Generally these are located posterior and 5 mm above the pinna Pins are placed with 8 inch-lbs of force gauged by use

of a torque wrench If there is concern for bone strength, it is recommended to use six pins or more to distribute the force more evenly When using less than 8 inch-lbs of torque, consider additional points of fixation

Ventral CSF Leak Management After Odontoidectomy

Ventral cerebrospinal fluid leaks following toidectomy are not uncommon and can be chal-lenging to manage The indications for this procedure are generally removal of a degenerative

odon-or rheumatoid pannus, decompression of an tious or pathologic compressive lesion, or trauma

infec-In all cases, the underlying dura may be adherent, attenuated, or frankly violated prior to surgical manipulation Thus, strategies for repair should be considered at the preoperative planning stage In this particular patient, primary repair by reapprox-imating the dura and suturing it closed was not possible A small piece of dural substitute was cut

to approximately 1 × 1 cm and placed over the native dura with a second overlapping piece placed inferiorly The tip of the uvula was then harvested, demucosalized, and placed over the dural substi-tute in a non-compressive fashion Fibrin glue was then sprayed over the onlay grafts At that point, there was no CSF leaking around the repair The longus colli were subsequently closed Muscle insertions of the clivus were preserved, so this final layer of closure appeared intact and no fur-ther grafts were used Merocels were placed to hold pressure over the superior aspect of the wound and remained in place until post-op day 5

Prior to leaving the operating room, the patient

underwent a tracheotomy This was performed to

protect the repair site and avoid endotracheal

intubation should that have been required The

patient also had an orogastric tube upon leaving

the operating room However, this was removed

after a percutaneous endoscopic gastrostomy

tube was placed on post-op day 2

The patient had a lumbar drain placed on

op day 1 and was drained at a rate of 10–15 cc/h

for 3 additional days On post-op day 5, the repair

was inspected via rigid endoscope There appeared

to be moist mucosa and secretions pooled in the

region but no clear CSF leak The lumbar drain and

merocels were removed at this point

Vertebral Artery Dissection

Management

Whether a vertebral artery dissection occurs due

to trauma or due to surgical injury to the vessel,

the essential management strategy is to assess for

collateral flow, ischemic sequelae, and to

con-sider anticoagulation or antiplatelet therapy If a

nondominant vertebral artery injury is identified

immediately post-op, angiography with

emboli-zation of the vessel may be an option If the

ver-tebral artery injury occurs secondary to placement

of instrumentation, then instrumentation of the

contralateral side should not be performed until

vascular imaging is obtained and the severity of

the injury is assessed

Discussion

Vertebral Artery Dissection

Vertebral artery occlusion has been described

previously in AAS In a case of reducible AAS in

a patient with RA, vertebral arteriography

dem-onstrated positional occlusion of the left VA [22]

associated with cerebral and cerebellar

symp-toms Posterior C1–C2 fusion prevented further

symptomatology and corrected the positional VA

insufficiency In a patient with AAS and

recur-rent cerebellar or brainstem symptoms, vertebral

artery angiography may be helpful Dynamic

angiographic imaging may be necessary—where

it can be undertaken in a safe manner Knowledge

of VA anatomy, and the presence of dissection or occlusion, is helpful for preoperative planning and may affect surgical timing, depending on the needs of peri-stroke medical management which includes antiplatelet medication administration

Halo Pin Cranial Penetration

Halo pin insertion is required in select cases of AAS Common complications of pin placement include superficial pin site infections, pressure sores, and pin site discomfort [23] More serious complications result from cranial pin penetration [24], which may be associated with the develop-ment of intracranial hematoma [25], cerebritis [23], CSF leak [26], and pneumocephalus and seizures [27]

Multiple cadaveric studies have been taken and demonstrate that 8 inch-lbs of torque may be optimal to prevent pin loosening while also avoiding cranial penetration [28, 29] The extent to which this applies to vulnerable populations, such as the elderly and in those with osteoporosis, is under ongoing investigation In a study of the elderly population, a cadaveric study

under-of >70-year-old specimens [30], it was found that

8 inch-lbs of torque remained safe for both anterolateral and posterolateral pin placements This study was corroborated by further cadaveric work in the elderly by Ebraheim and colleagues [31] Proper patient education is also crucial in preventing a number of cases of pin site penetra-tion, such as in the case of pin overtightening by patients without medical guidance [27] Special care should be undertaken in patients with osteo-porosis or in those with known risk factors for osteoporosis [25] Other contraindications for halo pin placement are the presence of cranial fractures, intracranial injuries, and soft tissue injuries of the skull or age < 3 Further investiga-tion of the relationship of pin torque and grade of osteoporosis, perhaps via CT imaging, is war-ranted Special attention should be paid to deter-mining if a threshold of skull thickness exists

beneath which pin placement may be unsafe

which may be measured by obtaining a CT of the

head before halo placement

Cerebrospinal Fluid Leak

Following Transoral Odontoidectomy

A transoral odontoidectomy may be required in

AAS to address ventral compression of the

cervi-cal spinal cord or to detether an irreducible

sub-luxation prior to posterior fusion A primary

concern of this anterior-based approach is

cere-brospinal fluid leakage, which is reported with

rates ranging from 0% to 6.3% following

tran-soral odontoidectomy [32–35] although rates

may be as high as 9% following transnasal

odon-toidectomy (2 of 22 cases in a review of the

lit-erature by Yu and colleagues [36]) This may

occur despite meticulous dissection because of

adhesions that obliterate the plane between the

odontoid tip and the dura that are often a sequelae

of long-term compression [36]

If recognized intraoperatively, primary repair

should be undertaken when feasible and may

uti-lize a combination of fat graft, uvula graft,

muco-sal flap, dural substitute, and/or fibrin glue If

persistent leakage occurs postoperatively, timely

recognition and external lumbar drainage are

uti-lized [34, 36] to avoid persistent leak with risks

of intracranial infection and meningitis

Summary Points

• Atlantoaxial instability results from the loss of

structural integrity of the C1–C2 articulation

Treatment is focused on restoration of proper

alignment, neural decompression, and

stabili-zation with fusion

• Atlantoaxial instability can arise from

con-genital, traumatic, inflammatory, infectious,

or neoplastic etiologies

• Patients with atlantoaxial instability have

varying presentations depending on the type

and etiology of the instability Patients may

present with pain or neurologic deficit Those

with rotatory AAS may present with the

clas-sic cock-robin head position Those with tebral artery injury may present with vertebrobasilar insufficiency

ver-• Radiographic evaluation of atlantoaxial joint stability and integrity of the transverse liga-ment include measurements of ADI (< 3 mm,

< 4 mm in pediatric population) and tion of the overhang of both C1 lateral masses on C2 (i.e., Rule of Spence, over-hang < 7 mm)

summa-• Surgical techniques depend on the type of subluxation and pathology and include poste-rior clamps, posterior wiring techniques, C1–C2 transarticular screw fixation, posterior C1 lateral mass screw with C2 pars or pedicular screw fixation, occipitocervical fixation, and anterior C1 lateral mass to C2 fixation Decompression may be completed either pos-teriorly with laminectomies or anteriorly with transoral surgery

• When halo immobilization is attempted, care should be taken in osteoporotic patients to avoid skull fractures associated with halo pins

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© The Author(s) 2018

P Mummaneni et al (eds.), Spinal Deformity, DOI 10.1007/978-3-319-60083-3_4

Mid-Cervical Kyphosis Surgery Complication

Dan Harwell and Frank La Marca

D Harwell

Department of Neurosurgery, University of Michigan

Medical School, 1500 E Medical Center Dr, 3470

Taubman Center, Ann Arbor, MI 48109, USA

F La Marca (*)

Department of Neurosurgery, University of Michigan,

Ann Arbor, MI, USA

e-mail: frank.lamarca@allegiancehealth.org

4

Case: Degenerative Cervical

Kyphosis with Myelopathy

Introduction

Degenerative cervical myelopathy is a

progres-sive spine disease and the most common cause of

spinal cord dysfunction in adults worldwide [1]

Cervical kyphosis can be defined as a loss of the

normal lordosis of the cervical spine required to

maintain overall cranio-spinal balance Though

typically a result of traumatic or iatrogenic injury,

degenerative changes and congenital conditions

are other leading causes Due to the change that

occurs in normal cervical biomechanics of

verte-bral segments and stabilizing tissues once

cervi-cal lordosis is lost, a vicious cycle can occur that

promotes progressive deformity With healthy

cervical lordosis, the instantaneous axis of

rota-tion (IAR) of each cervical vertebra should be

located anterior to the sagittal vertical axis The

anterior bony elements of the cervical spine resist

compressive forces, whereas the posterior

ele-ments and ligaele-ments resist tensile forces Initially, there is a balance of forces between the weight of the head and the lordotic cervical spine, such that the weight-bearing axis of the head is posterior to the vertebral bodies of C2–C7 along the sagittal vertical axis Once there is loss of lordosis, the weight-bearing axis is relatively and progres-sively shifted ventrally

The loss of the posterior tension band will force the vertebral body to bear more of the com-pressive force The neck musculature is placed at

a mechanical disadvantage in order to keep the head upright, and the cycle of a progressive kyphotic deformity is perpetuated Disc degen-eration as well as forward-tilted angulation of cervical end plates further contributes to the pro-gression of this deformity Progression of the kyphotic deformity can cause narrowing of the spinal canal with the spinal cord to be draped over the posterior aspect of the vertebral bodies where the kyphotic angle is maximal Flexion of the cervical spine increases compression of the cervical cord over the kyphotic segment(s) and can compromise the integrity of small feeder ves-sels along the anterior aspect of the cord This movement also increases the tension in the cord due to a tethering effect produced by dentate liga-ments and the cervical nerve roots The combina-tion of ischemic damage and cord tension initiates

a series of pathobiological events that can result

in irreversible histological damage and neurological impairment [2] Direct neuronal and axonal damage often results in myelomalacia

Presentation

Clinically, this cycle of progressive kyphosis leads

to mechanical neck pain, myelopathy, and potential

difficulty with swallowing and gaze (loss of the

horizon) in severe cases Table 4.1 lists common

symptoms and physical exam findings

Diagnosis

Advanced multi-planar spinal neuroimaging is

required Most often, the study of choice is MRI

which allows assessment of spinal canal

compro-mise, osseoligamentous cord compression, and

effacement of the cerebrospinal fluid with cord

deformation with T1 hypointensity and T2

hyper-intensity [3] CT is of value in assessing the bony

anatomy and whether fusion has occurred X-rays

are typically required to assess flexibility and

alignment

Treatment

In significantly symptomatic patients, surgery is

indicated Surgical decompression typically

results in substantial and clinically meaningful

improvements Evidence suggests that without

surgical decompression, 20–62% of patients with

symptomatic myelopathy will deteriorate by 1

point on the Japanese Orthopaedic Association

(JOA) scale 3–6 years after initial assessment [2]

Surgical decompression can be achieved from an

anterior and/or posterior approach

Factors to consider when choosing an approach include location and nature of the pathology need-ing to be addressed, patient’s clinical presentation and sagittal balance, and surgeon’s preference In regard to complications, surgery for degenerative cervical myelopathy is associated with around a 14% risk of complication [3] Most common complications are C5 palsy, dural tear, infection, and dysphagia

Case Presentation

A 68-year-old male presents with a 6-month tory of recurrent progressive arm and leg weak-ness, unsteady gait, falls, loss of manual dexterity, and neck pain The patient had progressive diffi-culty holding his head erect and difficulty seeing the horizon He had undergone 5 years prior a C3–C4 anterior cervical discectomy and fusion sup-plemented by a C2–C4 posterior cervical fusion (Figs 4.1 and 4.2) Physical exam reveals weak-ness in his arms and legs, hyperreflexia, and a positive Hoffman and Babinski sign His gait is ataxic Given the patient’s kyphotic deformity, a C5–C6 corpectomy with anterior and posterior fusion from C4 to T2 with intraoperative neuro-monitoring was performed to decompress the cord and correct the kyphosis (Fig 4.3) The patient emerged from anesthesia and had improved strength in all four extremities On postoperative day number two, the patient was unable to feed himself due to profound weakness in his bilateral deltoids and biceps

Discussion of Complication

Postoperative C5 palsy complicates between 1.6% and 12% of ventral decompressive proce-dures and up to 30% for posterior procedures [4, 5] The pathogenesis of C5 palsy is poorly understood and is believed to be multifactorial (Table 4.2) Hypotheses include (1) direct intra-operative neural injury, (2) “tethering” of the short C5 nerve root, and (3) ischemic and reper-fusion injury of the spinal cord [6] Other risk factors include corpectomy decompressions or foraminotomy decompressions greater than

Table 4.1 Common presenting symptoms and physical

exam findings for symptomatic degenerative cervical

Neck pain Difficulty swallowing

Upper/lower extremity

weakness

Hyperreflexia Paresthesias Hoffman and/or Babinski sign

Decreased dexterity Spastic gait

Unstable gait Loss of gaze of the horizon

15 mm Other theories exist such as the anterior

dural expansion following corpectomy in the

set-ting of restricted spinal cord movement possibly

causing C5 root dysfunction, particularly in cases

in which the ventral rootlets are adherent to the dura

or in OPLL C5 palsy appears to be more common

with increasing age, male patients, and multiple corpectomy levels [7 8] Other risks include severe foraminal stenosis and presence of T2 sig-nal change (Table 4.3) In addition, ossification

of the posterior longitudinal ligament (OPLL) has been shown to be a potential risk factor It is