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Neurocritical Care
Management of the
Neurosurgical Patient
Neurocritical Care
Management of
the Neurosurgical
Patient
Monisha Kumar, MD
Assistant Professor
Departments of Neurology, Neurosurgery, and Anesthesiology & Critical Care
Associate Director of Neurocritical Care Fellowship Program
Perelman School of Medicine at the University of Pennsylvania
Philadelphia, PA, USA

W. Andrew Kofke, MD, MBA, FCCM, FNCS

Professor, Director Neuroscience in Anesthesiology and Critical Care Program
Co-Director Neurocritical Care
Co-Director Perioperative Medicine and Pain Clinical Research Unit
Department of Anesthesiology and Critical Care
Department of Neurosurgery
University of Pennsylvania
Philadelphia, PA, USA

Joshua M. Levine, MD, FANA, FNCS

Chief, Division of Neurocritical Care, Department of Neurology
Co-Director, Neurocritical Care Program
Associate Professor, Departments of Neurology, Neurosurgery, and Anesthesiology and Critical Care
Perelman School of Medicine at the University of Pennsylvania
Philadelphia, PA, USA

James Schuster, MD, PhD

Associate Professor, Department of Neurosurgery
Director of Neurotrauma
Perelman School of Medicine at the University of Pennsylvania
Philadelphia, PA, USA

Edinburgh London New York Oxford Philadelphia St Louis Sydney Toronto

© 2018, Elsevier Inc. All rights reserved.

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Notices
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In medicine there are a few nodes of care where over a short
period of time a person’s life lies in the balance. The neuro-
critical care unit (NICU) is one such node. Though postop-
erative care units for neurosurgical patients have existed
for many decades the multidisciplinary neurocritical care
field is still very young, dating back only to the 1980s.
As a result, the evidence-base that underlies much of the
decision-making in the NICU is still being assembled. The
lessons-learned from experienced neurointensivists remains
the bedrock of the art of neurocritical care.
This textbook incorporates the wisdom of an impressive
cadre of dedicated physicians who clearly communicated
their art, as well as describing the evidence-base for their
craft. The focus on the neurosurgical patient places the
book in a special position in medical literature. Close work-
ing relationships between the patient’s neurosurgeon, neu-
roanesthesiologist, and the neurointensivist is crucial for
good patient care in the NICU, but is not by itself a replace-
ment for a working knowledge of each others concerns,
abilities, and processes. Understanding the neurosurgery
is as essential for the neurointensivist, as neurointensive
care is to the neurosurgeon. It would be impossible to pro-
vide quality care for the person transferred to the NICU
from the emergency department without knowledge of
what occurred in the emergency department. A similar
Foreword
knowledge of the events that occur in the operating room
is equally essential. However, the emergency department
is a much more familiar environment for the neurointensi-
vist than the operating room. This textbook, written by
neurosurgeons, neuroanesthesiologists, and neurointensi-
vists, defines the key issues needed to meld these two
approaches.
Dr. Kumar and her co-authors bring a unique viewpoint
that mimics the reality of the NICU where the patient care is
a complicated dance with multiple caregivers, the patient
and family. From my position at NIH it’s also important
to note that many of the chapters identify the evidence gaps
that need to be addressed to inform decision-making in the
NICU. Outlining these should enable neurointensivists to
engage in research to understand those interventions asso-
ciated with clinically important outcomes in specific
patients. Though professional agendas differ among care-
givers, a good final clinical outcome is shared by all, and
the body of knowledge displayed in the text is a wonderful
guide to the care of the neurosurgical patient in the NICU.
Walter Koroshetz, MD
Director, National Institute of
Neurological Disorders and Stroke
ix

Neurocritical Care is a burgeoning field dedicated to the
management of patients with life-threatening neurological
and neurosurgical illness as well as those at risk for neuro-
logical complications of systemic disease. Much of neuro-
intensive care unit (Neuro ICU) management focuses on
the postoperative neurosurgical patient. Treating neuro-
surgical patients without a comprehensive understanding
of what occurs in the operating room (OR) may severely
hinder the intensivist in the provision of optimal care. It is
imperative that neuro-intensivists be aware of the relevant
neuroanatomical structures, surgical approach, and anes-
thetic considerations as well as the range of known compli-
cations of elective and non-elective neurosurgery. This is
fundamental to the practice of neurocritical care. However,
the preoperative evaluation, perioperative assessment and
intraoperative management are not comprehensively
taught in the neurocritical care curriculum. This book is
intended to grant deeper insight into perioperative neuro-
surgical evaluations and anesthetic considerations that
may affect the intensive care management of these patients.
It is critical that this knowledge gap be sealed as the field
of neurocritical care matures. The knowledge gap is further
compounded by the fact that practitioners of neurocritical
care hail from a wide variety of primary specialties includ-
ing Internal Medicine, Emergency Medicine, General Sur-
gery, Anesthesiology and Neurology. The diversity of
specialties allows practitioners a varied skill set; however,
a standard and comprehensive set of skills may be elusive.
Although a fundamental understanding of neurosurgery,
including proper patient positioning, operative techniques
and relevant neuroanatomy, remain a prerequisite for
those caring for postoperative neurosurgical patients, it is
an oft-overlooked segment of clinical training.
Transitions in care and patient handoffs have evolved
dramatically over the last decade. Hand-offs in surgical spe-
cialties often focus on the operative intervention, whereas
hand-offs in medical specialties focus on the history of pre-
sent illness. These distinct approaches intersect in the
Neuro ICU, which is frequently a mixed medical-surgical
ICU. Surgical ICU sign-out rounds involves a review of
the anatomy, anesthesia and complications of the surgery
performed for each postoperative patient, in contradistinc-
tion to the individual patient’s initial presentation and
symptom chronology as is often done in the Neuro ICU.
Although reviewing the patient’s initial symptomatology
may be important, it is likely that the early ICU course
might be as much related to the operative procedure, as
to the presenting signs and symptoms. We are unaware
of a reference for the intensivist that provides this type of
perioperative information regarding neurosurgical patients
in a clear and concise manner. This was the impetus for this
textbook.
Preface
Furthermore, the options and methods for intraoperative
monitoring have grown over the past decade and will con-
tinue to do so. Physiological data gleaned from novel mon-
itors provide critical information about the individual
patient’s response to surgery and anesthesia. Understand-
ing the advantages and disadvantages of these monitoring
techniques is imperative to the provision of exemplary care
of the neurocritically-ill patient. Similarly, mounting evi-
dence suggests that critical information is progressively
omitted during points of transitions of care. Anticipatory
inquiry may enhance communication between OR and
ICU staff if providers receiving the patients are knowledge-
able enough to ask probing questions and to elicit details
that may be lost in translation.
The aim of this text, Neurocritical Care Management of the
Neurosurgical Patient, is to serve as the premier reference for
the intensive care management of neurosurgical patients.
Many available neurocritical care textbooks have focused
on particular disease states, pathophysiological conditions,
or medical complications. However, none has described the
specific neurosurgical procedures or anesthetic consider-
ations that impact the critical care management of these
patients.
This textbook is divided into 6 sections. Section 1 offers a
review of core neuroanesthesiology principles applied to the
operative care of neurosurgical patients. Chapters in this
section focus on neurophysiological effects of anesthetic
agents, procedural patient positioning, specific anesthetic
considerations for brain, spinal cord and endovascular neu-
rosurgery, intraoperative neuromonitoring, and intrao-
perative catastrophes.
The lion’s share of the volume is contained within
Sections 2-5. For the most part, a neurosurgeon or
neuro-interventionalist collaborated with a neurointensivist
to write each chapter. Section 2 focuses on types of craniot-
omy procedures, including vascular neurosurgery, neuro-
oncologic surgery, epilepsy surgery, functional neurosurgery
and trauma neurosurgery. Section 3 is devoted to spinal
surgery and Section 4 focuses on endovascular neurosur-
gery. Section 5 is dedicated to specialty procedures
including ventricular shunts and neuro-monitor placement,
combined neurosurgical procedures (e.g. with Otorhinolar-
yngology or Plastic Surgery) and peripheral neurosurgery.
Chapters in Sections 2-5 adhere to a prescribed struc-
ture and format. Each chapter is divided into 3 parts: Neu-
roanatomy and Procedure, Perioperative Considerations,
and ICU Complications. The first part, Neuroanatomy and
Procedure, reviews the relevant neuroanatomy and opera-
tive steps of the procedure. The second part, Perioperative
Considerations, describes the related neuro-monitoring,
operative position and anesthetic choices for the procedure.
The remainder of the chapter, ICU Complications, comprises
xi
xii Preface
an evidence-based review of the potential procedural com-
plications and the relevant critical care management strat-
egies. Section 6 is exclusively devoted to potential ICU
complications of neurosurgery including delayed emer-
gence, intracranial hypertension, hemodynamic complica-
tions, intracranial hypertension, or status epilepticus.
The editors are grateful that the Neuro ICUs at the Uni-
versity of Pennsylvania foster collaborative endeavors
between Neurology, Neurosurgery and Anesthesiology. It
is likely due to the fact that from its inception, the Penn
Neuro ICU represented a shared vision of the chairpersons
of the Departments of Neurology, Neurosurgery and Anes-
thesiology & Critical Care. The inherent nature of this
Neuro-ICU program has borne fruitful clinical, academic
and research programs that are nationally and
internationally recognized. These academic and clinical
endeavors have resulted in partnerships with experts in
neuroanesthesia, neurocritical care and neurosurgery,
many of whom have graciously contributed to this volume.
We believe that this textbook will have broad applicability
and will serve neurosurgeons, anesthesiologists, medical
intensivists, surgical intensivists as well as neurointensi-
vists. We hope that it will also serve as a reference for
trainees of varied backgrounds.
M. A. Kumar, MD
W. A. Kofke, MD, MBA
J. M. Levine, MD
J. M. Schuster, MD, PhD

Manish K. Aghi, MD, PhD
Department of Neurological Surgery, Center for Minimally
Invasive Skull Base Surgery, University of California,
San Francisco, CA, USA
Zarina S. Ali, MD
Assistant Professor, Department of Neurosurgery,
University of Pennsylvania, Philadelphia, PA, USA
Dorothea Altschul, MD
Clinical Assistant Professor of Neurology, Neurological
Surgery, Columbia University College of Physicians and
Surgeons, New York, NY, USA
Zirka H. Anastasian, MD
Assistant Professor of Anesthesiology, Department of
Anesthesiology, Columbia University Medical Center,
New York, NY, USA
Safdar Ansari, MD
Assistant Professor, Chief, Division of Neurocritical Care,
Department of Neurology, University of Utah School of
Medicine, Salt Lake City, UT, USA
William J. Ares, MD
Department of Neurological Surgery, University of
Pittsburgh Medical Center, Pittsburgh, PA, USA
Mark Attiah, BA
Medical Student, Perelman School of Medicine, University
of Pennsylvania, Philadelphia, PA, USA
Anthony M. Avellino, MD, MBA
Chief Executive Officer, OSF HealthCare Neuroscience
Service Line and Illinois Neurological Institute;
Professor of Neurosurgery and Pediatrics, University
of Illinois College of Medicine at Peoria, Peoria, IL,
USA
Rafi Avitsian, MD
Section Head, Neurosurgical Anesthesiology, Associate
Professor of Anesthesiology, Neuroanesthesia
Fellowship Program Director, Anesthesiology and
Neurological Institutes, Cleveland Clinic, Cleveland, OH,
USA
Neeraj Badjatia, MD, MSc
Chief of Neurocritical Care, Program in Trauma, Associate
Professor of Neurology, Neurosurgery, Anesthesiology,
University of Maryland School of Medicine, Baltimore,
MD, USA
List of Contributors
Robert L. Bailey, BS, MD
Physician, Department of Neurosurgery, Paoli Hospital,
Paoli, IN, USA
Nicholas Bastidas, MD, FAAP
Attending, Plastic Surgery, Assistant Professor, Surgery,
Hofstra Northwell School of Medicine, Manhasset, NY,
USA
Paulomi Bhalla, MD
Neurocritical Care Fellow, Department of Neurology,
Hospital of the University of Pennsylvania, Philadelphia,
PA, USA
Adarsh Bhimraj, MD
Head, Section of Neurologic Infectious Diseases, Cleveland
Clinic, Cleveland, OH, USA
Joshua T. Billingsley, MD, MS
Cerebrovascular Surgery, Department of Neurosurgery,
University of Florida at Orlando Health, Orlando, FL, USA
Thomas P. Bleck, MD
Professor and Associate Chief Medical Officer,
Departments of Neurological Sciences, Neurosurgery,
Anesthesiology, and Medicine, Rush University
Medical Center, Chicago, IL, USA
Christine Boone, BS
MD, PhD Candidate, Department of Neurosurgery, The
Johns Hopkins University School of Medicine, Baltimore,
MD, USA
Steven Brem, MD
Chief, Neurosurgical Oncology, Co-Director, Penn Brain
Tumor Center, Department of Neurosurgery, Abramson
Cancer Center, Perelman School of Medicine, University
of Pennsylvania, Philadelphia, PA, USA
Vivek Buch, MD
Neurosurgery Resident, Department of Neurosurgery,
Hospital of the University of Pennsylvania, Philadelphia,
PA, USA
Richard W. Byrne, MD
Professor and Chairman, Department of Neurosurgery,
Rush University Medical Center, Chicago, IL, USA
Daniel P. Cahill, MD, PhD
Associate Professor, Department of Neurosurgery,
Massachusetts General Hospital, Boston, MA, USA
xiii
xiv List of Contributors
Justin M. Caplan, MD
Resident Department of Neurosurgery, Johns Hopkins
University School of Medicine, Baltimore, MD, USA
Nohra Chalouhi, MD
Department of Neurological Surgery, Thomas Jefferson
University Hospital, Philadelphia, PA, USA
Catherine S. Chang, MD
Resident Division of Plastic Surgery, University of
Pennsylvania, Philadelphia, PA, USA
Jason J. Chang, MD
Assistant Professor of Neurological Surgery, Oregon Health
& Science University, Center for Health & Healing,
Portland, OR, USA
Steven D. Chang, MD
Robert C. and Jeannette Powell Professor, Director,
Stanford Neuromolecular Innovations Program,
Director, Stanford Neurogenetics Oncology Program,
Co-Director, Stanford CyberKnife Program, Department
of Neurosurgery, Stanford University School of
Medicine, Stanford, CA, USA
Navjot Chaudhary, MD
Clinical Assistant Professor, Department of Neurosurgery,
Stanford University, Stanford, CA, USA
H. Isaac Chen, MD
Assistant Professor, Department of Neurosurgery, Hospital
of the University of Pennsylvania, Philadelphia, PA,
USA
Randall M. Chesnut, MD, FCCM, FACS
Department of Neurological Surgery and Orthopaedics
and Sports Medicine, University of Washington School
of Medicine, Harborview Medical Center, University of
Washington School of Global Health, Seattle, WA,
USA
E. Antonio Chiocca, MD, PhD, FAANS
Harvey W. Cushing Professor of Neurosurgery, Established
by the Daniel E. Ponton Fund, Harvard Medical School,
Neurosurgeon-in-Chief and Chairman, Department of
Neurosurgery, Co-Director, Institute for the
Neurosciences at the Brigham, Brigham and Women’s/
Faulkner Hospital, Surgical Director, Center for
Neurooncology, Dana-Farber Cancer Institute, Boston,
MA, USA
Rohan Chitale, MD
Assistant Professor, Department of Neurosurgery,
Vanderbilt University Medical Center, Nashville, TN,
USA
Claudia F. Clavijo, MD
Assistant Professor, Department of Anesthesiology,
University of Colorado School of Medicine, Aurora, CO,
USA
William T. Curry, Jr., MD
Associate Professor and Attending Neurosurgeon, Director
of Neurosurgical Oncology, Department of
Neurosurgery, Massachusetts General Hospital,
Harvard Medical School, Boston, MA, USA
Andrew Dailey, MD
Associate Professor, Department of Neurosurgery,
University of Utah School of Medicine, Salt Lake City,
UT, USA
Rahul Damani, MD, MPH
Assistant Professor, Division of Vascular Neurology and
Neurocritical Care, Department of Neurology, Baylor
College of Medicine, Houston, TX, USA
Daniel J. DiLorenzo, MD, PhD, MBA
Functional and Epilepsy Neurosurgery Fellow, Department
of Neurosurgery, Rush University Medical Center,
Chicago, IL, USA
Christopher F. Dowd, MD
Professor, Department of Radiology and Biomedical
Imaging, University of California, San Francisco, San
Francisco, CA USA
Emad N. Eskanadar, MD
Professor in Surgery, Charles Anthony Pappas Chair of
Neurosciences, Harvard Medical School, Department of
Neurosurgery, Massachusetts General Hospital, Boston,
MA, USA
James J. Evans, MD
Professor, Department of Neurological Surgery, Thomas
Jefferson University, Philadelphia, PA, USA
Brenda G. Fahy, MD, MCCM
Associate Chair and Chief, Division of Critical Care,
Department of Anesthesiology, University of Florida,
Gainesville, FL, USA
Christopher J. Farrell, MD
Assistant Professor, Department of Neurological Surgery,
Thomas Jefferson University, Philadelphia, PA, USA
Anna K. Finley Caulfield, MD
Clinical Associate Professor, Department of Neurology and
Neurological Sciences, Stanford University, Stanford,
CA, USA
Alana M. Flexman, MD
Assistant Professor, Department of Anesthesiology,
Pharmacology and Therapeutics, University of British
Columbia, Vancouver, BC, Canada
Sunil V. Furtado, MS, MCh, DNB
Clinical Instructor, Department of Neurosurgery,
Stanford University School of Medicine, Stanford,
CA, USA

Alexander J. Gamble, DO
Resident in Neurosurgery, Hofstra Northwell School of
Medicine, Manhasset, NY, USA
Paul A. Gardner, MD
Associate Professor, Department of Neurological
Surgery, University of Pittsburgh School of Medicine,
Co-Director, Center for Cranial Base Surgery,
University of Pittsburgh Medical Center, Pittsburgh,
PA, USA
John G. Gaudet, MD
Assistant Professor of Anesthesiology, Department of
Anesthesiology, Columbia University Medical Center,
New York, NY, USA
Emily J. Gilmore
Assistant Professor of Neurology, Department of
Neurology, Yale University School of Medicine, New
Haven, CT, USA
C. Rory Goodwin, MD, PhD
Neurosurgery Resident, Department of Neurosurgery, The
Johns Hopkins University School of Medicine, Baltimore,
MD, USA
William B. Gormley, MD, MPH
Director, Neurosurgical Critical Care, Brigham and
Women’s Hospital, Department of Neurosurgery,
Harvard Medical School, Boston, MA, USA
M. Sean Grady, MD
Charles Harrison Frazier Professor and Chairman,
Department of Neurosurgery, The University of
Pennsylvania, Philadelphia, PA, USA
Ramesh Grandhi, MD
Department of Neurological Surgery, University of
Pittsburgh Medical Center, Pittsburgh, PA, USA
Benjamin F. Gruenbaum, MD
Resident Physician, Department of Anesthesiology, Yale
University School of Medicine, New Haven, CT, USA
Shaun E. Gruenbaum, MD
Clinical Fellow, Neurosurgical Anesthesiology,
Department of Anesthesiology, Yale University School of
Medicine, New Haven, CT, USA
James S. Harrop, MD
Professor of Neurological and Orthopedic Surgery, Thomas
Jefferson University, Philadelphia, PA, USA
J. Claude Hemphill, III, MD
Professor, Department of Neurology and Neurological
Surgery, Kenneth Rainin Chair in Neurocritical Care,
University of California, San Francisco, Co-Director,
Brain and Spinal Cord Injury Center, Director,
Neurocritical Care, San Francisco General Hospital, San
Francisco, CA, USA
List of Contributors xv
Todd M. Herrington, MD, PhD
Instructor in Neurology, Fellow in Movement Disorders,
Department of Neurology, Massachusetts General
Hospital, Boston, MA, USA
Lawrence J. Hirsch
Professor of Neurology, Department of Neurology,
Yale University School of Medicine, New Haven,
CT, USA
Kyle S. Hobbs, MD
Neurocritical care fellow, Division of Neurocritical Care
and Stroke, Department of Neurology, Stanford
University School of Medicine, Stanford, CA, USA
Brian L. Hoh, MD
James and Newton Eblen Professor, Department of
Neurosurgery, Chief, Division of Cerebrovascular
Surgery, University of Florida, Gainesville, FL, USA
Yin C. Hu, MD
Assistant Professor, Westchester Neurovascular
Institute, Westchester Medical Center, Department
of Neurosurgery, New York Medical College,
Valhalla, NY, USA
Christina Huang, MD
Department of Neurological Surgery, Keck School of
Medicine, University of Southern California, Los
Angeles, CA, USA
Judy Huang, MD
Professor of Neurosurgery, Program Director,
Neurosurgery Residency Program, Fellowship Director,
Cerebrovascular Neurosurgery, Johns Hopkins
University School of Medicine, Department of
Neurosurgery, Baltimore, MD, USA
Robert W. Hurst, MD
Professor of Radiology, Department of Radiology, Hospital
of the University of Pennsylvania, Children’s Hospital of
Philadelphia, Philadelphia, PA, USA
Michael E. Ivan, MD
Department of Neurological Surgery, University of Miami,
Chief of Service, Cranial and Neuro-oncology, JSCH,
Director of Research, University of Miami Brain Tumor
Initiative, Miami, FL, USA
Pascal Jabbour, MD
Division Director of Neurovascular Surgery and
Endovascular Neurosurgery, Department of
Neurological Surgery, Thomas Jefferson University
Hospital, Philadelphia, PA, USA
Ian Kaminsky, MD
Assistant Professor, Department of Radiology, Tufts
University, School of Medicine, Interventional
Neuroradiologist, Lahey Hospital & Medical Center,
Burlington, MA, USA
xvi List of Contributors
Suhail Kanchwala, MD
Assistant Professor of Surgery, Division of Plastic Surgery,
University of Pennsylvania, Philadelphia, PA, USA
Gregory Kapinos, MD, MS, FASN
Attending, Neurocritical Care, Assistant Professor,
Neurosurgery and Neurology, Hofstra Northwell School
of Medicine, Manhasset, NY, USA
Craig Kilburg, MD
Resident, Department of Neurosurgery, University of Utah
School of Medicine, Salt Lake City, UT, USA
Koffi M. Kla, MD
Assistant Professor, Department of Anesthesiology,
Vanderbilt University School of Medicine, Nashville, TN,
USA
W. Andrew Kofke, MD, MBA, FCCM, FNCS
Professor, Director Neuroscience in Anesthesiology
and Critical Care Program, Co-Director Neurocritical
Care, Co-Director Perioperative Medicine and Pain
Clinical Research Unit, Department of Anesthesiology
and Critical Care, Department of Neurosurgery,
University of Pennsylvania, Philadelphia, PA, USA
David Kung, MD
Fellow, Neurovascular Surgery and Endovascular
Neurosurgery, Thomas Jefferson University,
Philadelphia, PA, USA
Shih-Shan Lang, MD
Instructor, Division of Neurosurgery, Children’s Hospital
of Philadelphia, Philadelphia, PA, USA
Sean D. Lavine, MD
Clinical Associate Professor in Neurological Surgery,
Columbia College of Physicians and Surgeons,
New York, NY, USA
Peter Le Roux, MD, FACS
Brain and Spine Center, Lankenau Medical Center,
Wynnewood, PA, USA
Lorri A. Lee, MD
Professor, Departments of Anesthesiology and
Neurological Surgery, Vanderbilt University School of
Medicine, Nashville, TN, USA
Vincent Lew, MD
Department of Anesthesia and Perioperative Care,
University of California, San Francisco, CA, USA
Caitlin Loomis, MD
Assistant Professor, Department of Neurology, Yale
University, New Haven, CT, USA
Timothy Lucas, MD, PhD
Assistant Professor of Neurosurgery, Department of
Neurosurgery, Hospital of the University of
Pennsylvania, Philadelphia, PA, USA
K.H. Kevin Luk, MD, MS
Assistant Professor, Department of Anesthesiology and
Pain Medicine, University of Washington, Seattle,
WA, USA
Tracy S. Ma, MD
Neurosurgery Resident, Department of Neurosurgery,
Perelman School of Medicine, University of Pennsylvania,
Philadelphia, PA, USA
Brian Mac Grory
Resident Physician Department of Neurology, Yale
University School of Medicine, New Haven, CT, USA
Luke Macyszyn, MD, MA
Assistant Professor of Neurosurgery and Orthopedics,
David Geffen School of Medicine at UCLA, Los Angeles,
CA, USA
Stephen T. Magill, MD, PhD
Resident Physician, Department of Neurological Surgery,
University of California, San Francisco, San Francisco,
CA, USA
Geoffrey T. Manley, MD, PhD
Professor, Vice-Chairman, Department of Neurological
Surgery, University of California, San Francisco, Chief,
Neurological Surgery, Co-Director, Brain and Spinal
Cord Injury Center, San Francisco General Hospital, San
Francisco, CA, USA
Edward M. Manno, MD FCCM, FANA, FAAN, FAHA
Head, Neurological Intensive Care Unit, Cleveland Clinic,
Cleveland, OH, USA
Neena I. Marupudi, MD, MS
Neurosurgery Resident, Wayne State University School of
Medicine, Detroit, MI, USA
Hesham Masoud, MD
Assistant Professor of Neurology, Neurosurgery and
Radiology, SUNY Upstate Medical University, Syracuse,
NY, USA
Christopher M. Maulucci, MD
Assistant Professor, Department of Neurosurgery, Tulane
University, New Orleans, LA, USA
Christopher Melinosky, MD
Neurocritical Care Fellow, Department of Neurology,
University of Maryland School of Medicine, Baltimore,
MD, USA
Jennifer Gutwald Miller, MD
Attending, Neurocritical Care, Christiana Care Health
System, Newark, DE, USA
Bradley J. Molyneaux, MD, PhD
Assistant Professor, Departments of Neurology and Critical
Care Medicine, University of Pittsburgh Medical Center,
Pittsburgh, PA, USA

Bryan Moore, MD
Hospital of the University of Pennsylvania, Division of
Neurocritical Care, Department of Neurology,
Philadelphia, PA, USA
Patricia L. Musolino, MD, PhD
Instructor, Department of Neurology, Massachusetts
General Hospital, Boston, MA, USA
Raj K. Narayan, MD, FACS
Professor and Chairman, Department of Neurosurgery,
Hofstra Northwell School of Medicine and Executive
Director, Northwell Neuroscience Institute,
Manhasset, NY, USA
Sandra Narayanan, MD, FAHA
Assistant Professor, Depts. of Neurosurgery and
Neurology, Wayne State University School of
Medicine, Detroit, MI, USA
Neeraj Naval, MD
Assistant Professor of Neurology, Neurosurgery and
Anesthesiology and Critical Care Medicine, Johns
Hopkins University School of Medicine, Department
of Neurology, Director, Neurosciences Critical Care,
Johns Hopkins Bayview Medical Center, Baltimore,
MD, USA
Cuong Nguyen, MD
Hospital of the University of Pennsylvania, Division of
Interventional Neuroradiology, Department of
Radiology, Philadelphia, PA, USA
Peggy Nguyen
Department of Neurology, Keck School of Medicine,
University of Southern California, Los Angeles,
CA, USA
Thanh Nguyen, MD, FRCP
Associate Professor, Departments of Neurology, Radiology
and Neurosurgery, Boston University School of
Medicine, Boston, MA, USA
Raul G. Nogueira, MD
Professor of Neurology, Neurosurgery and Radiology,
Emory University School of Medicine, Marcus Stroke &
Neuroscience Center, Grady Memorial Hospital,
Atlanta, GA, USA
Alexander Norbash, MD, MHCM
Professor and Chairman, Department of Radiology,
University of California, San Diego CA, USA
David Okonkwo, MD, PhD
Associate Professor, Department of Neurological
Surgery, University of Pittsburgh Medical Center,
Pittsburgh, PA, USA
Mark E. Oppenlander, MD
Clinical Assistant Professor, Department of Neurosurgery,
University of Michigan, Ann Arbor, MI, USA
List of Contributors xvii
Santiago Ortega Gutierrez, MD, MSc
Clinical Assistant Professor, Departments of
Neurology, Anesthesia, Neurosurgery &
Radiology, University of Iowa Hospitals & Clinics,
Iowa City, IA, USA
Bryan A. Pukenas, MD
Assistant Professor of Radiology, Department of
Radiology, Hospital of the University of Pennsylvania,
Children’s Hospital of Philadelphia, Philadelphia,
PA, USA
Alfredo Quiñones-Hinojosa, MD, FAANS, FACS
William J. and Charles H. Mayo Professor, Neurologic
Surgery Chair, Mayo Clinic College of Medicine,
Jacksonviille, FL, USA
Preethi Ramchand, MD
Neurology Resident, Department of Neurology, Perelman
School of Medicine, University of Pennsylvania,
Philadelphia, PA, USA
Jordina Rincon-Torroella, MD
Post-doctoral Fellow, Department of Neurosurgery, The
John Hopkins University, Baltimore, MD, USA
Jonathan Rosand, MD, MSc
Professor and Medical Director of the Neurosciences
Intensive Care Unit, Chief, Division of Neurocritical Care
and Emergency Neurology, Department of Neurology,
Massachusetts General Hospital, Harvard Medical
School, Boston, MA, USA
Robert H. Rosenwasser, MD
Chairman, Department of Neurological Surgery,
Thomas Jefferson University Hospital, Philadelphia,
PA, USA
W. Caleb Rutledge, MD
Department of Neurological Surgery, Center for Minimally
Invasive Skull Base Surgery, University of California,
San Francisco, CA, USA
R. Alexander Schlichter, MD
Chief of Neuroanesthesia, Department of Anesthesiology
and Critical Care, Perelman School of Medicine,
University of Pennsylvania, Philadelphia, PA, USA
James M. Schuster, MD, PhD
Associate Professor of Neurological Surgery, Director of
Neurotrauma, University of Pennsylvania,
Philadelphia, PA, USA
Daniel M. Sciubba, MD
Director, Spine Tumor and Spine Deformity Research,
Co-Director, Spinal Column Biomechanics and Surgical
Outcomes, Associate Professor of Neurological Surgery,
Oncology, Orthopaedic Surgery, Radiation Oncology
and Molecular Radiation Sciences, Department of
Neurosurgery, The Johns Hopkins University School
of Medicine, Baltimore, MD, USA
xviii List of Contributors
Benjamin K. Scott, MD
Assistant Professor, Department of Anesthesiology,
University of Colorado School of Medicine, Aurora,
CO, USA
Alfred Pokmeng See, MD
Neurosurgery Resident, Brigham and Women’s Hospital,
Department of Neurosurgery, Harvard Medical School,
Boston, MA, USA
Ganesh M. Shankar, MD, PhD
Instructor, Department of Neurosurgery, Massachusetts
General Hospital, Boston, MA, USA
Yoram Shapira, MD, PhD
Professor and Chairman, Department of Anesthesiology
and Critical Care, Ben-Gurion University of the Negev,
Beer-Sheva, Israel
Deepak Sharma, MBBS, DM, MD
Professor and Division Chief, Neuroanesthesiology &
Perioperative Neurosciences, Department of
Anesthesiology and Pain Medicine, University of
Washington, Seattle, WA, USA
Kevin N. Sheth, MD
Chief, Division of Neurocritical Care and Emergency
Neurology; Chief, Clinical Research, Department of
Neurology; Director, Neurosciences Intensive Care Unit,
Yale School of Medicine and Yale New Haven Hospital,
New Haven, CT, USA
Lori A. Shutter, MD, FCCM, FNCS
Professor, Departments of Critical Care Medicine,
Neurology and Neurosurgery, University of Pittsburgh
School of Medicine, Medical Director, Neurovascular
Intensive Care Unit, University of Pittsburgh Medical
Center, Pittsburgh, PA, USA
James E. Siegler, MD
Resident Physician, Department of Neurology, Hospital
of the University of Pennsylvania, Philadelphia,
PA, USA
Michelle J. Smith, MD
Hospital of the University of Pennsylvania, Department of
Neurosurgery, Philadelphia, PA, USA
Carl H. Snyderman, MD, MBA
Professor, Departments of Otolaryngology and
Neurological Surgery, University of Pittsburgh School of
Medicine, Co-Director, Center for Cranial Base Surgery,
University of Pittsburgh Medical Center, Pittsburgh,
PA, USA
Gary K. Steinberg, MD, PhD
Bernard and Ronni Lacroute–William Randolph
Hearst Professor of Neurosurgery and the
Neurosciences, Chairman, Department of
Neurosurgery, Stanford University School of
Medicine, Stanford, CA, USA
Michael F. Stiefel, MD, PhD, FAANS
Director, Capital Institute for Neurosciences, Director,
Stroke and Cerebrovascular Center, Capital Health
System, Pennington, NJ, USA
Geoffrey P. Stricsek, MD
Resident Physician, Department of Neurological
Surgery, Thomas Jefferson University, Philadelphia,
PA, USA
Jose I. Suarez, MD
Professor and Head, Division of Vascular Neurology and
Neurocritical Care, Department of Neurology, Baylor
College of Medicine, Houston, TX, USA
Gene Sung, MD, MPH
Department of Neurology, Keck School of Medicine,
University of Southern California, Los Angeles, CA, USA
Peter Syre, MD
Chief Resident, Department of Neurosurgery, University of
Pennsylvania, Philadelphia, PA, USA
Pekka O. Talke, MD
Professor, Department of Anesthesia and Perioperative
Care, University of California, San Francisco, San
Francisco, CA, USA
Rafael J. Tamargo, MD
Walter E. Dandy Professor of Neurosurgery, Professor of
Neurosurgery and Otolaryngology-Head and Neck
Surgery, Director of Cerebrovascular Neurosurgery,
Neurosurgical Co-Director, The Johns Hopkins
Neurocritical Care Unit, Johns Hopkins University
School of Medicine, Department of Neurosurgery,
Baltimore, MD, USA
Robert Taylor, MD
Stroke and Neurovascular Center of Central California,
Santa Barbara, CA, USA
Anurag Tewari, MD
Neuroanesthesia Fellow, Anesthesia Institute, Cleveland
Clinic, Cleveland, OH, USA
Stavropoula Tjoumakaris, MD
Department of Neurological Surgery, Thomas Jefferson
University Hospital, Philadelphia, PA, USA
Chitra Venkatasubramanian, MBBS, MD, MSc
Clinical Associate Professor, Division of Neurocritical
care and Stroke, Department of Neurology,
Stanford University School of Medicine, Stanford,
CA, USA
Andrew S. Venteicher, MD, PhD
Resident physician, Department of Neurosurgery,
Massachusetts General Hospital, Harvard Medical
School, Boston, MA, USA

Michael S. Weinstein, MD
Associate Professor of Surgery and Critical Care
Medicine, Thomas Jefferson University, Philadelphia,
PA, USA
Peggy White, MD
Assistant Professor of Anesthesiology, Department of
Anesthesiology, University of Florida, Gainesville,
FL, USA
Anthony J. Wilson, MD
Resident, Division of Plastic Surgery, University of
Pennsylvania, Philadelphia, PA, USA
James M. Wright, MD
Department of Neurological Surgery, Case Western
Reserve School of Medicine, Cleveland, OH, USA
Debbie Yi, MD
Assistant Professor, Department of Emergency Medicine,
UC San Francisco, San Francisco, CA, USA
List of Contributors xix
Patricia Zadnik, MD
Resident Physician, Department of Neurosurgery, Hospital
of the University of Pennsylvania, Philadelphia, PA, USA
Eric L. Zager, MD
Professor of Neurosurgery, Department of
Neurosurgery, University of Pennsylvania,
Philadelphia, PA, USA
Mario Zanaty, MD
Senior Clinical Research Fellow, Department of
Neurological Surgery, Thomas Jefferson
University Hospital, Philadelphia, PA, USA
Alexander Zlotnik, MD, PhD
Associate Professor, Department of Anesthesiology
and Critical Care, Ben-Gurion University of the
Negev, Beer-Sheva, Israel

We would like to express our sincere gratitude and appre-
ciation to all the contributors to this volume. We also thank
the editorial, design and production staff at Elsevier, in par-
ticular: Charlotta Kryhl, Sharon Nash, Trinity Hutton, and
Julie Taylor who have been particularly helpful in produc-
ing this volume. We would like to thank Dr. Rae Allain, for-
merly of the Massachusetts General Hospital, for planting
Acknowledgements
the seed that would grow into this textbook. Also we would
like to thank the nurses in the clinic, operating room and
intensive care unit who care for our patients as we could
not do our job without them. Finally, we would like to
thank our patients and their families; we are grateful for
the opportunity to be a part of their treatment, cure and
recovery.
xxi
 Dedications

To the nurses in the clinic, operating room and intensive

care unit who care for our patients.
Monisha Kumar
W. Andrew Kofke
Joshua M. Levine
James M. Schuster

To my parents who motivated me, my girls who

inspire me, my husband who encourages me and CC
who supports me.

To RJS: for teaching me, training me, and giving me

the confidence to accomplish, one ML at a time.
Monisha Kumar

xxiii
 1 Effects of Anesthetics,
Operative Pharmacotherapy,
and Recovery from Anesthesia
ZIRKA H. ANASTASIAN and JOHN G. GAUDET
Introduction
Even after completion of a neurosurgical intervention, intrao-
perative factors, including anesthetic agents, pharmacother-
apy, and surgery, may have lasting effects that persist
through recovery. The goal of this chapter is to discuss the
effects of intraoperative factors, such as anesthetic effect
and surgical manipulation, on postoperative recovery,
including respiratory function, nausea and vomiting, glucose
control, temperature variations, pain management, and
delirium and cognitive dysfunction.
Key Concepts
• Anesthetics, sedatives, and opioids impair respiratory arousal
by reducing chemoresponsiveness to hypoxemia and
hypercarbia.
• The effect of anesthetics on respiratory muscles depends
on the agent, the dose, the patient’s state of consciousness,
and the specific muscle group.
• Risk factors for postoperative respiratory depression in
patients with obstructive sleep apnea include the severity
of sleep apnea, the dose of systemic opioids, the use of
sedatives, the site and invasiveness of surgical procedure, and
the potential for apnea during rapid eye movement (REM)
rebound.
• When neuromuscular blockade is employed, it is necessary to
monitor the degree of neuromuscular blockade and consider
adequacy and potential side effects of reversal of
neuromuscular blockade.
Respiratory Muscle Effects
The muscles involved in respiration are skeletal muscles
and can be classified by their anatomical function into
two groups: (1) upper airway dilators and (2) respiratory
pump muscles. Upper airway dilator muscles counterbal-
ance the negative inspiratory pressure generated by
the respiratory pump muscle to permit airflow during
inspiration.1
Surgery itself can have direct effects on respiratory pump
muscles by functional disruption (injury of muscle), postoper-
ative pain leading to restrictions on ventilation, and phrenic
nerve injury resulting in diaphragm dysfunction. Other fac-
tors that affect diaphragmatic dysfunction postoperatively
include inflammation2 and reflex vagal inhibition.3 Indirect
effects of abdominal surgery may increase intraabdominal
pressure. Increased intraabdominal pressure decreases chest
wall compliance and increases the work of breathing, further
taxing the muscles of the respiratory pump.1
Upper airway muscles are generally more sensitive to
anesthetics and sedatives than respiratory pump muscles.
Animal trials have shown that although volatile anes-
thetics, barbiturates, and benzodiazepine anesthetics all
decrease neural input to both upper airway (hypoglossal
nerve) and respiratory pump muscles (phrenic nerve), the
decrease of upper airway neural input is much more than
respiratory pump muscles.4 In human clinical studies, even
subhypnotic concentrations of propofol, isoflurane, and
sevoflurane increase the incidence of pharyngeal dysfunc-
tion. This places patients at increased risk for aspiration of
pharyngeal contents during recovery of anesthesia. The
effect on the pharyngeal contraction pattern may be most
pronounced in patients treated with propofol because pro-
pofol use results in markedly reduced pharyngeal contrac-
tion.5 In contrast, ketamine reduces neural input to both
the upper airway and respiratory muscles equally. Reduc-
tion in neural input to the upper airway muscles is much
less with ketamine relative to the other classes of anes-
thetics.4 Ketamine has no inhibitory effect on genioglossus
activity. Unlike other anesthetics, ketamine preserves a
high level of upper airway dilator muscle activity, similar
to that of conscious patients.6 Ketamine, however, is a sial-
agogue, a property that can occasionally be problematic.
Opioid analgesics cause respiratory depression via both
upper airway dilator and respiratory pump muscle dysfunc-
tion. Opioids reduce genioglossus activity in animals,
decrease vagal motor neuron activity in the laryngeal
abductors, and increase vagal motor neuronal activity in
adductors.7–9 These changes result in increased upper air-
way resistance and possibly vocal cord closure, as well as
pharyngeal airflow obstruction.9 Opioid analgesia also
increases abdominal muscle activity, which produces a
rapid decrease in end-expiratory lung volume and func-
tional residual capacity, contributing to a higher degree
of atelectasis.10 Chest wall rigidity also occurs with the
use of opioids, even when dosed conservatively.11
Clinical Pearl
Upper airway muscles are generally more affected by
anesthetics and sedatives than respiratory pump muscles.
3
4 SECTION 1 • Neuroanesthesia and Perioperative Care
Controlled ventilation immobilizes the diaphragm and
disrupts diaphragmatic function. Controlled ventilation is
associated with proteolysis in the diaphragm, which over
a long period leads to diaphragmatic atrophy and dysfunc-
tion.12 As little as 18 hours of controlled ventilation results
in diaphragmatic atrophy and decreases contractile func-
tion.13 Duration of controlled ventilation correlates with
thinning, injury, and atrophy of the diaphragm.14,15
Neuromuscular blocking agents (NMBAs) are often used
during surgery to provide immobility and optimal operat-
ing conditions. Train-of-four (TOF) ratios are customary
measures to assess neuromuscular blockade at muscle
groups. The TOF ratio value is determined by the ratio of
the last twitch height to the first twitch height after a
TOF twitches. Recovery at the adductor pollicis is often used
for this assessment because the hand is generally conve-
nient and available for monitoring purposes. A TOF ratio
of 0.6 or more predicts acceptable recovery of forced vital
capacity,16,17 and for many years recovery to a TOF ratio
of 0.7 was considered indicative of adequate recovery of
neuromuscular function.18 Recovery from NMBA gener-
ally occurs sooner at the diaphragm than peripheral mus-
cles, such as the hand muscles. Therefore tidal volumes are
usually preserved, whereas residual paralysis may still be
noted by peripheral monitoring.19,20 However, a TOF ratio
of 0.6 and even 0.8 may be insufficient to ensure recovery
of respiratory function. TOF ratios of <1.0 are associated
with decreased forced inspiratory volume in one second
(FIV1), upper airway obstruction, and impaired pharyngeal
function and impaired ability to swallow.16,21
Even when nerve stimulators are used, subjective tactile or
visual evaluation of the evoked response to indirect nerve
stimulation is notoriously inaccurate. Once the TOF ratio
exceeds 0.4, most clinicians cannot detect the presence of
any fade in the twitches upon four stimuli.22 A very strong
case can be made for the routine administration of a nonde-
polarizing reversal agent (cholinesterase inhibitor), unless it
can be objectively demonstrated that complete recovery
(TOF ratio >0.9) has occurred spontaneously.23,24 As little
as 0.015 to 0.025 mg/kg of neostigmine is required at a
TOF count of four with minimal fade, whereas 0.04 to
0.05 mg/kg is needed at a TOF count of two or three.23
Neuromuscular blockade reversal is not without conse-
quence, however. Neostigmine, in clinically recommended
doses, can actually cause neuromuscular transmission fail-
ure when given to patients who have already recovered
from neuromuscular block.25 Cholinesterase inhibitors
may cause neuromuscular transmission failure by various
mechanisms, including the desensitization of acetylcholine
receptors,26 block of neuromuscular transmission, or open
channel block.27,28 Neostigmine, when given in the
absence of postsynaptic neuromuscular block, also impairs
upper airway dilator volume, genioglossus muscle func-
tion, and diaphragmatic function.28 Thus patients fully
recovered from the effects of NMBAs given unwarranted
reversal may develop secondary neuromuscular impair-
ment. Neostigmine can also have other systemic effects,
including bradycardia, bronchorrhea, bronchospasm, and
alimentary peristalsis, muscarinic cholinergic effects that
require concomitant administration of an anticholinergic
drug such as atropine or glycopyrrolate.
Clinical Pearl
Monitoring of neuromuscular blockade is necessary to
evaluate for residual blockade when muscle relaxants have
been used. Clinical examination for fade in TOF ratio is not
dependable.
Anesthetic Effect on Respiratory
Control
At 1 minimum alveolar concentration (MAC), the concentra-
tion at which 50% of patients do not move in response to
a painful stimulus, all volatile anesthetics (in absence of
other depressants) increase respiratory rate, decrease tidal
volume, decrease minute ventilation, and increase the
arterial PCO2. The order of the respiratory depressant effect,
as measured by the increase in arterial PCO2n is enflurane>
desflurane  isoflurane > sevoflurane  halothane.29 Volatile
anesthetics abolish the ventilatory response to hypoxia in ani-
mals and humans in a dose-dependent manner.30,31 The
peripheral chemoreceptors are the site responsible for this
action.32 Volatile anesthetics also decrease the ventilatory
response to hypercapnia, but the response to hypercapnia is
more resistant than the response to hypoxia.33 At subanes-
thetic concentrations, similar to those that would be
found in patients recovering from anesthesia (0.1 MAC),
volatile anesthetics reduce the acute hypoxic response
by 30% to 50%. The order of potency is halotha-
ne> enflurane > sevoflurane > isoflurane > desflurane. This
is reflective of the extent to which these agents are metabo-
lized. This effect is probably mediated through a preferential
action on the peripheral chemoreflex loop.34 Low-dose volatile
anesthetics also uncouple the association between peripheral
chemoreceptor activity and hypoxic ventilatory depression.34
The effect of subanesthetic volatile anesthetics on the hyper-
capnic ventilatory response is minimal or absent.35
Clinical Pearl
At subanesthetic concentrations, volatile anesthetics reduce
the acute hypoxic response.
Anesthetic Effects on Bronchial
Tree, Mucociliary Function, and
Surfactant Production
Volatile anesthetics are potent bronchodilators that relax
airway smooth muscle by directly depressing smooth mus-
cle contractility. This effect is thought to result from direct
effects on bronchial epithelium and indirect inhibition of
reflex neural pathways. Animal models suggest that halo-
thane (1 MAC), enflurane (1 MAC), and isoflurane (1.5
MAC) produce a similar reduction in bronchial airway
resistance.36 In vitro models demonstrate that isoflurane
preferentially relaxes the bronchiole versus the bronchus.37
Halothane, enflurane, sevoflurane, and isoflurane do not
 1 • Effects of Anesthetics, Operative Pharmacotherapy, and Recovery from Anesthesia 5

affect baseline pulmonary resistance and dynamic pulmo- Sleeping CNS

nary compliance, but do attenuate increases in resistance
and decreases in compliance due to histamine.38 In addi-
tion to volatile anesthetics, intravenous anesthetics affect
NREM sleep Risk factors REM sleep
bronchial tone. Ketamine has a bronchodilator effect that Decreased baseline Sao2
may be due to inhibition of catecholamine reuptake and Increased baseline Paco2
action as a sympathomimetic agent.39 Propofol also has FEV1 < 50% predicted
bronchoprotective properties by reducing basal airway Irregular respiration
Stable respiration
tone and histamine-induced bronchoconstrictions in ani- Increased upper Increased upper airway
mal studies. Propofol also has a vagolytic effect on the airway resistance resistance
airway.40,41 Mild decrease in Substantial decrease in
Foreign matter is removed from the tracheobronchial hypercapnic and hypercapnic and
tree by the upward clearance of the ciliated respiratory epi- hypoxic hypoxic respiratory
thelium. Impaired ciliary motility in anesthetized or inten- respiratory center center responsiveness
responsiveness Inhibited intercostal
sive care patients may predispose them to respiratory
muscles
complications, including infections and atelectasis. Poorly Reduced FRC
humidified inspiratory gases, cuffed endotracheal tubes,
high fractional inspired O2, and positive pressure ventila-
tion are known to reduce ciliary movement and decrease Severe hypoventilation
Mild
mucus production. Halothane, enflurane, nitrous oxide hypoventilation
Increased V/Q inequality
with halothane, and nitrous oxide with opioid all produce from reduced FRC
dose-dependent decreases of mucociliary movement in
dogs.42,43 Human studies with isoflurane show no inhibi-
Mild excess Severe prolonged
tion in mucus production; however, data are conflicting excess hypoxemia
regarding the impact on ciliary motion.44,45 Intravenous hypoxemia
anesthetics, including propofol, dexmedetomidine, and Fig. 1.1 Effect of nonrapid eye movement (NREM) and rapid eye move-
thiopental, have no effect on ciliary function. Administra- ment (REM) sleep on nocturnal arterial hemoglobin saturation in patients
tion of ketamine and fentanyl at high doses increases ciliary with severe to very severe COPD, with FEV1 generally less than 50% pre-
dicted. Boldface type indicates differences between NREM and REM
beat frequency. sleep contributing to hypoxemia. CNS, central nervous system; COPD,
Lastly, volatile anesthetics cause a progressive, reversible chronic obstructive pulmonary disease; FRC, functional residual capacity
reduction in phosphatidylcholine, the main lipid compo- (end-expiratory lung volume); PaCO2, partial arterial pressure of carbon
nent of surfactant. The reversibility was within 2 hours dioxide; SaO2, arterial oxygen saturation (%) of hemoglobin, usually
in culture.46 expressed in as a percentage; V./Q., pulmonary alveolar/pulmonary
capillary ventilation/perfusion inequality. (Adapted from Barkoukis, TJ
& Littner, MR. Therapy in Sleep Medicine. Copyright © 2012 Elsevier,
Inc. All rights reserved.)

Anesthesia Effects on Respiratory

Arousal from Sleep, Rapid Eye
Movement Rebound, and
Obstructive Sleep Apnea
Anesthetics, sedatives, and opioids impair respiratory
arousal, defined as arousal from sleep due to respiratory
stimuli. These agents reduce chemoresponsiveness to hyp-
oxia47 and hypercarbia,48 suppress the reflexive respon-
siveness to negative upper airway pressure,49 and depress
the magnitude of wakefulness.
During REM sleep, there is hypotonia of voluntary mus-
cles. Electromyogram activity is at the lowest level of any
stage of sleep.50 Neural drive to the upper airway dilators
is decreased, and this predisposes the patient to airway
instability and episodes of hypoxemia.51 REM sleep also
reduces the hypoxic ventilatory drive and the hypercarbic
ventilatory response. Therefore REM rebound (i.e.,
increased REM sleep due to sleep deprivation or anesthetic
inhibition of REM sleep) results in more episodes of hypox-
emia due to impaired respiratory arousal52 (see Fig. 1.1).
The effect of anesthetics on REM rebound varies according
to the specific agent. Six hours of treatment with volatile
anesthesia in mice caused REM rebound,53 but 3 hours
of isoflurane in human volunteers had no effect on REM
sleep.54 Benzodiazepines and opioids cause REM rebound
upon discontinuation.55 Propofol has no effect on REM
rebound.56
Obstructive sleep apnea (OSA) is a syndrome character-
ized by periodic, partial, or complete obstruction in the
upper airway during sleep. This, in turn, causes repetitive
arousal from sleep to restore airway patency. The airway
obstruction may also cause episodic sleep-associated oxy-
gen desaturation, episodic hypercarbia, and cardiovascu-
lar dysfunction. In the postoperative period, patients
with OSA, even if asymptomatic, present special chal-
lenges that must be addressed to minimize the risk of
perioperative morbidity and mortality. Risk factors for
postoperative respiratory depression may include the
severity of the underlying sleep apnea, administration of
opioids or sedatives, site and extent of the surgical proce-
dure, and the potential for apnea during REM rebound.
Postoperative interventions to manage OSA patients
who may be susceptible to the aforementioned risks
should take into consideration (1) postoperative analgesia,
(2) oxygenation, (3) patient positioning, and (4) monitor-
ing. Recently published guidelines57 relevant to the post-
operative management of patients with OSA include the
following:
6 SECTION 1 • Neuroanesthesia and Perioperative Care

A. Provide evidence supporting the use of postoperative

continuous positive airway pressure (Category A3-B • Low Risk (10–20%)
evidence).58 • No prophylaxis or single therapy
B. Suggest consideration of a regional anesthesia tech- • Dexamethasone 4–8mg
nique. This is in the setting of insufficient literature to • Rescue: Ondansetron
evaluate outcomes associated with different types of
postoperative analgesia (regional versus systemic anal-
gesia and effects of basal rates of analgesia) on patients • Risk Factors
with OSA. • 0 RF=10% • Intermediate Risk (20–40%)
C. Suggest consideration of providing supplemental • Propofol/antiemetic
• 1 RF=20%
oxygenation, but this is in the setting of insufficient • Combination antiemetics
literature. • 2 RF=40% • Rescue: Drug from a different class
D. Support positioning patients in a nonsupine fashion • 3 RF=60%
(Category B1-B evidence).59 • 4 RF=80%
E. Support using postoperative pulse oximetry monitoring
(Category B3-B evidence).60 • High Risk (60–80%)
• Multimodal therapy
• TlVA with propofol
• Combinations antiemetics
Effects of Anesthetics and Surgery on • Minimal opioids
Postoperative Nausea and Vomiting Fig. 1.2 Risk factors and PONV management strategy. (Adapted from
Keyes, M. Management of postoperative nausea and vomiting in ambu-
latory surgery: the big little problem. Clinics in Plastic Surgery. Copyright
Key Concepts © 2013 Elsevier, Inc.)

• Postoperative nausea and vomiting (PONV) is multifactorial

involving anesthetic risk factors, surgical risk factors, and Table 1.1 Risk of PONV
individual risk factors. Risk Factors Female sex
• Prevention and treatment of PONV should focus on Nonsmoker
identification of risk factors, reduction of baseline risk factors, History of PONV
and intervention based on a multimodal prophylaxis and Use of post op opioids
treatment regimen.
• Some neurosurgical procedures, particularly those involving Risk of PONV 10%: No risk factor
20%: One risk factor
the posterior fossa, are at higher risk of PONV. 40%: Two risk factors
60%: Three risk factors
80%: Four risk factors
General anesthesia using volatile anesthetics is associ-
ated with an average incidence of PONV ranging between
20% and 30% for general surgery patients, 50% for crani- administration of appropriate prophylaxis.65 Antiemetics
otomy patients, and even higher for infratentorial craniot- that are commonly used, the classes, mechanisms, and
omy.61,62 Development of PONV is multifactorial, involving common side effects are as follows:
anesthetic, surgical, and individual risk factors (see 5-hydroxytryptamine (5-HT3) receptor antagonists
Fig. 1.2). Anesthetic risk factors include the use of volatile (ondansetron, dolasetron, granisetron, and tropisetron).66
anesthetics, nitrous oxide, and intraoperative and postoper- There are no effects on cerebral hemodynamics or intracra-
ative opioids. The emetogenic effect of the inhaled anes- nial pressure with minimal added sedation.67 Side effects
thetics and opioids appears to be dose related.61,63 The include the potential to produce a headache, dizziness,68
duration of surgery also affects the likelihood of PONV. and a possibility to produce a dystonic/encephalopathic
For each 30-minute increase in duration, the risk of PONV reaction.69
increases by 60% from baseline. However, patient-specific Metoclopramide is a D2 and 5-HT3 antagonist.70 It
factors, including female sex, nonsmoking status, and his- increases gastric motility.71 It can produce dystonic reac-
tory of PONV, may be the most important determinants. A tions, which can include respiratory insufficiency and
validated scoring system based on risk factors includes extrapyramidal symptoms. It is therefore contraindicated
female gender, nonsmoker, history of PONV, and adminis- in patients with Parkinson’s disease.
tration of postoperative opioids, with a corresponding risk Corticosteroids (dexamethasone) have an unclear mech-
of 10% for no risk factors, 20% for one risk factor, 40% anism on decreasing nausea and vomiting, but it is thought
for two, 60% for three, and 80% for four risk factors64 to be related to antiinflammatory effects, a direct effect on
(see Table 1.1). the solitary tract nucleus, interaction with serotonin
Nausea and vomiting after neurosurgery may increase and receptor proteins NK1 and NK2, regulation of the
the risk of systemic hypertension, vagal maneuvers, and hypothalamic–pituitary–adrenal axis, and reduction of
increased venous postoperative bleeding. Anesthesiology pain and thus the use of opioids.72 Side effects include blood
guidelines to prevent PONV focus on identification of glucose abnormalities and genital pain/burning upon
risk factors, reduction of exacerbating factors, and administration.
 1 • Effects of Anesthetics, Operative Pharmacotherapy, and Recovery from Anesthesia
Propofol in low doses is an antiemetic of an unclear mech-
anism. The residual antiemetic properties postoperatively
make propofol a popular choice or adjunct for an anesthetic
in a patient who is at high risk for nausea and vomiting
postoperatively.68
Phenothiazines (promethazine and prochlorperazine)
are D2 antagonists with moderate antihistamine and anti-
cholinergic properties.70 They can produce extrapyramidal
reactions.68
Phenylethylamine (ephedrine) is a sympathomimetic
agent that has been used as an antiemetic in the obstetrical
and abdominal surgery populations.73 It does increase
heart rate and blood pressure.
Butyrophenones (droperidol, haloperidol) are D2 recep-
tor antagonists.70 They have minimal effect on cerebral
hemodynamics or intracranial pressure and tend to
decrease blood pressure. Side effects include mild sedation,
dysphoria, and extrapyramidal side effects. It is therefore
contraindicated in patients with Parkinson’s disease and
prolonged QT interval.
Antihistamines (dimenhydrinate, hydroxyzine) block
histamine receptors in the nucleus of the solitary tract.
They can produce some sedation.68
Anticholinergic (transdermal scopolamine) medica-
tions act centrally and block impulses from vestibular
nuclei to higher areas in the central nervous system
and reticular activating system.68,74 The central cholin-
ergic antagonism can lead to delirium, which can be
reversed with physostigmine, a centrally acting cholines-
terase inhibitor. It also can result in mild sedation and
dizziness.
Neurokinin antagonists (aprepitant) act by blocking the
binding of substance P (a regulatory neuropeptide) to NK1
receptors in vagal afferents in the gastrointestinal tract and
in regions of the central nervous system. Common side
effects include fatigue, headache, and constipation.75
In general, combination therapy has superior efficacy
compared with monotherapy for PONV prophylaxis, and
drugs with different mechanisms of action should be used
in combination to optimize efficacy.76
Postoperatively, when a prophylactic dose of an antie-
metic has failed, a rescue dose should be chosen from
another mechanistic class. To repeat a prophylactic dose
in the first 6 hours after administration has not been shown
to be effective.77
Effects of Anesthetics and Surgery on
Postoperative Glycemic Control
Key Concept
Optimal glucose management, particularly in patients with acute
brain insult, remains a controversial issue because both
hypoglycemia and hyperglycemia appear to result in critical
adverse effects.
Many preclinical studies conclusively demonstrate the
deleterious effects of hyperglycemia in the ischemic
7
brain.78,79 Also numerous retrospective studies have
reported an association between hyperglycemia and
adverse outcomes in humans with various types of neuro-
logical problems.80 Sieber et al. reported that routine elec-
tive neurosurgery was associated with levels of
hyperglycemia thought to be high enough to exacerbate
ischemic brain damage.81 Thus the stage was set for needed
prospective randomized studies. In 2001 Van den Berghe
et al. reported on the use of intensive insulin therapy
targeted to tight blood glucose control (target range 80–
110 mg/dL) in critically ill surgical patients. This and
subsequent studies from her group resulted in
recommendations calling for the widespread use of inten-
sive insulin therapy (IIT) in critically ill patients.82 To
address the safety of IIT administered to postoperative neu-
rosurgical patients, tight blood glucose control with IIT
resulted in a three-fold increase in the risk of iatrogenic
hypoglycemia.83 The Normoglycemia in Intensive Care
Evaluation-Survival Using Glucose Algorithm Regulation
trial, a large (6104 patients), multicenter, international,
randomized trial, reported that in adult intensive care unit
(ICU) patients, IIT targeted to tight blood glucose control
(target range 81–108 mg/dL), compared with conven-
tional glucose control (target <144–180 mg/dL), resulted
in higher mortality.84
Optimal glucose management, particularly in patients
with acute brain injury and those undergoing neurosur-
gery, remains a controversial issue. Both hypoglycemia
and hyperglycemia appear to result in critical adverse
effects. Although there may be benefit in controlling hyper-
glycemia in neurocritical care and neurosurgical ICU
patients,85–87 the actual incidence and impact of hypogly-
cemia remain unknown. This may be due to the fact that
the temporal relationship to ictus, optimal level of control,
and the impact of confounding factors such as stress or ste-
roid administration remains unknown. More information is
needed about the correlation of peripheral glucose levels
with intracellular levels in the brain, particularly in the
ischemic or potentially ischemic brain. Current guidelines
suggest that hyperglycemic levels above 180 to 200 mg%
warrant insulin therapy.88
The widespread use of glucocorticoids in the neurosur-
gical ICU affects optimal glucose management. Glucocor-
ticoids stabilize the blood–brain barrier and increase
absorption of cerebrospinal fluid. They are beneficial
when administered in low doses (e.g., 10 mg of dexa-
methasone) in preventing PONV and are commonly used
in neurosurgery to reduce vasogenic edema in primary
and metastatic tumors. The administration of a single
dose of dexamethasone will, however, increase blood
glucose concentration significantly in both diabetic and
nondiabetic patients.89,90
Clinical Pearl
Although hyperglycemia has negative consequences,
hypoglycemia can be regional in the injured brain and
should be avoided.
8 SECTION 1 • Neuroanesthesia and Perioperative Care
Effects of Anesthetics and Surgery
on Temperature Regulation
Key Concepts
• Hypothermia has both deleterious and potentially
neuroprotective effects when performed intraoperatively and
postoperatively.
• Rewarming should be done gradually and with caution to
avoid complications.
Abnormal body temperature results from an imbalance
between heat loss and heat production. Radiation, conduc-
tion, convection, and evaporation mechanisms contribute
to heat loss.91 The hypothalamus is responsible, in large
part, for maintaining core temperature within a normal
range (35.0–37.5°C, 95.0–99.5°F).92 It receives afferent
peripheral input from C (warm) and Aδ (cold) fibers and reg-
ulates both heat production (basal metabolic rate, shivering)
and heat distribution (peripheral vasomotor tone, sweat) via
efferent autonomic and endocrine signals.93 Disruption of
afferent or efferent signaling, as well as hypothalamic dys-
function, may lead to hypothermia (any core temperature
below 35°C) or hyperthermia (any core temperature above
37.5°C) as measured centrally (pulmonary artery, bladder,
nasopharynx, lower esophagus, tympanic membrane) or
peripherally (axilla, mouth, rectum). Core temperature is
usually higher than peripheral temperature. Core hypother-
mia is graded as mild (32–35.0°C, 90–95.0°F), moderate
(28–32°C, 82–90°F), severe (20–28°C, 68–82°F), or pro-
found (less than 20°C, 68°F). Severe hyperthermia (any core
temperature above 40.0°C, 104.0°F) is sometimes referred
to as hyperpyrexia.94
Whereas hypothermia is frequently observed following
administration of general anesthesia, the onset of hyper-
thermia is rare but should prompt immediate investigation
because it may be the expression of anaphylaxis or abnor-
mal drug reaction.95 Malignant hyperthermia is most con-
cerning and potentially lethal, but quite rare. Most general
anesthetic drugs affect both peripheral vasomotor tone and
hypothalamic function but preserve sweat mechanisms
and afferent hypothalamic input.96 Initially after induction
of general anesthesia, heat loss is accelerated due to redis-
tribution of blood flow to peripheral tissues. Skin warming
before induction attenuates this phenomenon by reducing
the thermic gradient between the central and peripheral
compartments.97 Drugs such as ketamine98 and midazo-
lam,99 as well as nitrous oxide100 may help preserve vaso-
motor tone and decrease heat loss. During maintenance of
general anesthesia, the hypothalamic temperature set
point gets readjusted to a lower temperature due to drug-
related effects. Inhibition of shivering by muscle relaxants
further decreases heat production.101 During neuraxial
anesthesia, the combination of sympatholytic vasoplegia
and altered afferent signaling leads to hypothermia from
accelerated heat loss and abnormal elevation in apparent
temperature, respectively.102 Under such circumstances,
skin warming may fail to prevent hypothermia.103 Heat
loss is also exacerbated by the frequent administration of
hypnotic drugs to produce sedation in combination with
neuraxial anesthesia.
The effects of general and/or neuraxial anesthesia may
either balance or exacerbate temperature changes com-
monly observed in brain or spinal cord injury. After brain
injury, hypothalamic dysfunction or stress-induced
immune modulation may result in hypothermia or hyper-
thermia.104 In patients with altered mental status, fever is
also commonly due to environmental exposure and
bronchoaspiration. After spinal cord injury, although pro-
longed immobility may present with hyperthermia due to
infectious or thrombotic complications, neurogenic vaso-
plegia can be responsible for significant heat loss.105
Fever is clearly associated with worse clinical outcomes
in patients with neurological injury.106 Although hypo-
thermia has multiple systemic deleterious side effects, it
may also have neuroprotective effects in patients with trau-
matic brain injury (TBI) or massive stroke.107,108 Mild
hypothermia attenuates secondary cerebral insults due to
intracranial hypertension after TBI.109 In stroke patients,
therapeutic effects of hypothermia are equivocal despite
robust benefits in animal models. In absence of strong evi-
dence from clinical trials, therapeutic hypothermia should
be considered for treatment of massive stroke with intracra-
nial hypertension.110 Unclear benefits of therapeutic hypo-
thermia in a clinical setting are due in part to the
deleterious effects of rewarming.111 Patients with brain
or spinal cord injury should be rewarmed carefully before
initiation of emergence. As a general rule, the more severe
the injury and/or degree of hypothermia, the more progres-
sive and closely monitored rewarming should be. In all
cases of brain or spinal cord injury, hyperthermia should
be avoided, as it is clearly deleterious.112
Clinical Pearl
Hypothermia is common during and after surgery and may
be neuroprotective in some cases, but hyperthermia is clearly
deleterious and should be avoided.
Effects of Anesthetics and Surgery
on Pain and Pain Control
Key Concepts
• Multimodal analgesia, including acetaminophen, nonsteroidal
antiinflammatory drugs (NSAIDs), local anesthetics,
gabapentinoids, ketamine, and opioids, should be considered
in chronic pain patients or patients at risk of developing
chronic pain.
• Whenever necessary, collaboration with a pain specialist
should be considered.
Up to two-thirds of patients suffer from postoperative pain
after craniotomy.113 Compared with supratentorial proce-
dures, patients undergoing infratentorial craniotomy report
more severe pain scores. Such poor outcomes are at least in
part due to avoidance or underutilization of opioids to reduce
the sedation associated with their use. They also result from
a presumed lack of need for analgesics, as well as difficulties
in assessing pain during recovery from brain surgery.
 1 • Effects of Anesthetics, Operative Pharmacotherapy, and Recovery from Anesthesia
Pain after spine surgery represents a particularly difficult
challenge. These patients often have chronic pain, signifi-
cant disability, and psychological distress, and many have
had prior neurosurgery.114 The challenge in managing
pain after spine surgery resides in treating patients with
multiple predictors of severe postoperative pain and analge-
sic consumption.115 Factors clearly associated with difficult
postoperative pain management include chronic pain inde-
pendent of opioid tolerance, significant disability with psy-
chological distress, major surgery, or reoperation after
failed surgery.114 In the presence of such risk factors, the
perioperative analgesic plan should be made and adjusted
in collaboration with a pain specialist.
Opioids remain the mainstay of analgesia after neurosur-
gical procedures. Although most share common pharma-
codynamical properties (μ receptor agonism), their
pharmacokinetic profiles tend to differ significantly.116
Whenever rapid neurological recovery from anesthetic
effect is required, drugs with shorter half-lives are usually
favored. Unless complemented with other nonopioid anal-
gesics, use of such short-acting drugs may result in subop-
timal postoperative analgesia. Alternatively, drugs with
longer half-lives may be preferred to optimize analgesia dur-
ing emergence and recovery whenever pain management is
anticipated to be problematic. Opioid-induced side effects
include respiratory depression, sedation, and prolonged
immobilization. Perioperative analgesia should be managed
in collaboration with a pain specialist in presence of respira-
tory risk factors such as obesity, sleep apnea, or obstructive
or restrictive lung disease. Nausea, vomiting, constipation,
and slow gastric emptying with delayed enteral nutrition
may also complicate their use.117 Prolonged duration of
high opioid plasma levels has been associated with increas-
ing sensitivity to noxious stimuli (opioid-induced hyperalge-
sia)118 and immunosuppression.119 In order to reduce the
incidence and severity of opioid-induced side effects, modern
analgesic management relies on a multimodal approach that
combines opioids with coanalgesics.120
Acetaminophen may be used as an adjunctive to treat
mild to moderate postoperative pain. In patients with fever,
it may also induce a significant decrease in temperature
within 15 minutes. Compared with the oral or rectal routes,
IV acetaminophen may be beneficial. However, due to the
relatively high cost of the IV formulation, physicians
remain hesitant to use it.121
The use of NSAIDs such as ketorolac after neurosurgical
procedures remains controversial. On one hand, ketorolac
is a nonsedating drug with potent analgesic activity that
has been demonstrated to reduce postoperative opioid
requirements.122 On the other hand, ketorolac has an inhib-
itory effect on both platelet function123 and bone
formation,124 a key determinant for the success of spinal
fusion procedures. In the absence of strong clinical evidence,
ketorolac should be used cautiously, if at all, after intracra-
nial surgery125 or spinal fusion procedures.126 In addition,
NSAIDs should be avoided in patients with, or at risk for,
renal dysfunction and gastrointestinal bleeding.127
Ketamine has potent antinociceptive effects in the spinal
cord at subanesthetic concentrations.128 It may also have
beneficial antiinflammatory effects.129 The combination of
a low-dose bolus (0.1–0.5 mg/kg preferably administered
before incision) and a continuous infusion (2–5 mcg/kg/
min) may improve postoperative pain management while
9
decreasing opioid consumption without increasing the risk
of aberrant excitatory cortical, hippocampal, and limbic
hallucinogenic activity observed at higher dosages.
Although the use of ketamine during craniotomy remains
very controversial, there is preliminary clinical evidence
indicating ketamine may be beneficial in sedated, ventilated
patients with severe traumatic brain injury.130 It should be
considered for patients with chronic pain and opioid depen-
dence undergoing spine surgery.131
Gabapentinoids, such as gabapentin and pregabalin, are
oral anticonvulsant drugs. They block calcium channels,
which are upregulated in dorsal root ganglia and contrib-
ute to neuropathic pain symptoms (hyperalgesia, allody-
nia) after nerve injury. A heterogeneous body of clinical
studies shows they may also have antinociceptive, opioid-
sparing, and anxiolytic properties.128 Their use as analge-
sic premedication before craniotomy is very controversial
due to a high incidence of dizziness and sedation, most com-
monly in the elderly and/or in patients with renal dysfunc-
tion.132 Gabapentinoids appear to be most beneficial in
patients undergoing major spine surgery; however, timing
and optimal dosage remain unclear.133
Finally, postoperative pain may also be attenuated using
local anesthetics to reduce transmission of the nociceptive
signal from the peripheral to the central nervous system.
During craniotomy, regional scalp block using lidocaine,
bupivacaine, or ropivacaine before incision has been shown
to reduce postoperative pain and opioid consumption.
Addition of low-dose epinephrine to the local anesthetic
solution may help prolong duration of the block without
systemic hemodynamic effects.134 Local anesthetics may
also be administered in the epidural space or intravenously
in patients undergoing major spine surgery. Combined epi-
dural/general anesthesia with postoperative epidural anal-
gesia may produce better pain control and a lower surgical
stress response than general anesthesia with postoperative
systemic opioid analgesia. However, patients with epidural
catheters should be carefully monitored and referred to a
pain specialist postoperatively due to the potential signifi-
cant side effects of sympathetic blockade.135 Alternatively,
perioperative IV administration of lidocaine may improve
postoperative pain management after complex spine proce-
dures. The evidence supporting this strategy remains lim-
ited; further research is needed to confirm preliminary
results, demonstrate safety, and clarify dosage.136
Effects of Anesthetics and Surgery
on Consciousness and Cognition
Key Concepts
• Postoperative delirium (POD) and postoperative cognitive
decline (POCD) are frequently encountered in the elderly after
surgery.
• Management should rely on early identification of patients at
risk and avoidance of any disruption of cerebral physiology
until the mechanisms leading to POD and POCD are
elucidated.
• Treatment can include reduction of psychological and
physiological perioperative stress and use of
dexmedetomidine and antipsychotics.
10 SECTION 1 • Neuroanesthesia and Perioperative Care
POD and POCD are two distinct forms of brain dysfunc-
tion that are frequently encountered mostly in the elderly
after major surgery.137 Although it is unclear whether both
disorders share common pathophysiological mechanisms,
they have clearly been associated with an increased
risk of complications leading to longer hospital stays,
significantly higher costs, and higher mortality rates.138
Rapid, often fluctuant alterations of consciousness are
the hallmark of POD. Psychomotor changes (agitation or,
more commonly, hypoactivity) and acute cognitive distur-
bances are other important signs frequently observed
alongside an abnormal sleep/wake cycle or disturbed
visual/auditory perception. POD typically presents 1 to
3 days after surgery; it may persist for several days to
weeks. Several diagnostic scales using Diagnostic and Statis-
tical Manual of Mental Disorders criteria are available for use
in multiple settings, including the ICU.139 In some situa-
tions of an apparent hypoactive cognitive state, consider-
ation should be given to nonconvulsive seizures, which
have been reported in up to 19% of ICU patients.140
POCD has a subtler, subacute presentation dominated by
memory loss and executive dysfunction leading to inability
to perform simple activities of daily living. POCD usually
presents weeks to months after surgery; it may be only
partially reversible over a period of several months. The
diagnosis of POCD must be confirmed by the results of a
time-consuming battery of neurocognitive tests, adminis-
tered by trained personnel, showing significant decline
from baseline evaluation.141 Education and awareness of
POCD are of considerable importance because many
patients and their families may not be aware of the poten-
tial scope of this disease.
Because the stress response to surgery appears to play a
central role in development of postoperative brain dysfunc-
tion, strategies aimed at reducing tissue injury and/or lim-
iting its impact on the brain may be beneficial. Minimally
invasive surgical techniques are associated with lower rates
of POD.142 Their role in decreasing the risk of POCD
remains unclear. Similarly, effective attenuation of the
pain-induced stress response using a multimodal, opioid-
sparing analgesic strategy may be beneficial during
and after surgery.143 Other neuroprotective strategies tar-
geting the perioperative inflammatory activation or the
neuroendocrine response are being investigated.144
Finally, reduction of psychological perioperative stress
using reassurance, orientation, and maintenance of sen-
sory input from visual or auditory aids has been shown
to be as efficient as, if not more than, other strategies.145
Clearly, management should rely on early identification
of patients at risk (Table 1.2) and avoidance of any disrup-
tion of cerebral physiology until the mechanisms leading to
POD and POCD are elucidated. Patient management rely-
ing on a multimodal, multidisciplinary strategy is most suc-
cessful when initiated before surgery and continued
postoperatively.146 Overall, conditions associated with
insufficient cerebral oxygen or energy delivery (hypoxemia,
anemia, hypotension, hypoglycemia, stroke), excessive
cerebral metabolism (hyperthermia, seizure activity, sub-
stance withdrawal), and any acute homeostatic imbalance
(renal or hepatic dysfunction, drug toxicity, systemic
inflammation) should be identified as early as possible
and treated promptly. Whereas most hypnotic drugs have
Table 1.2 Predisposing and Precipitating Factors
for Postoperative Delirium
Predisposing factors Precipitating factors
Reduced cognitive reserve Polymedication
(advanced age, cognitive Drugs affecting the central nervous
impairment) system
Sensory impairment Pain
(visual, auditory) Urinary obstruction/catheterization
Frailty Hypoxemia
(malnutrition, dehydration) Hypotension
Substance dependence Infection
(alcohol, drugs) Electrolyte abnormalities
Severe illness with organ Environmental changes
dysfunction
Apolipoprotein E4 genotype Sleep/wake disturbances
been shown to increase the risk of POD irrespective of
dose or duration of administration, dexmedetomidine
may be advantageous and should be considered for seda-
tion or as a complement for general anesthesia in patients
at risk.147 Interestingly, recent evidence indicates excessive
depth of anesthesia, as measured with electroencephalog-
raphy, may correlate with a higher risk of both POD and
POCD.148
Anticholinergic drugs used for reversal of muscle paral-
ysis have been suspected to contribute to the development
of POD and POCD; however, recent reports have failed to
confirm this hypothesis.149 Antipsychotic medications
have been successfully used for prevention and treatment
of hyperactive POD. The precise underlying mechanism
remains unclear; some authors suggest it may convert
hyperactive episodes of POD into hypoactive ones without
resolving the issue.150 In absence of a reversible cause for
brain dysfunction, they may be administered cautiously.
Atypical antipsychotics such as risperidone or olanzapine
have a better side effect profile but are available for oral
administration only. Alternatively, haloperidol may be
administered intravenously or intramuscularly.151
Clinical Pearl
Management of POD and POCD should focus on early
identification of patients at risk and minimizing disruption of
cerebral physiology.
Summary
The effects of anesthetics, agents given during surgery, and
surgery itself can have an effect on the recovering patient.
Patients who are at an increased risk for postoperative
respiratory dysfunction, PONV, hyperglycemia, hypother-
mia, pain, and cognitive dysfunction should be identified
by preoperative risk factors, and the postoperative manage-
ment should take into consideration the intraoperative
course and management.
 1 • Effects of Anesthetics, Operative Pharmacotherapy, and Recovery from Anesthesia
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 2 Patient Positioning for
Neurosurgical Procedures
SHAUN E. GRUENBAUM, BENJAMIN F. GRUENBAUM, YORAM SHAPIRA, and
ALEXANDER ZLOTNIK
Introduction
Perhaps more so than in any other surgical specialty,
patient positioning is a critical component of neurosurgical
procedures. Whereas most other surgeries are performed in
the supine position with little input or assistance from the
anesthesiologist, positioning for neurosurgical procedures
requires cooperation between the surgeon, anesthesiolo-
gist, and nursing staff.
Correct patient positioning is essential to ensure ade-
quate surgical access, surgeon comfort, and minimal risk
for patient injury. There are several positions commonly
employed for neurosurgical procedures. It is essential that
all operating room personnel have a comprehensive
understanding of the various positions employed for neu-
rosurgical procedures, as well as the unique risks and pos-
sible postoperative implications associated with that
position.
The four major positions utilized for neurosurgical proce-
dures include the supine, lateral, prone, and sitting posi-
tions. Patients should be carefully evaluated prior to
surgery, and the benefits of a particular position as they
pertain to surgical access and comfort for the surgeon
should be weighed against the specific risks.
Each step of positioning the patient should be a cooper-
ative effort and should be accomplished in an efficient
and safe manner. Communication is vital to minimize
patient risk. Care and diligence should be taken when fixing
the patient’s head in a stereotaxic frame, positioning the
head and neck, and positioning the patient’s body. The
general principles of patient positioning are discussed at
length in the literature. In this chapter, we will focus our
discussion on the specific considerations that pertain to
positioning patients for neurosurgical procedures.
General Principles
Key Concepts
• Positioning the patient is an important part of the
neurosurgical procedure and should be planned during the
preoperative evaluation.
• Positioning the extremities should be done under the
guidelines of the American Society of Anesthesiologists
Practice Advisory for the Prevention of Perioperative
Peripheral Neuropathies.
• Temporary disconnection of the patient’s monitors, lines, and
ventilator may be necessary during positioning and when
turning the head of the bed; this should be done efficiently
and with the coordination of the operating room staff.
The general goals of patient positioning for neurosurgical
procedures are to provide optimal surgical exposure while
maintaining patient safety. Positioning the patient is an
important component of the neurosurgical procedure,
and this step is perhaps more critical than in any other
specialty. Whereas positioning for most other surgical spe-
cialties usually involves little input by anesthesiologists,
positioning the patient for neurosurgical procedures should
be a collaborative effort between the surgical, anesthesia,
and nursing staff.1 Especially in long surgeries, poor posi-
tioning may result in significant comorbidity secondary
to direct effects of positioning or indirect effects related to
suboptimal anatomical orientation.
Many patient positions have unique associated risks,
which must be appreciated by the surgical, nursing, and
anesthesia staff.2 The risks of a particular position must be
weighed against the benefits of surgical access and comfort.
The patient should be thoroughly evaluated in the preoper-
ative clinic, and the optimal position should be considered
and planned at that time. The operating room nurses and
anesthesiologist should be notified as early as possible about
the planned patient position so they can prepare all neces-
sary equipment. The anesthesiologist should be able to
anticipate potential complications associated with the
planned position and be prepared to treat accordingly.
The basic principles of patient positioning with regard to
appropriate padding and positioning the extremities should
be based on the American Society of Anesthesiologists
Practice Advisory for the Prevention of Perioperative
Peripheral Neuropathies3 (Table 2.1). The patient’s eyes
should be taped after induction of general anesthesia,
and eye lubrication should be considered for long proce-
dures. The arms should be maintained in a neutral position,
with arm abduction limited to 90 degrees. The bony prom-
inences of the extremities should be padded well to prevent
compression and breakdown of the skin, as well as periph-
eral neuropathies.
After induction of general anesthesia and placement of
arterial and venous lines, the operating room table is typi-
cally rotated 90 degrees or 180 degrees away from the
anesthesiologist. For a brief period, the patients may be dis-
connected from the monitoring devices, vascular lines, and
ventilation circuit. This requires careful coordination
15
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towards the whole free colored population of the United States. I
understand that policy to comprehend: First, the complete
suppression of all anti-slavery discussion; second, the expulsion
of the entire free people of the United States; third, the
nationalization of slavery; fourth, guarantees for the endless
perpetuation of slavery and its extension over Mexico and
Central America. Sir, these objects are forcibly presented to us in
the stern logic of passing events, and in all the facts that have
been before us during the last three years. The country has
been and is dividing on these grand issues. Old party ties are
broken. Like is finding its like on both sides of these issues, and
the great battle is at hand. For the present the best
representative of the slavery party is the Democratic party. Its
great head for the present is President Pierce, whose boast it
was before his election, that his whole life had been consistent
with the interests of slavery—that he is above reproach on that
score. In his inaugural address he reassures the South on this
point, so there shall be no misapprehension. Well, the head of
the slave power being in power it is natural that the pro-slavery
elements should cluster around his administration, and that is
rapidly being done. The stringent protectionist and the free-
trader strike hands. The supporters of Fillmore are becoming the
supporters of Pierce. Silver Gray Whigs shake-hands with
Hunker Democrats, the former only differing from the latter in
name. They are in fact of one heart and one mind, and the union
is natural and perhaps inevitable. Pilate and Herod made
friends. The key-stone to the arch of this grand union of forces of
the slave party is the so-called Compromise of 1850. In that
measure we have all the objects of our slaveholding policy
specified. It is, sir, favorable to this view of the situation, that the
whig party and the democratic party bent lower, sunk deeper,
and strained harder in their conventions, preparatory to the late
presidential election to meet the demands of slavery. Never did
parties come before the northern people with propositions of
such undisguised contempt for the moral sentiment and religious
ideas of that people. They dared to ask them to unite with them
in a war upon free speech, upon conscience, and to drive the
Almighty presence from the councils of the nation. Resting their
platforms upon the fugitive slave bill they have boldly asked this
people for political power to execute its horrible and hell-black
provisions. The history of that election reveals with great
clearness, the extent to which slavery has “shot its leprous
distillment” through the lifeblood of the nation. The party most
thoroughly opposed to the cause of justice and humanity
triumphed, while the party only suspected of a leaning toward
those principles was overwhelmingly defeated, and some say
annihilated. But here is a still more important fact, and still better
discloses the designs of the slave power. It is a fact full of
meaning, that no sooner did the democratic party come into
power than a system of legislation was presented to all the
legislatures of the Northern States designed to put those States
in harmony with the fugitive slave law, and with the malignant
spirit evinced by the national government towards the free
colored inhabitants of the country. The whole movement on the
part of the States bears unmistakable evidence of having one
origin, of emanating from one head, and urged forward by one
power. It was simultaneous, uniform, and general, and looked
only to one end. It was intended to put thorns under feet already
bleeding; to crush a people already bowed down; to enslave a
people already but half free; in a word, it was intended and well
calculated to discourage, dishearten, and if possible to drive the
whole free colored people out of the country. In looking at the
black law then recently enacted in the State of Illinois one is
struck dumb by its enormity. It would seem that the men who
passed that law, had not only successfully banished from their
minds all sense of justice, but all sense of shame as well; these
law codes propose to sell the bodies and souls of the blacks to
provide the means of intelligence and refinement for the whites;
to rob every black stranger who ventures among them to
increase their educational fund.
“While this kind of legislation is going on in the States, a pro-
slavery political board of health is being established at
Washington. Senators Hale, Chase, and Sumner are robbed of
their senatorial rights and dignity as representatives of sovereign
States, because they have refused to be inoculated with the pro-
slavery virus of the times. Among the services which a senator is
expected to perform, are many that can only be done efficiently
as members of important committees, and the slave power in the
Senate, in saying to these honorable senators, you shall not
serve on the committees of this body, took the responsibility of
insulting and robbing the States which has sent them there. It is
an attempt at Washington to decide for the States who the
States shall send to the Senate. Sir, it strikes me that this
aggression on the part of the slave power did not meet at the
hands of the proscribed and insulted senators the rebuke which
we had a right to expect from them. It seems to me that a great
opportunity was lost, that the great principle of senatorial
equality was left undefended at a time when its vindication was
sternly demanded. But it is not to the purpose of my present
statement to criticize the conduct of friends. Much should be left
to the discretion of anti-slavery men in Congress. Charges of
recreancy should never be made but on the most sufficient
grounds. For of all places in the world where an anti-slavery man
needs the confidence and encouragement of his friends, I take
Washington—the citadel of slavery—to be that place.
“Let attention now be called to the social influences
operating and coöperating with the slave power of the time,
designed to promote all its malign objects. We see here the
black man attacked in his most vital interests: prejudice and hate
are systematically excited against him. The wrath of other
laborers is stirred up against him. The Irish, who, at home,
readily sympathize with the oppressed everywhere, are instantly
taught when they step upon our soil to hate and despise the
negro. They are taught to believe that he eats the bread that
belongs to them. The cruel lie is told them, that we deprive them
of labor and receive the money which would otherwise make its
way into their pockets. Sir, the Irish-American will find out his
mistake one day. He will find that in assuming our avocation, he
has also assumed our degradation. But for the present we are
the sufferers. Our old employments by which we have been
accustomed to gain a livelihood are gradually slipping from our
hands: every hour sees us elbowed out of some employment to
make room for some newly arrived emigrant from the Emerald
Isle, whose hunger and color entitle him to special favor. These
white men are becoming house-servants, cooks, stewards,
waiters, and flunkies. For aught I see they adjust themselves to
their stations with all proper humility. If they cannot rise to the
dignity of white men, they show that they can fall to the
degradation of black men. But now, sir, look once more! While
the colored people are thus elbowed out of employment; while a
ceaseless enmity in the Irish is excited against us; while State
after State enacts laws against us; while we are being hunted
down like wild beasts; while we are oppressed with a sense of
increasing insecurity, the American Colonization Society, with
hypocrisy written on its brow, comes to the front, awakens to
new life, and vigorously presses its scheme for our expatriation
upon the attention of the American people. Papers have been
started in the North and the South to promote this long cherished
object—to get rid of the negro, who is presumed to be a standing
menace to slavery. Each of these papers is adapted to the
latitude in which it is published, but each and all are united in
calling upon the government for appropriations to enable the
Colonization Society to send us out of the country by steam.
Evidently this society looks upon our extremity as their
opportunity, and whenever the elements are stirred against us,
they are stimulated to unusual activity. They do not deplore our
misfortunes, but rather rejoice in them, since they prove that the
two races cannot flourish on the same soil. But, sir, I must
hasten. I have thus briefly given my view of one aspect of the
present condition and future prospects of the colored people of
the United States. And what I have said is far from encouraging
to my afflicted people. I have seen the cloud gather upon the
sable brows of some who hear me. I confess the case looks bad
enough. Sir, I am not a hopeful man. I think I am apt to
undercalculate the benefits of the future. Yet, sir, in this
seemingly desperate case, I do not despair for my people. There
is a bright side to almost every picture, and ours is no exception
to the general rule. If the influences against us are strong, those
 for us are also strong. To the inquiry, will our enemies prevail in
the execution of their designs—in my God, and in my soul, I
believe they will not. Let us look at the first object sought for by
the slavery party of the country, viz., the suppression of the anti-
slavery discussion. They desire to suppress discussion on this
subject, with a view to the peace of the slaveholder and the
security of slavery. Now, sir, neither the principle nor the
subordinate objects, here declared, can be at all gained by the
slave power, and for this reason: it involves the proposition to
padlock the lips of the whites, in order to secure the fetters on
the limbs of the blacks. The right of speech, precious and
priceless, cannot—will not—be surrendered to slavery. Its
suppression is asked for, as I have said, to give peace and
security to slaveholders. Sir, that thing cannot be done. God has
interposed an insuperable obstacle to any such result. “There
can be no peace, saith my God, to the wicked.” Suppose it were
possible to put down this discussion, what would it avail the
guilty slaveholder, pillowed as he is upon the heaving bosoms of
ruined souls? He could not have a peaceful spirit. If every anti-
slavery tongue in the nation were silent—every anti-slavery
organization dissolved—every anti-slavery periodical, paper,
pamphlet, book, or what not, searched out, burned to ashes, and
their ashes given to the four winds of heaven, still, still the
slaveholder could have no peace. In every pulsation of his heart,
in every throb of his life, in every glance of his eye, in the breeze
that soothes, and in the thunder that startles, would be waked up
an accuser, whose cause is, ‘thou art verily guilty concerning thy
brother.’”

This is no fancy sketch of the times indicated. The situation

during all the administration of President Pierce was only less
threatening and stormy than that under the administration of James
Buchanan. One sowed, the other reaped. One was the wind, the
other was the whirlwind. Intoxicated by their success in repealing the
Missouri compromise—in divesting the native-born colored man of
American citizenship—in harnessing both the Whig and Democratic
parties to the car of slavery, and in holding continued possession of
the national government, the propagandists of slavery threw off all
disguises, abandoned all semblance of moderation, and very
naturally and inevitably proceeded under Mr. Buchanan, to avail
themselves of all the advantages of their victories. Having legislated
out of existence the great national wall, erected in the better days of
the republic, against the spread of slavery, and against the increase
of its power—having blotted out all distinction, as they thought,
between freedom and slavery in the law, theretofore, governing the
Territories of the United States, and having left the whole question of
the legislation or prohibition of slavery to be decided by the people of
a Territory, the next thing in order was to fill up the Territory of
Kansas—the one likely to be first organized—with a people friendly
to slavery, and to keep out all such as were opposed to making that
Territory a free State. Here was an open invitation to a fierce and
bitter strife; and the history of the times shows how promptly that
invitation was accepted by both classes to which it was given, and
the scenes of lawless violence and blood that followed.
All advantages were at first on the side of those who were for
making Kansas a slave State. The moral force of the repeal of the
Missouri compromise was with them; the strength of the triumphant
Democratic party was with them; the power and patronage of the
federal government was with them; the various governors, sent out
under the Territorial government, was with them; and, above all, the
proximity of the Territory to the slave State of Missouri favored them
and all their designs. Those who opposed the making Kansas a
slave State, for the most part were far away from the battleground,
residing chiefly in New England, more than a thousand miles from
the eastern border of the Territory, and their direct way of entering it
was through a country violently hostile to them. With such odds
against them, and only an idea—though a grand one—to support
them, it will ever be a wonder that they succeeded in making Kansas
a free State. It is not my purpose to write particularly of this or of any
other phase of the conflict with slavery, but simply to indicate the
nature of the struggle, and the successive steps, leading to the final
result. The important point to me, as one desiring to see the slave
power crippled, slavery limited and abolished, was the effect of this
Kansas battle upon the moral sentiment of the North: how it made
abolitionists before they themselves became aware of it, and how it
rekindled the zeal, stimulated the activity, and strengthened the faith
of our old anti-slavery forces. “Draw on me for $1,000 per month
while the conflict lasts,” said the great-hearted Gerrit Smith. George
L. Stearns poured out his thousands, and anti-slavery men of smaller
means were proportionally liberal. H. W. Beecher shouted the right
word at the head of a mighty column; Sumner in the Senate spoke
as no man had ever spoken there before. Lewis Tappan representing
one class of the old opponents of slavery, and William L. Garrison
the other, lost sight of their former differences, and bent all their
energies to the freedom of Kansas. But these and others were
merely generators of anti-slavery force. The men who went to
Kansas with the purpose of making it a free State, were the heroes
and martyrs. One of the leaders in this holy crusade for freedom,
with whom I was brought into near relations, was John Brown,
whose person, house, and purposes I have already described. This
brave old man and his sons were amongst the first to hear and heed
the trumpet of freedom calling them to battle. What they did and
suffered, what they sought and gained, and by what means, are
matters of history, and need not be repeated here.
When it became evident, as it soon did, that the war for and
against slavery in Kansas was not to be decided by the peaceful
means of words and ballots, but that swords and bullets were to be
employed on both sides, Captain John Brown felt that now, after long
years of waiting, his hour had come, and never did man meet the
perilous requirements of any occasion more cheerfully,
courageously, and disinterestedly than he. I met him often during this
struggle, and saw deeper into his soul than when I met him in
Springfield seven or eight years before, and all I saw of him gave me
a more favorable impression of the man, and inspired me with a
higher respect for his character. In his repeated visits to the East to
obtain necessary arms and supplies, he often did me the honor of
spending hours and days with me at Rochester. On more than one
occasion I got up meetings and solicited aid to be used by him for
the cause, and I may say without boasting that my efforts in this
respect were not entirely fruitless. Deeply interested as
“Ossawatamie Brown” was in Kansas he never lost sight of what he
called his greater work—the liberation of all the slaves in the United
States. But for the then present he saw his way to the great end
through Kansas. It would be a grateful task to tell of his exploits in
the border struggle, how he met persecution with persecution, war
with war, strategy with strategy, assassination and house-burning
with signal and terrible retaliation, till even the blood-thirsty
propagandists of slavery were compelled to cry for quarter. The
horrors wrought by his iron hand cannot be contemplated without a
shudder, but it is the shudder which one feels at the execution of a
murderer. The amputation of a limb is a severe trial to feeling, but
necessity is a full justification of it to reason. To call out a murderer at
midnight, and without note or warning, judge or jury, run him through
with a sword, was a terrible remedy for a terrible malady. The
question was not merely which class should prevail in Kansas, but
whether free-state men should live there at all. The border ruffians
from Missouri had openly declared their purpose not only to make
Kansas a slave state, but that they would make it impossible for free-
state men to live there. They burned their towns, burned their farm-
houses, and by assassination spread terror among them until many
of the free-state settlers were compelled to escape for their lives.
John Brown was therefore the logical result of slaveholding
persecutions. Until the lives of tyrants and murderers shall become
more precious in the sight of men than justice and liberty, John
Brown will need no defender. In dealing with the ferocious enemies
of the free-state cause in Kansas he not only showed boundless
courage but eminent military skill. With men so few and odds against
him so great, few captains ever surpassed him in achievements,
some of which seem too disproportionate for belief, and yet no voice
has yet called them in question. With only eight men he met, fought,
whipped, and captured Henry Clay Pate with twenty-five well-armed
and well-mounted men. In this battle he selected his ground so
wisely, handled his men so skillfully, and attacked his enemies so
vigorously, that they could neither run nor fight, and were therefore
compelled to surrender to a force less than one-third their own. With
just thirty men on another memorable occasion he met and
vanquished 400 Missourians under the command of General Read.
These men had come into the territory under an oath never to return
to their homes in Missouri till they had stamped out the last vestige
of the free-state spirit in Kansas. But a brush with old Brown instantly
took this high conceit out of them, and they were glad to get home
upon any terms, without stopping to stipulate. With less than 100
men to defend the town of Lawrence, he offered to lead them and
give battle to 1,400 men on the banks of the Waukerusia river, and
was much vexed when his offer was refused by General Jim Lane
and others, to whom the defense of the place was committed. Before
leaving Kansas he went into the border of Missouri and liberated a
dozen slaves in a single night, and despite of slave laws and
marshals, he brought these people through a half dozen States and
landed them safe in Canada. The successful efforts of the North in
making Kansas a free State, despite all the sophistical doctrines, and
the sanguinary measures of the South to make it a slave State,
exercised a potent influence upon subsequent political forces and
events in the then near future. It is interesting to note the facility with
which the statesmanship of a section of the country adapted its
convictions to changed conditions. When it was found that the
doctrine of popular sovereignty (first I think invented by General
Cass, and afterwards adopted by Stephen A. Douglas) failed to
make Kansas a slave State, and could not be safely trusted in other
emergencies, southern statesmen promptly abandoned and
reprobated that doctrine, and took what they considered firmer
ground. They lost faith in the rights, powers, and wisdom of the
people and took refuge in the Constitution. Henceforth the favorite
doctrine of the South was that the people of a territory had no voice
in the matter of slavery whatever; that the Constitution of the United
States, of its own force and effect, carried slavery safely into any
territory of the United States and protected the system there until it
ceased to be a territory and became a State. The practical operation
of this doctrine would be to make all the future new States
slaveholding States, for slavery once planted and nursed for years in
a territory would easily strengthen itself against the evil day and defy
eradication. This doctrine was in some sense supported by Chief
Justice Taney, in the infamous Dred Scott decision. This new ground,
however, was destined to bring misfortune to its inventors, for it
divided for a time the democratic party, one faction of it going with
John C. Breckenridge and the other espousing the cause of Stephen
A. Douglas; the one held firmly to the doctrine that the United States
Constitution, without any legislation, territorial, national, or otherwise,
by its own force and effect, carried slavery into all the territories of
the United States; the other held that the people of a territory had the
right to admit slavery or reject slavery, as in their judgment they
might deem best. Now, while this war of words—this conflict of
doctrines—was in progress, the portentous shadow of a stupendous
civil war became more and more visible. Bitter complaints were
raised by the slaveholders that they were about to be despoiled of
their proper share in territory won by a common valor, or bought by a
common treasure. The North, on the other hand, or rather a large
and growing party at the North, insisted that the complaint was
unreasonable and groundless; that nothing properly considered as
property was excluded or meant to be excluded from the territories;
that southern men could settle in any territory of the United States
with some kinds of property, and on the same footing and with the
same protection as citizens of the North; that men and women are
not property in the same sense as houses, lands, horses, sheep,
and swine are property, and that the fathers of the Republic neither
intended the extension nor the perpetuity of slavery; that liberty is
national, and slavery is sectional. From 1856 to 1860 the whole land
rocked with this great controversy. When the explosive force of this
controversy had already weakened the bolts of the American Union;
when the agitation of the public mind was at its topmost height; when
the two sections were at their extreme points of difference; when
comprehending the perilous situation, such statesmen of the North
as William H. Seward sought to allay the rising storm by soft,
persuasive speech, and when all hope of compromise had nearly
vanished, as if to banish even the last glimmer of hope for peace
between the sections, John Brown came upon the scene. On the
night of the 16th of October, 1859, there appeared near the
confluence of the Potomac and Shenandoah rivers, a party of 19
men—14 white and 5 colored. They were not only armed
themselves, but they brought with them a large supply of arms for
such persons as might join them. These men invaded the town of
Harper’s Ferry, disarmed the watchman, took possession of the
arsenal, rifle factory, armory, and other government property at that
place, arrested and made prisoners of nearly all the prominent
citizens in the neighborhood, collected about 50 slaves, put bayonets
into the hands of such as were able and willing to fight for their
liberty, killed 3 men, proclaimed general emancipation, held the
ground more than thirty hours, were subsequently overpowered and
nearly all killed, wounded, or captured by a body of United States
troops under command of Col. Robert E. Lee, since famous as the
rebel General Lee. Three out of the nineteen invaders were captured
while fighting, and one of them was Capt. John Brown—the man
who originated, planned, and commanded the expedition. At the time
of his capture Capt. Brown was supposed to be mortally wounded,
as he had several ugly gashes and bayonet wounds on his head and
body, and apprehending that he might speedily die, or that he might
be rescued by his friends, and thus the opportunity to make him a
signal example of slaveholding vengeance, would be lost, his
captors hurried him to Charlestown, 10 miles further within the
border of Virginia, placed him in prison strongly guarded by troops,
and before his wounds were healed he was brought into court,
subjected to a nominal trial, convicted of high-treason and inciting
slaves to insurrection, and was executed.
His corpse was given up to his woe-stricken widow, and she,
assisted by anti-slavery friends, caused it to be borne to North Elba,
Essex county, N. Y., and there his dust now reposes amid the silent,
solemn, and snowy grandeurs of the Adirondacks. This raid upon
Harper’s Ferry was as the last straw to the camel’s back. What in the
tone of southern sentiment had been fierce before became furious
and uncontrollable now. A scream for vengeance came up from all
sections of the slave States and from great multitudes in the North.
All who were supposed to have been any way connected with John
Brown were to be hunted down and surrendered to the tender
mercies of slaveholding and panic-stricken Virginia, and there to be
tried after the fashion of John Brown’s trial, and of course to be
summarily executed.
On the evening when the news came that John Brown had taken
and was then holding the town of Harper’s Ferry, it so happened that
I was speaking to a large audience in National Hall, Philadelphia.
The announcement came upon us with the startling effect of an
earthquake. It was something to make the boldest hold his breath. I
saw at once that my old friend had attempted what he had long ago
resolved to do, and I felt certain that the result must be his capture
and destruction. As I expected, the next day brought the news that
with two or three men he had fortified and was holding a small
engine house, but that he was surrounded by a body of Virginia
militia, who thus far had not ventured to capture the insurgents, but
that escape was impossible. A few hours later and word came that
Colonel Robert E. Lee with a company of United States troops had
made a breach in Capt. Brown’s fort, and had captured him alive
though mortally wounded. His carpet bag had been secured by
Governor Wise, and that it was found to contain numerous letters
and documents which directly implicated Gerritt Smith, Joshua R.
Giddings, Samuel G. Howe, Frank P. Sanborn, and myself. This
intelligence was soon followed by a telegram saying that we were all
to be arrested. Knowing that I was then in Philadelphia, stopping with
my friend, Thomas J. Dorsey, Mr. John Hern, the telegraph operator,
came to me and with others urged me to leave the city by the first
train, as it was known through the newspapers that I was then in
Philadelphia, and officers might even then be on my track. To me
there was nothing improbable in all this. My friends for the most part
were appalled at the thought of my being arrested then or there, or
while on my way across the ferry from Walnut street wharf to
Camden, for there was where I felt sure the arrest would be made,
and asked some of them to go so far as this with me merely to see
what might occur, but upon one ground or another they all thought it
best not to be found in my company at such a time, except dear old
Franklin Turner—a true man. The truth is, that in the excitement
which prevailed my friends had reason to fear that the very fact that
they were with me would be a sufficient reason for their arrest with
me. The delay in the departure of the steamer seemed unusually
long to me, for I confess I was seized with a desire to reach a more
northern latitude. My friend Frank did not leave my side till “all
ashore” was ordered and the paddles began to move. I reached New
York at night, still under the apprehension of arrest at any moment,
but no signs of such event being made, I went at once to the Barclay
street ferry, took the boat across the river and went direct to
Washington street, Hoboken, the home of Mrs. Marks, where I spent
the night, and I may add without undue profession of timidity, an
anxious night. The morning papers brought no relief, for they
announced that the government would spare no pains in ferretting
out and bringing to punishment all who were connected with the
Harper’s Ferry outrage, and that papers as well as persons would be
searched for. I was now somewhat uneasy from the fact that sundry
letters and a constitution written by John Brown were locked up in
my desk in Rochester. In order to prevent these papers from falling
into the hands of the government of Virginia, I got my friend Miss
Ottilia Assing to write at my dictation the following telegram to B. F.
Blackall, the telegraph operator in Rochester, a friend and frequent
visitor at my house, who would readily understand the meaning of
the dispatch:

“B. F. Blackall, Esq.,

“Tell Lewis (my oldest son) to secure all the important papers
in my high desk.”

I did not sign my name, and the result showed that I had rightly
judged that Mr. Blackall would understand and promptly attend to the
request. The mark of the chisel with which the desk was opened is
still on the drawer, and is one of the traces of the John Brown raid.
Having taken measures to secure my papers the trouble was to
know just what to do with myself. To stay in Hoboken was out of the
question, and to go to Rochester was to all appearance to go into the
hands of the hunters, for they would naturally seek me at my home if
they sought me at all. I, however, resolved to go home and risk my
safety there. I felt sure that once in the city I could not be easily
taken from there without a preliminary hearing upon the requisition,
and not then if the people could be made aware of what was in
progress. But how to get to Rochester became a serious question. It
would not do to go to New York city and take the train, for that city
was not less incensed against the John Brown conspirators than
many parts of the South. The course hit upon by my friends, Mr.
Johnston and Miss Assing, was to take me at night in a private
conveyance from Hoboken to Paterson, where I could take the Erie
railroad for home. This plan was carried out and I reached home in
safety, but had been there but a few moments when I was called
upon by Samuel D. Porter, Esq., and my neighbor, Lieutenant-
Governor Selden, who informed me that the governor of the State
would certainly surrender me on a proper requisition from the
governor of Virginia, and that while the people of Rochester would
not permit me to be taken South, yet in order to avoid collision with
the government and consequent bloodshed, they advised me to quit
the country, which I did—going to Canada. Governor Wise in the
meantime, being advised that I had left Rochester for the State of
Michigan, made requisition on the governor of that State for my
surrender to Virginia.
The following letter from Governor Wise to President James
Buchanan (which since the war was sent me by B. J. Lossing, the
historian,) will show by what means the governor of Virginia meant to
get me in his power, and that my apprehensions of arrest were not
altogether groundless:

[Confidential.]
Richmond, Va., Nov. 13, 1859.
To His Excellency, James Buchanan, President of the United States, and to the
Honorable Postmaster-General of the United States:

Gentlemen—I have information such as has caused me,

upon proper affidavits, to make requisition upon the Executive of
Michigan for the delivery up of the person of Frederick Douglass,
a negro man, supposed now to be in Michigan, charged with
murder, robbery, and inciting servile insurrection in the State of
Virginia. My agents for the arrest and reclamation of the person
so charged are Benjamin M. Morris and William N. Kelly. The
latter has the requisition, and will wait on you to the end of
obtaining nominal authority as post-office agents. They need be
very secretive in this matter, and some pretext for traveling
 through the dangerous section for the execution of the laws in
this behalf, and some protection against obtrusive, unruly, or
lawless violence. If it be proper so to do, will the postmaster-
general be pleased to give to Mr. Kelly, for each of these men, a
permit and authority to act as detectives for the post-office
department, without pay, but to pass and repass without
question, delay or hindrance?
Respectfully submitted by your obedient servant,
Henry A. Wise.

There is no reason to doubt that James Buchanan afforded

Governor Wise all the aid and coöperation for which he was asked. I
have been informed that several United States marshals were in
Rochester in search of me within six hours after my departure. I do
not know that I can do better at this stage of my story than to insert
the following letter, written by me to the Rochester Democrat and
American:

Canada West, Oct 31st, 1859.

Mr. Editor:
I notice that the telegraph makes Mr. Cook (one of the
unfortunate insurgents at Harper’s Ferry, and now a prisoner in
the hands of the thing calling itself the Government of Virginia,
but which in fact is but an organized conspiracy by one part of
the people against another and weaker) denounce me as a
coward, and assert that I promised to be present in person at the
Harper’s Ferry insurrection. This is certainly a very grave
impeachment whether viewed in its bearings upon friends or
upon foes, and you will not think it strange that I should take a
somewhat serious notice of it. Having no acquaintance whatever
with Mr. Cook, and never having exchanged a word with him
about Harper’s Ferry insurrection, I am disposed to doubt if he
could have used the language concerning me, which the wires
attribute to him. The lightning when speaking for itself, is among
the most direct, reliable, and truthful of things; but when
speaking of the terror-stricken slaveholders at Harper’s Ferry, it
has been made the swiftest of liars. Under its nimble and
trembling fingers it magnifies 17 men into 700 and has since
filled the columns of the New York Herald for days with its
interminable contradictions. But assuming that it has told only
the simple truth as to the sayings of Mr. Cook in this instance, I
have this answer to make to my accuser: Mr. Cook may be
perfectly right in denouncing me as a coward; I have not one
word to say in defense or vindication of my character for
courage; I have always been more distinguished for running than
fighting, and tried by the Harper’s-Ferry-insurrection-test, I am
most miserably deficient in courage, even more so than Cook
when he deserted his brave old captain and fled to the
mountains. To this extent Mr. Cook is entirely right, and will meet
no contradiction from me, or from anybody else. But wholly,
grievously and most unaccountably wrong is Mr. Cook when he
asserts that I promised to be present in person at the Harper’s
Ferry insurrection. Of whatever other imprudence and
indiscretion I may have been guilty, I have never made a
promise so rash and wild as this. The taking of Harper’s Ferry
was a measure never encouraged by my word or by my vote. At
any time or place, my wisdom or my cowardice, has not only
kept me from Harper’s Ferry, but has equally kept me from
making any promise to go there. I desire to be quite emphatic
here, for of all guilty men, he is the guiltiest who lures his
fellowmen to an undertaking of this sort, under promise of
assistance which he afterwards fails to render. I therefore
declare that there is no man living, and no man dead, who if
living, could truthfully say that I ever promised him, or anybody
else, either conditionally, or otherwise, that I would be present in
person at the Harper’s Ferry insurrection. My field of labor for the
abolition of slavery has not extended to an attack upon the
United States arsenal. In the teeth of the documents already
published and of those which may hereafter be published, I
affirm that no man connected with that insurrection, from its
noble and heroic leader down, can connect my name with a
single broken promise of any sort whatever. So much I deem it
proper to say negatively. The time for a full statement of what I
know and of all I know of this desperate but sublimely
disinterested effort to emancipate the slaves of Maryland and
Virginia from their cruel taskmasters, has not yet come, and may
never come. In the denial which I have now made, my motive is
more a respectful consideration for the opinions of the slave’s
friends than from my fear of being made an accomplice in the
general conspiracy against slavery, when there is a reasonable
hope for success. Men who live by robbing their fellowmen of
their labor and liberty have forfeited their right to know anything
of the thoughts, feelings, or purposes of those whom they rob
and plunder. They have by the single act of slaveholding,
voluntarily placed themselves beyond the laws of justice and
honor, and have become only fitted for companionship with
thieves and pirates—the common enemies of God and of all
mankind. While it shall be considered right to protect oneself
against thieves, burglars, robbery, and assassins, and to slay a
wild beast in the act of devouring his human prey, it can never
be wrong for the imbruted and whip-scarred slaves, or their
friends, to hunt, harass, and even strike down the traffickers in
human flesh. If any body is disposed to think less of me on
account of this sentiment, or because I may have had a
knowledge of what was about to occur, and did not assume the
base and detestable character of an informer, he is a man
whose good or bad opinion of me may be equally repugnant and
despicable.
Entertaining these sentiments, I may be asked why I did not
join John Brown—the noble old hero whose one right hand has
shaken the foundation of the American Union, and whose ghost
will haunt the bed-chambers of all the born and unborn
slaveholders of Virginia through all their generations, filling them
with alarm and consternation. My answer to this has already
been given; at least impliedly given—“The tools to those who
can use them!” Let every man work for the abolition of slavery in
his own way. I would help all and hinder none. My position in
regard to the Harper’s Ferry insurrection may be easily inferred
from these remarks, and I shall be glad if those papers which
have spoken of me in connection with it, would find room for this
brief statement. I have no apology for keeping out of the way of
those gentlemanly United States marshals, who are said to have
paid Rochester a somewhat protracted visit lately, with a view to
an interview with me. A government recognizing the validity of
the Dred Scott decision at such a time as this, is not likely to
have any very charitable feelings towards me, and if I am to
meet its representatives I prefer to do so at least upon equal
terms. If I have committed any offense against society I have
done so on the soil of the State of New York, and I should be
perfectly willing to be arraigned there before an impartial jury;
but I have quite insuperable objections to being caught by the
hounds of Mr. Buchanan, and “bagged” by Gov. Wise. For this
appears to be the arangement. Buchanan does the fighting and
hunting, and Wise “bags” the game. Some reflections may be
made upon my leaving on a tour to England just at this time. I
have only to say that my going to that country has been rather
delayed than hastened by the insurrection at Harper’s Ferry. All
know that I had intended to leave here in the first week of
November.
Frederick Douglass.”
 CHAPTER X.
THE BEGINNING OF THE END.

My connection with John Brown—To and from England—Presidential contest

—Election of Abraham Lincoln.

WHAT was my connection with John Brown, and what I knew of his
scheme for the capture of Harper’s Ferry, I may now proceed to
state. From the time of my visit to him in Springfield, Mass., in 1847,
our relations were friendly and confidential. I never passed through
Springfield without calling on him, and he never came to Rochester
without calling on me. He often stopped over night with me, when we
talked over the feasibility of his plan for destroying the value of slave
property, and the motive for holding slaves in the border States. That
plan, as already intimated elsewhere, was to take twenty or twenty-
five discreet and trustworthy men into the mountains of Virginia and
Maryland, and station them in squads of five, about five miles apart,
on a line of twenty-five miles; each squad to co-operate with all, and
all with each. They were to have selected for them, secure and
comfortable retreats in the fastnesses of the mountains, where they
could easily defend themselves in case of attack. They were to
subsist upon the country roundabout. They were to be well armed,
but were to avoid battle or violence, unless compelled by pursuit or
in self-defense. In that case, they were to make it as costly as
possible to the assailing party, whether that party should be soldiers
or citizens. He further proposed to have a number of stations from
the line of Pennsylvania to the Canada border, where such slaves as
he might, through his men, induce to run away, should be supplied
with food and shelter and be forwarded from one station to another
till they should reach a place of safety either in Canada or the
Northern States. He proposed to add to his force in the mountains
any courageous and intelligent fugitives who might be willing to
remain and endure the hardships and brave the dangers of this
mountain life. These, he thought, if properly selected, on account of
their knowledge of the surrounding country, could be made valuable
auxiliaries. The work of going into the valley of Virginia and
persuading the slaves to flee to the mountains, was to be committed
to the most courageous and judicious man connected with each
squad.
Hating slavery as I did, and making its abolition the object of my
life, I was ready to welcome any new mode of attack upon the slave
system which gave any promise of success. I readily saw that this
plan could be made very effective in rendering slave property in
Maryland and Virginia valueless by rendering it insecure. Men do not
like to buy runaway horses, nor to invest their money in a species of
property likely to take legs and walk off with itself. In the worse case,
too, if the plan should fail, and John Brown should be driven from the
mountains, a new fact would be developed by which the nation
would be kept awake to the existence of slavery. Hence, I assented
to this, John Brown’s scheme or plan for running off slaves.
To set this plan in operation, money and men, arms and
ammunition, food and clothing, were needed; and these, from the
nature of the enterprise, were not easily obtained, and nothing was
immediately done. Captain Brown, too, notwithstanding his rigid
economy, was poor, and was unable to arm and equip men for the
dangerous life he had mapped out. So the work lingered till after the
Kansas trouble was over, and freedom was a fact accomplished in
that Territory. This left him with arms and men, for the men who had
been with him in Kansas, believed in him, and would follow him in
any humane but dangerous enterprise he might undertake.
After the close of his Kansas work, Captain Brown came to my
house in Rochester, and said he desired to stop with me several
weeks; “but,” he added, “I will not stay unless you will allow me to
pay board.” Knowing that he was no trifler and meant all he said, and
desirous of retaining him under my roof, I charged three dollars a
week. While here, he spent most of his time in correspondence. He
wrote often to George L. Stearns of Boston, Gerrit Smith of