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THE
NeuroICU BOOK
Lee-FM_pi-xxx.indd 1 5/15/17 8:01 PM

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THE
NeuroICU BOOK
Second Edition
Editor
Kiwon Lee, MD, FACP, FAHA, FCCM

Vice Chairman, Department of Neurosurgery for Critical Care
Associate Professor, Neurosurgery and Neurology
Chief, Division of Neurocritical Care
Director, Neuroscience and Neurotrauma ICU
The University of Texas Medical School at Houston
Mischer Neuroscience Institute
Memorial Hermann—Texas Medical Center
Houston, Texas
New York Chicago San Francisco Athens London Madrid

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With love, this book is again dedicated to my father, Duckhee Lee, who has shown
me diligence and love; to my mother, Younghee Lee, who has taught me how to
become a leader with legacy; to my one and only sister, Katelyn Jongmee Lee;
to my dearest daughters, Sophia Koen Lee and Estelle Charin Lee, who constantly
bring me happiness even when I am under stress; and to my lovely wife,
Kyongsook Lee, without whose support I certainly would not be at where
I am today. I am also grateful to all my colleagues, trainees,
and medical students as we continue our journey as a team of healers
and teachers for our patients and their families.

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Contents
Contributors xiii
Foreword xxv
Preface xxvii
Acknowledgments xxix
Section 1 Neurocritical Care Diseases................................................................ 1

Section Editor: Neeraj Badjatia, MD, MSc, FCCM
1. Subarachnoid Hemorrhage........................................................................................... 1
2. Intracerebral Hemorrhage........................................................................................... 36
Fred Rincon, MD, MSc, FACP, FCCP, FCCM and Stephan A. Mayer, MD, FCCM
3. Status Epilepticus............................................................................................................ 52
David Roh, MD, and Jan Claassen, MD, PhD, FNCS
4. Neurotrauma.................................................................................................................... 80
Wan-Tsu W. Chang, MD, and Neeraj Badjatia, MD, MSc, FCCM
5. Acute Ischemic Stroke................................................................................................... 93

Joshua Z.Willey, MD, MS
6. Neuromuscular Diseases.............................................................................................125
Jennifer Frontera, MD, and Ivan Rocha Ferreira da Silva, MD
7. Paroxysmal Sympathetic Hyperactivity.................................................................147

Sophie Samuel, PharmD, BCPS, H. Alex Choi, MD, and
8. CNS Infection...................................................................................................................155
Syed Omar Shah, MD, MBA, and Fred Rincon, MD, MSc, FACP, FCCP, FCCM
9. ICU Management of Brain Tumors...........................................................................174

Simon Hanft, MD, and Michael B. Sisti, MD, FACS
10. Inflammatory and Demyelinating CNS Diseases................................................203

H. Alex Choi, MD, Sang-Bae Ko, MD, PhD, Mubashir Pervez, MD,
Robert J. Brown, MD, and Kiwon Lee, MD, FACP, FAHA, FCCM
vii

viii Contents
11. Cardiac Arrest and Anoxic Brain Injury...................................................................214

Tiffany Chang, MD, Rishi Malhotra, MD, and
12. Fulminant Hepatic Failure...........................................................................................230

H. Alex Choi, MD, Sang-Beom Jeon, MD, PhD, and
13. Encephalopathy and Delirium..................................................................................239

Nancy J. Edwards, MD, and Kiwon Lee, MD, FACP, FAHA, FCCM
Section 2 Neurocritical Care Monitoring.................................................. 249

Section Editor: Jan Claassen, MD, PhD, FNCS
14. Management of Increased Intracranial Pressure................................................249

Kiwon Lee, MD, FACP, FAHA, FCCM, and Stephan A. Mayer, MD, FCCM
15. Continuous Electroencephalogram Monitoring in the ICU............................262

Emily J. Gilmore, MD, and Jan Claassen, MD, PhD, FNCS
16. Multimodality Neuromonitoring..............................................................................289

Raimund Helbok, MD, Pedro Kurtz, MD, PhD, and Jan Claassen, MD, PhD, FNCS
17. Advanced Hemodynamic Monitoring....................................................................325

Pedro Kurtz, MD, PhD, and Kiwon Lee, MD, FACP, FAHA, FCCM
18. Evoked Potentials in the Operating Room and ICU...........................................338

Errol Gordon, MD, and Jan Claassen, MD, PhD, FNCS
19. Neurophysiologic Decision Support Systems.....................................................351

Michael J. Schmidt, PhD, MSc, and Soojin Park, MD, FAHA
20. Sedation ............................................................................................................................361

Amy L. Dzierba, PharmD, BCPS, BCCCP, FCCM,
Vivek K. Moitra, MD, and Robert N. Sladen, MBChB, MRCP, FRCP
21. Fever and Temperature Modulation........................................................................378

Aashish Anand, MD, Joseph Haymore, CRNP, and
Neeraj Badjatia, MD, MSc, FCCM
Section 3 Neurosurgery..........................................................................................................397
Section Editors: E. Sander Connolly, Jr., MD, FACS, and Arthur L. Day, MD
22. External Ventricular Drain Management and

Ventriculoperitoneal Shunts......................................................................................397
Nikita G. Alexiades, MD, Jason A. Ellis, MD, and E. Sander Connolly, Jr., MD, FACS

Contents ix
23. Endovascular Surgical Neuroradiology..................................................................416

Blake E. S. Taylor, MD, Nathan Manning, MBBS, FRANZCR, and
Philip M. Meyers, MD, FACR, FSIR, FAHA
24. Brain Aneurysm, AVM, and Bypass Surgery..........................................................460

Jason A. Ellis, MD, and E. Sander Connolly, Jr., MD, FACS
25. Carotid Endarterectomy and Extracranial-Intracranial Bypass......................473

Jason A. Ellis, MD, and E. Sander Connolly, Jr., MD, FACS
26. Postcraniotomy Complication Management............................................................ 482

Blake E. S. Taylor, MD, Christopher P. Kellner, MD, and
E. Sander Connolly, Jr., MD, FACS
27. Spine Trauma...................................................................................................................505

Ryan Kitagawa, MD, and Daniel H. Kim, MD, FACS, FAANS
28. Pediatric Neurosurgery................................................................................................520

Stephen L. Katzen, MD, Stephen A. Fletcher, DO, Manish N. Shah, MD, and
David I. Sandberg, MD, FAANS, FACS, FAAP
Section 4 Trauma and Surgical Intensive Care................................547

Section Editors: Joseph S. Meltzer, MD, and Vivek K. Moitra, MD
29. Thoracic Trauma and Cardiothoracic Intensive Care Unit Management........547

Steven Miller, MD, and Vivek K. Moitra, MD
30. Abdominal Trauma........................................................................................................560

Brian Woods, MD
31. Traumatic Vascular Injuries.........................................................................................575

John Rollo, MD, and Joseph S. Meltzer, MD
32. Abdominal Emergencies.............................................................................................586

Carlee Clark, MD
33. Genitourinary Emergencies........................................................................................609

Francis Macchio, MD
34. Critical Care Ultrasound...............................................................................................622

Oliver Panzer, MD, and Wolf Benjamin Kratzert, MD
Section 5 Cardiovascular Section..........................................................................645

Section Editor: Umesh K. Gidwani, MD, MS, FCCP, FCCM, FACC
35. Acute Coronary Syndrome.........................................................................................645

Umesh K. Gidwani, MD, MS, FCCP, FCCM, FACC

x Contents
36. Rhythm Disturbances in Critically Ill Patients......................................................660

Anurag Singh, MD, Umesh K. Gidwani, MD, MS, FCCP, FCCM, FACC,
and Vivek Reddy, MD
37. Acute Decompensated Heart Failure......................................................................680

Ruwanthi Titano, MD, Raymond Bietry, MD, and Sean Pinney, MD
38. Cardiogenic Shock and Intraaortic Balloon Pump.............................................696

Samit K. Shah, MD, Radha Gopalan, MD, and Umesh K. Gidwani,
MD, MS, FCCP, FCCM, FACC
39. Management of Cardiopulmonary Devices at the End of Life......................709

Raman Sharma, MD, Neha Dangayach, MD, and Umesh K. Gidwani,
MD, MS, FCCP, FCCM, FACC
40. The Role of ECMO in Cardiopulmonary Failure in Adults................................722

Darryl Abrams, MD, and Daniel Brodie, MD
Section 6 Pulmonary Diseases....................................................................................739

Section Editor: David B. Seder, MD, FCCP, FCCM, FNCS
41. The Neurocritical Care Airway...................................................................................739

Avinash B. Kumar, MD, FCCM, FCCP, and
David B. Seder, MD, FCCP, FCCM, FNCS
42. Mechanical Ventilation.................................................................................................757

Brian M. Fuller, MD, MSCI
43. Acute Respiratory Distress Syndrome....................................................................786

Luciana Mascia, MD, PhD, Anna Teresa Mazzeo, MD, Federico Bilotta, MD,
and Vito Fanelli, MD, PhD
44. Deep Vein Thrombosis and Pulmonary Embolism.............................................799

Geno J. Merli, MD, MACP, FHM, FSVM, Photi Galanis, MD, Geoffrey O. Ouma, DO,
MS, Luis Eraso, MD, and Lynda Thomson, PharmD, CACP
45. Percutaneous Tracheostomy......................................................................................814

Akshu Balwan, MBChB, and David B. Seder, MD, FCCP, FCCM, FCNS
46. Bronchoscopy in the NeuroICU.................................................................................826

Akshu Balwan, MBChB, and David B. Seder, MD, FCCP, FCCM, FNCS
Section 7 Renal and Electrolyte Disorders.............................................841

Section Editor: Lawrence S. Weisberg, MD
47. Acute Kidney Injury.......................................................................................................841

Jean-Sebastien Rachoin, MD, and Lawrence S. Weisberg, MD

Contents xi
48. Renal Replacement Therapies...................................................................................857

Andrew Davenport, MD
49 Disorders of Water Homeostasis: Hypo- and Hypernatremia........................869

Lawrence S. Weisberg, MD
50. Management of Systemic Blood Pressure in the NeuroICU...........................889

Samia Mian, MD, Thilagavathi Venkatachalam, MD, and
Christopher B. McFadden, MD
Section 8 Hematology...............................................................................................................901
Section Editor: Louis M. Aledort, MD, MACP
51. Disseminated Intravascular Coagulation..............................................................901

Caroline Cromwell, MD, and Louis M. Aledort, MD, MACP
52. Bleeding Disorders and Coagulopathy Reversal................................................906

Caroline Cromwell, MD, and Louis M. Aledort, MD, MACP
Section 9 Infectious Disease...........................................................................................919

Section Editor: Fred Rincon, MD, MSc, FACP, FCCP, FCCM
53. Sepsis and Septic Shock..............................................................................................919

Daniel De Backer, MD, and Fabio Silvio Taccone, MD
54. Antimicrobial Therapies in the ICU..........................................................................935

Glenn Oettinger, PharmD, BCPS, and Luyi Kathy Zhang, MD
55. Catheter-Related Bloodstream Infections.............................................................952

Jacqueline S. Urtecho, MD, and Deena M. Athas, MD
56. Common Infections in the ICU..................................................................................960

Miranda Tan, MD, and David Oxman, MD
Section 10 Nutrition and Endocrinology..................................................975

Section Editor: Kiwon Lee, MD, FACP, FAHA, FCCM
57. Nutrition and Metabolic Support.............................................................................975

Dong Wook Kim, MD, and David S. Seres, MD
58. Endocrine Disorders in Critical Illness.....................................................................988

Nancy J. Edwards, MD, and Kiwon Lee, MD, FACP, FAHA, FCCM

xii Contents
Section 11 Ethics and End-of-Life Issues....................................................993

Section Editor: Kiwon Lee, MD, FACP, FAHA, FCCM
59. Brain Death and Organ Donation............................................................................993

Jeremy T. Ragland, MD, Guillermo Linares, MD, Mireia Anglada, MD, and
Index 1011

Contributors
Darryl Abrams, MD Deena M. Athas, MD

Division of Pulmonary, Allergy and Clinical Assistant Professor
Critical Care Thomas Jefferson University
Columbia University College of Philadelphia, Pennsylvania
Physicians and Surgeons Chapter 55
New York, New York
Chapter 40 Neeraj Badjatia, MD, MSc, FCCM
Chief, Neurocritical Care
Louis M. Aledort, MD, MACP Associate Professor of Neurology,
The Mary Weinfeld Professor of Neurosurgery, and Anesthesiology
Clinical Research in Hemophilia University of Maryland School of
Division of Hematology and Medical Medicine
Oncology Baltimore, Maryland
Department of Medicine Chapters 4, 21
The Mount Sinai School of Medicine
New York, New York Akshu Balwan, MBChB
Chapters 51, 52 Departments of Medicine and Critical
Care Services
Nikita G. Alexiades, MD Maine Medical Center
Department of Neurological Surgery Portland, Maine
Columbia University Medical Center Chapters 45, 46
New York, New York
Chapter 22 Raymond Bietry, MD
The Mount Sinai Hospital
Aashish Anand, MD New York, New York
University of Maryland Medical Chapter 37
Center
Baltimore, Maryland Federico Bilotta, MD
Chapter 21 Assistant Professor, Dipartimento di
Anestesiologia e Rianimazione
Mireia Anglada, MD Università di Torino
Germans Trias i Pujol Hospital Ospedale S. Giovanni Battista
Intensive Care Unit Torino, Italy
Barcelona, Spain Chapter 43
Chapter 59
xiii

xiv Contributors
Daniel Brodie, MD H. Alex Choi, MD

Division of Pulmonary, Allergy, and Assistant Professor, Department of
Critical Care Neurology
Columbia University College of Assistant Professor, Department of
Physicians and Surgeons Neurosurgery
New York, New York The University of Texas Health
Chapter 40 Sciences Center at Houston
McGovern Medical School
Robert J. Brown, MD Houston, Texas
Assistant Professor of Neurosurgery Chapters 7, 10, 12
and Neurology
The University of Texas Medical Jan Claassen, MD, PhD, FNCS
School at Houston Associate Professor of Neurology
Memorial Hermann-Texas Medical Head of Neurocritical Care
Center and Medical Director of the
The Mischer Neuroscience Institute Neurological Intensive Care Unit
Houston, Texas Columbia University College of
Chapter 10 Physicians and Surgeons
New York, New York
Tiffany Chang, MD Chapters 3, 15, 16, 18
Assistant Professor of Neurosurgery
and Neurology Carlee Clark, MD
The University of Texas Medical Associate Professor
School at Houston Department of Anesthesia and
Memorial Hermann-Texas Medical Perioperative Medicine
Center Medical University of South Carolina
The Mischer Neuroscience Institute Charleston, South Carolina
Houston, Texas Chapter 32
Chapter 11
E. Sander Connolly, Jr., MD, FACS
Bennett M Stein Professor of
Wan-Tsu W. Chang, MD
Neurological Surgery
Assistant Professor of Emergency
Vice Chairman of Neurosurgery
Medicine
Director, Cerebrovascular Research
University of Maryland School of
Laboratory
Medicine
Surgical Director, Neuro-Intensive
Baltimore, Maryland
Care Unit
Chapter 4
Columbia University Medical Center
New York, New York
Chapters 22, 24, 25, 26

Contributors xv
Caroline Cromwell, MD Amy L. Dzierba, PharmD, BCPS,

Assistant Professor of Medicine BCCCP, FCCM
Division of Hematology and Medical Clinical Pharmacist, Medical Intensive
Oncology Care Unit
Department of Medicine Department of Pharmacy
The Mount Sinai School of Medicine NewYork-Presbyterian/Columbia
New York, New York Medical Center
Chapters 51, 52 New York, New York
Chapter 20
Neha Dangayach, MD
Assistant Professor of Neurology and Nancy J. Edwards, MD
Neurosurgery Neurocritical Care
Mount Sinai Medical Center and Assistant Professor of Neurosurgery
Icahn School of Medicine at and Neurology
Mount Sinai The University of Texas Medical
New York, New York School at Houston
Chapter 39 Memorial Hermann-Texas Medical
Center
Ivan Rocha Ferreira da Silva, MD The Mischer Neuroscience Institute
Cerebrovascular Center Houston, Texas
Neurological Institute, Cleveland Chapters 13, 58
Clinic
Cleveland, Ohio Jason A. Ellis, MD
Chapter 6 Department of Neurological Surgery
Andrew Davenport, MD New York, New York
University College London Center Chapters 22, 24, 25
for Nephrology
Royal Free Hospital Vito Fanelli, MD, PhD
London, England Assistant Professor, Dipartimento di
Chapter 48 Anestesiologia e Rianimazione
Università di Torino
Daniel De Backer, MD Ospedale S. Giovanni Battista
Department of Intensive Care Torino, Italy
Centre Hospitalier Interrégional Edith Chapter 43
Cavelle (CHIEC) Hospitals
Université libre de Bruxelles Stephen A. Fletcher, DO
Brussels, Belgium Associate Professor, Division of
Chapter 53 Pediatric Neurosurgery
University of Texas Health Sciences
Center at Houston
Houston, Texas
Chapter 28

xvi Contributors
Jennifer Frontera, MD Emily J. Gilmore, MD

Associate Professor of Medicine Assistant Professor of Neurology
(Neurology) Staff Neurointensivist, Neuroscience
Cleveland Clinic Lerner College Intensive Care Unit
of Medicine Division of Neurocritical Care and
Staff, Cerebrovascular Center Emergency Neurology
Neurological Institute, Cleveland Yale University School of Medicine
Clinic New Haven, Connecticut
Staff, Department of Cellular and Chapter 15
Molecular Medicine
Cleveland, Ohio Radha Gopalan, MD
Chapter 6 Associate Professor, Medicine and
Cardiology
Brian M. Fuller, MD, MSCI The Mount Sinai Hospital
Assistant Professor, Emergency New York, New York
Medicine Chapter 38
Assistant Professor, Anesthesiology–
Critical Care Errol Gordon, MD
Washington University School of Assistant Professor of Neurosurgery
Medicine in St. Louis and Neurology
St. Louis, Missouri The Mount Sinai School of Medicine
Chapter 42 Division of Neuro-Critical Care
Mount Sinai Hospital
Photi Galanis, MD New York, New York
Thomas Jefferson University Chapter 18
Department of Medicine
Philadelphia, Pennsylvania Simon Hanft, MD
Chapter 44 Assistant Professor of Neurosurgery
Rutgers Robert Wood Johnson
Umesh K. Gidwani, MD, MS, FCCP, Medical School
FCCM, FACC New Brunswick, New Jersey
Associate Professor, Cardiology, Chapter 9
Pulmonary, Critical Care and
Sleep Medicine Joseph Haymore, CRNP
Chief, Cardiac Critical Care Nurse Practitioner
Zena and Michael A. Wiener Washington Adventist Hospital
Cardiovascular Institute Takoma Park, Maryand
Director, Cardiac ICU Senior Nurse Practitioner
Institute of Critical Care Medicine University of Maryland Medical
Mount Sinai Hospital Center
New York, New York Baltimore, Maryland
Chapters 35, 36, 38, 39 Chapter 21

Contributors xvii
Raimund Helbok, MD Dong Wook Kim, MD

Department of Neurology, Assistant Professor of Medicine
Neurocritical Care Unit Boston University School of Medicine
Medical University of Innsbruck Boston Medical Center
Innsbruck, Austria Boston , Massachusetts
Chapter 16 Chapter 57
Sang-Beom Jeon, MD, PhD Ryan Kitagawa, MD

Associate Professor of Neurology Assistant Professor, Department of
Ulsan University College of Medicine Neurosurgery
Asan Medical Center The University of Texas Health
Seoul, Korea Sciences Center at Houston
Chapter 12 McGovern Medical School
Houston, Texas
Stephen L. Katzen, MD Chapter 27
Associate Professor, Division of
Pediatric Neurosurgery Sang-Bae Ko, MD, PhD
University of Texas Health Sciences Assistant Professor of Neurology
Center at Houston Seoul National University Hospital
Houston, Texas Seoul, Korea
Christopher P. Kellner, MD Wolf Benjamin Kratzert, MD

Assistant Professor of Neurosurgery Department of Anesthesiology
Department of Neurosurgery Ronald Reagan UCLA Medical Center
Icahn School of Medicine at Santa Monica, California
Mount Sinai Chapter 34
New York, New York
Chapter 26 Avinash B. Kumar, MD, FCCM, FCCP
Director, Neurosciences Intensive
Daniel H. Kim, MD, FACS, FAANS Care Unit
Professor of the Vivian L. Smith Associate Professor, Anesthesiology
Department of Neurosurgery and Critical Care
Director of Reconstructive Spinal and Associate Professor, Neurology
Peripheral Nerve Surgery Vanderbilt University
Nancy, Clive and Pierce Runnells Nashville, Tennessee
Distinguished Chair in Neuroscience Chapter 41
University of Texas McGovern Medical
School
Houston, Texas
Chapter 27

xviii Contributors
Pedro Kurtz, MD, PhD Francis J. Macchio, MD

Department of Intensive Care Medicine Assistant Professor
Hospital Copa Star Department of Anesthesiology
Rio de Janeiro, Brasil Hofstra-Northwell School of
Department of Intensive Care Medicine Medicine
Paulo Niemeyer State Brain Institute Hempstead, New York
Rio de Janeiro, Brasil Chapter 33
Chapters 16, 17
Rishi Malhotra, MD
Kiwon Lee, MD, FACP, FAHA, FCCM Assistant Professor of The Saul R.
Vice Chairman, Department of Korey Department of Neurology
Neurosurgery for Critical Care Medicine (Critical Care) and
Associate Professor, Neurosurgery and Neurological Surgery
Neurology Albert Einstein College of Medicine
Chief, Division of Critical Care Montefiore Medical Center
Director, Neuroscience and Bronx, New York
Neurotrauma ICU Chapter 11
Director, Neuroscience Intermediate
ICU Nathan Manning, MBBS, FRANZCR
Director, Neuroscience Program West Florey Institute of Neuroscience
Medical System Melbourne, Australia
The University of Texas Medical Chapter 23
School at Houston
Mischer Neuroscience Institute Luciana Mascia, MD, PhD
Memorial Hermann-Texas Medical Associate Professor, Dipartimento di
Center Anestesiologia e Rianimazione
Houston, Texas Università di Torino
Chapters 1, 7, 10, 11, 12, 13, 14, 17, 58, Ospedale S. Giovanni Battista
59 Torino, Italy
Chapter 43
Guillermo Linares, MD
Assistant Professor, Neurology, Stephan A. Mayer, MD, FCCM
Neurosurgery, Radiology Director, Neurological Intensive
Director, Neuro-Interventional Services Care Unit
Temple University Medical Center Columbia University Medical Center
Philadelphia, Pennsylvania Professor of Neurology and Neurosurgery
Chapter 59 Columbia University College of
Physicians and Surgeons
New York, New York
Chapters 2, 14

Contributors xix
Anna Teresa Mazzeo, MD Philip M. Meyers, MD, FACR, FSIR,

Associate Professor, Dipartimento di FAHA
Anestesiologia e Rianimazione Professor of Radiology and
Università di Torino Neurological Surgery
Ospedale S. Giovanni Battista Director, Neuroendovascular Services
Torino, Italy Columbia University College of
Chapter 43 Physicians and Surgeons
New York-Presbyterian/Columbia
Christopher B. McFadden, MD University Medical Center
Associate Professor of Medicine New York, New York
Cooper Medical School of Rowan Chapter 23
University
Division of Nephrology Samia Mian, MD
Cooper University Health Care Assistant Professor of Medicine
Camden, New Jersey Cooper Medical School of Rowan
Chapter 50 University
Division of Nephrology
Joseph S. Meltzer, MD Cooper University Health Care
Clinical Associate Professor Camden, New Jersey
Department of Anesthesiology Chapter 50
Director, Cardiothoracic Intensive
Care Unit Steven Miller, MD
David Geffen Medical School Assistant Professor at CUMC
Ronald Reagan UCLA Medical Department of Anesthesiology
Center Columbia University Medical Center
Los Angeles, California NewYork-Presbyterian Hospital
Chapter 31 New York, New York
Chapter 29
Geno Merli, MD, MACP, FHM,
FSVM Vivek K. Moitra, MD
Professor of Medicine and Surgery Allen I. Hyman Associate Professor
Co-Director, Jefferson Vascular of Critical Care Anesthesiology at
Center CUMC
Sidney Kimmel Medical College Chief, Division of Critical Care Medicine
Thomas Jefferson University Medical Director, CTICU and SICU
Hospitals Program Director, Critical Care
Philadelphia, Pennsylvania Medicine Fellowship
Chapter 44 Department of Anesthesiology,
PH 527-B
College of Physicians & Surgeons of
Columbia University
New York, New York
Chapters 20, 29

xx Contributors
Glenn Oettinger, PharmD, BCPS Mubashir Pervez, MD

Emergency Medicine Pharmacy Fellow physician, Division of
Specialist Neurocritical Care
Clinical Assistant Professor The University of Texas Medical
Thomas Jefferson University School at Houston
Philadelphia, Pennsylvania Mischer Neuroscience Institute
Chapter 54 Memorial Hermann-Texas Medical
Center
Geoffrey O. Ouma, DO, MS Houston, Texas
Assistant Professor of Medicine and Chapter 10
Surgery
Sidney Kimmel Medical College at Sean Pinney, MD
Thomas Jefferson University Hospital Associate Professor, Medicine and
Philadelphia, Pennsylvania Cardiology
Chapter 44 Director, Pulmonary Hypertension
Program
David Oxman, MD The Mount Sinai Hospital
Thomas Jefferson University Hospital New York, New York
Philadelphia, Pennsylvania Chapter 37
Chapter 56
Jean-Sebastien Rachoin, MD
Oliver Panzer, MD Assistant Professor of Medicine
Assistant Professor of Anesthesiology Cooper Medical School of Rowan
Columbia University College of University
Physicians and Surgeons Associate Division Head, Hospital
New York-Presbyterian/Columbia Medicine
University Medical Center Critical Care Medicine
New York, New York Cooper University Hospital
Chapter 34 Camden, New Jersey
Chapter 47
Soojin Park, MD, FAHA
Assistant Professor of Neurology Jeremy T. Ragland, MD
Columbia University College of Assistant Professor of Neurosurgery
Physicians and Surgeons and Neurology
Assistant Attending Physician at Division of Neurocritical Care
New York-Presbyterian/Columbia The University of Texas Health Science
University Medical Center Center at Houston
New York, New York Memorial Hermann-Texas Medical
Chapter 19 Center
The Mischer Neuroscience Institute
Houston, Texas
Chapter 59

Contributors xxi
Vivek Reddy, MD David I. Sandberg, MD, FAANS,

Director, Cardiac Arrhythmia Services FACS, FAAP
The Mount Sinai Hospital Professor and Chief, Division of
New York, New York Pediatric Neurosurgery
Chapter 36 University of Texas Health Sciences
Center at Houston
Fred Rincon, MD, MSc, FACP, FCCP, Houston, Texas
FCCM Chapter 28
Assistant Professor of Neurology and
Neurological Surgery Michael J. Schmidt, PhD, MSc
Department of Neurological Surgery Assistant Professor of
Thomas Jefferson University Neuropsychology in Neurology
Jefferson Medical College Director of Neuro-ICU
Division of Neurotrauma and Neuromonitoring and Informatics
Critical Care Columbia University College of
Methodist Hospital Division of Thomas Physicians and Surgeons
Jefferson University Hospital New York, New York
Philadelphia, Pennsylvania Chapter 19
Chapters 2, 8
David B. Seder, MD, FCCP, FCCM,
David Roh, MD FNCS
Assistant Professor of Neurology Director, Neurocritical Care
Division of Neurocritical Care Department of Critical Care Services
Columbia University College of Maine Medical Center
Physicians and Surgeons Portland, Maine
New York-Presbyterian/Columbia Tufts University School of Medicine
University Medical Center Associate Professor of Medicine
New York, New York Boston, Massachusetts
Chapter 3 Chapters 41, 45, 46
John Rollo, MD David S. Seres, MD

Pathology Director of Medical Nutrition
St. Louis, Missouri Associate Professor of Medicine
Chapter 31 Institute of Human Nutrition
Sophie Samuel, PharmD, BCPS New York, New York
Critical Care Clinical Specialist, Chapter 57
Neurosciences
Memorial Hermann-Texas
Medical Center
Department of Pharmacy Services
Houston, Texas
Chapter 7

xxii Contributors
Manish N. Shah, MD Michael B. Sisti, MD, FACS

Assistant Professor, Pediatric James G. McMurtry Associate Professor
Neurosurgery of Clinical Neurosurgery, Radiation
University of Texas Health Sciences Oncology & Otolaryngology
Center at Houston Co-Director, The Center for
Houston, Texas Radiosurgery
Chapter 28 Department of Neurosurgery
Columbia University College of
Samit K. Shah, MD Physicians and Surgeons
Fellow, Advanced Heart Failure and Columbia University Medical Center
Transplant New York, New York
Yale New Haven Hospital Chapter 9
New Haven, Connecticut
Chapter 38 Robert N. Sladen, MBChB, MRCP,
FRCP
Syed Omar Shah, MD, MBA Professor and Executive Vice-Chair
Assistant Professor of Neurology and of Anesthesiology
Neurological Surgery Chief, Division of Critical Care
Department of Neurological Surgery Department of Anesthesiology
Thomas Jefferson University Columbia University College of
Division of Critical Care and Physicians and Surgeons
Neurotrauma New York-Presbyterian/Columbia
Jefferson Hospital for Neurosciences University Medical Center
Philadelphia, Pennsylvania New York, New York
Raman Sharma, MD Fabio Silvio Taccone, MD

Fellow, Division of Cardiology Department of Intensive Care
Zena and Michael A. Wiener Erasme University Hospital
Cardiovascular Institute and Université Libre de Bruxelles
Institute of Critical Care Medicine Brussels, Belgium
Mount Sinai Medical Center and Icahn Chapter 53
School of Medicine at Mount Sinai
New York, New York Miranda Tan, MD
Chapter 39 Internal Medicine
Thomas Jefferson University Hospital
Anurag Singh, MD Philadelphia, Pennsylvania
Professor of Oncology Chapter 56
Director of Radiation Research
Roswell Park Cancer Institute Blake E.S. Taylor, MD
Buffalo, New York Resident, Neurological Surgery
Chapter 36 Rutgers New Jersey Medical School
Newark, New Jersey
Chapters 23, 26

Contributors xxiii
Lynda Thomson, PharmD, CACP Joshua Z. Willey, MD, MS

Advanced Practice Pharmacist Assistant Professor of Neurology
Jefferson Vascular Center Columbia University College of
Thomas Jefferson University Hospital Physicians and Surgeons
Philadelphia, Pennsylvania Department of Neurology, Division
Chapter 44 of Stroke
New York Presbyterian Hospital/
Ruwanthi Titano, MD Columbia University Medical
The Mount Sinai Hospital Center
New York, New York New York, New York
Jacqueline S. Urtecho, MD Brian Woods, MD

Temple University Hospital Assistant Professor of Anesthesiology
Philadelphia, Pennsylvania Department of Anesthesiology
Chapter 55 Columbia University College of
Physicians and Surgeons
Thilagavathi Venkatachalam, MD New York-Presbyterian/Columbia
Assistant Professor of Medicine University Medical Center
Cooper Medical School of Rowan New York, New York
University Chapter 30
Division of Hospital Medicine
Cooper University Health Care Luyi Kathy Zhang, MD
Camden, New Jersey Internal Medicine Specialist
Chapter 50 North Shore University Hospital
Manhassett, New York
Lawrence S. Weisberg, MD Chapter 54
Professor of Medicine
UMDNJ-Robert Wood Johnson
Medical School
Head, Division of Nephrology
Deputy Chief, Department of
Medicine
Cooper University Hospital
Camden, New Jersey
Chapters 47, 49


Foreword
Three converging realities provide the raisons d’etre for this new edition of The
NeuroICU Book. First, management of neurological and neurosurgical patients
is becoming increasingly complex and fluid as diagnostic and therapeutic
options increase. There are few “standards of care” that have not substantially
changed over the past few years. Second, as our population increases, engages
in risky behavior, and ages, the burden of trauma and neurological disease
threatens to overwhelm our hospitals. The number of physicians and other
staff who need training to care for these patients is truly exploding. Finally,
evidence-based protocol-driven care improves quality metrics, value and
patient centered outcomes. Every hospital and healthcare system now accepts
and is adapting to this new reality of medical practice. Nowhere are these
themes more evident than in the NeuroICU, hence the need for a comprehen-
sive, authoritative, and easily negotiated reference for medical staff managing
patients in this environment.
This second edition of The NeuroICU Book builds on the huge success of the
first edition published in 2012. The interactive, case-driven format of the first
edition is retained, with practical recommendations that consider the myriad
possible responses of patients to our interventions. Little is predictable in the
NeuroICU, and this book prepares the reader for the unexpected. The second
edition follows the general organization of the first, with expanded coverage of
encephalopathy, spine trauma, pediatric neurosurgery, and newer cardiovascular
interventions such as extracorporeal membrane oxygenation.
Dr Lee has assembled an all-star lineup of authors; they are interdisciplinary
leaders in their fields. Rarely will one find a more comprehensive and authoritative
compilation within the front and back covers of any textbook. The chapters are
all edited for consistent style, so that each topic is not only covered with the same
degree of expertise and depth, but once familiar with the approach, the reader can
easily find within each chapter the coverage they are seeking.
Finally, while this text will be most useful to those who work full-time in the
NeuroICU, it is a welcome addition to the bookshelf of any clinician taking care
of hospitalized neurological and neurosurgical patients. The new reality of neuro-
logical care is that a large percentage of hospitalized patients will spend some time
in the NeuroICU, or require ICU-level care while in the ED, endovascular suite,
or other non-ICU setting. Hence patients are frequently co-managed by clinicians
who will care for the patient before they transition into, or after they move out of,
xxv

xxvi Foreword
the NeuroICU. As a vascular neurologist, I frequently dive into the “non-stroke”

chapters to help me understand what Dr Lee and his staff are doing or would be
doing with my patients!
James C. Grotta, MD
June 26, 2016

Preface
A lot has happened since the first edition of this book and my departure from New
York City to arrive in Houston, Texas. The field of neurology continued to evolve,
especially in the area of therapeutics. Multiple class I-type of evidence emerged
from intraarterial thrombectomy studies showing its undeniable, outcome-
improving intervention, when combined with intravenous rt-PA compared to
intravenous thrombolysis alone in 2015. This ground-breaking study result, along
with other therapeutic advances in other neurological subspecialties, further
transformed the field of neurology from merely admiring phenomenology to
more time-sensitive interventional field. The field of neurocritical care is at the
forefront of therapeutic efforts, as our daily practice focuses on resuscitating and
reversing multiple organ failures.
The idea of neurologic critical care is to provide acute medical therapies and
appropriate interventions promptly by constantly monitoring the patients in one
area by specially trained physicians and nurses. Injured brains do not wait for
consults to show up and have a low threshold for irreversible damages. “Time
is brain” in many situations, and it is of paramount importance that neurocriti-
cal care team must physically staff the unit 24/7 and act quickly in the event of
neuro-emergencies. Patients with acute, severe brain injuries are often accompa-
nied by other organ failures at the time of initial presentation or during the ICU
stay. Therefore, neurointensivists must be trained to handle not only the brain,
but also rest of the body. This textbook is written for that very reason. Readers
will once again find this textbook being not just about the brain and spine. It is
about all organ insufficiencies and failures along with neurologic illnesses. After
the success and popularity of the first edition, the second edition again emphasizes
and focuses on one principle: practicality. This book is easy to read and full of real
cases that one may encounter in a neurocritical care unit. The flow of content is
in the form of dialogue. You will feel like you are making rounds with me. By
discussing and focusing on multiple challenging problems, and by paying attention
to all organs rather just the brain, it is my hope that you would find this textbook
extremely helpful for both daily practices as well as for board examinations.

Houston, Texas
xxvii


Acknowledgments
This second edition is a proud product of many leading academic physicians and
surgeons at numerous medical institutions including Columbia University College
of Physicians and Surgeons, University of Texas Health Science Center at Houston,
UMDNJ Robert Wood Johnson Medical School, Cooper Medical School of Rowan
University, Mount Sinai School of Medicine, Thomas Jefferson University Jefferson
Medical College, University of California at Los Angeles David Geffen School
of Medicine, and Washington University School of Medicine. I would like to
thank Andrew Moyer, an executive editor, and Christie Naglieri, a senior project
development editor at McGraw-Hill both of whom have been tremendously
supportive throughout the entire process. I would like to sincerely thank all my
section editors: Neeraj Badjatia, MD, MSc, FCCM, Jan Claassen, MD, PhD, FNCS,
E. Sander Connolly, Jr., MD, FACS, Arthur L. Day, MD, Joseph Meltzer, MD,
Umesh K. Gidwani, MD, MS, FCCP, FCCM, FACC, David B. Seder, MD, FCCP,
FCCM, FNCS, Lawrence S. Weisberg, MD, Louis M. Aledort, MD, MACP,
Fred Rincon, MD, MSc, FACP, FCCP, FCCM, and Guillermo Linares, MD.
From the beginning, my friend and colleague Fred Rincon, MD has been
extremely helpful in recruiting authors and once again contributed significantly
for this second edition, hence my personal thanks to him. Special thanks to my
new section editors Arthur Day, MD and Umesh K. Gidwani, MD, MS, FCCP,
FCCM, FACC, both have been very supportive for my project as well. Last but not
least, I would like to thank James C. Grotta, MD, who always inspires me, for kindly
providing the Foreword.
xxix


SECTION 1
Neurocritical Care
Diseases
Section Editor: Neeraj Badjatia, MD, MSc, FCCM
CHAPTER Subarachnoid Hemorrhage

1 Kiwon Lee, MD, FACP, FAHA, FCCM
A 49-year-old man with history of hypertension and hyperlipidemia presents with

a sudden onset of severe bifrontal headache followed by nausea. The headache,
the worst headache he had ever experienced, came on suddenly. The patient
vomited on his way to the nearby emergency department (ED) and became
obtunded in the ambulance. On arrival to the ED, he was intubated for airway protection as his
mental status continued to worsen. About 30 minutes after the onset of the initial symptoms, he
progressed to stuporous mental status. He was able to flex his elbows bilaterally to painful stimu-
lation. Brainstem reflexes were all intact. Stat head computed tomography (CT) (Figure 1-1)
revealed acute subarachnoid hemorrhage (SAH) filling the basal cistern, bilateral sylvian fissures
with thick hemorrhages along with early radiographic evidence for hydrocephalus, and intraven-
tricular hemorrhage (IVH) mainly in the fourth ventricle. The local ED physicians decided to
transfer the patient immediately to the nearest tertiary medical center. During the emergent
transfer, patient stopped responding to any painful stimuli and had only intact brainstem reflexes.
On arrival at the neuroscience intensive care unit (NeuroICU), the following is the clinical
observation: Patient is intubated with endotracheal tube, is in coma, decerebrate posturing to
painful stimulation, has intact corneal reflexes, pupils 5 mm in diameter briskly constricting to
3 mm bilaterally to light, intact oculocephalic reflexes, and positive bilateral Babinski signs.
Vital signs on arrival to the NeuroICU: heart rate, 110 bpm in sinus tachycardia; respira-
tion rate, 20 breaths per minute on the set rate of 14 breaths per minute on assist con-
trol–volume control mechanical ventilation; temperature, 99.3°F; and blood pressure (BP),
190/100 mm Hg by cuff pressure.
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2 SECTION 1 • Neurocritical Care Diseases
Figure 1-1. Axial CT images of the brain without contrast.
Lee_Ch01_p0001-0035.indd 2 5/15/17 7:30 PM

Diseases
Neurocritical Care
CHAPTER 1 • Subarachnoid Hemorrhage 3
What are the initial steps for resuscitating acute aneurysmal SAH in
this case?
ABC and EVD. You must optimize cerebral perfusion pressure (CPP) for all poor-grade SAH
The clinical and radiographic presentation of this case is consistent with poor grade (initially
Hunt and Hess [HH] grade IV, which quickly progressed to grade V while in transit to the tertiary care
center) acute aneurysmal SAH. Airway, breathing, and circulation (ABC) have all been addressed,
although the BP is high at this time. The very first step in managing this patient is ventricular drain,
the second step is ventricular drain, and the third step is ensuring that the ventricular drain you have
just placed is working (ie, draining bloody cerebrospinal fluid [CSF] adequately when the drain is
open, and maintaining good waveforms when the drain is clamped). After ABC, placing external
ventricular drain (EVD) is the most crucial, lifesaving, important early step for managing patients
with high-grade acute SAH with poor mental status and IVH. The presence of IVH complicates the
natural course of both intracerebral hemorrhage (ICH) as well as SAH cases. IVH is often associated
with development of an acute obstructive hydrocephalus, which may lead to vertical eye movement
impairment and depressed level of arousal by its mass effect on the thalamus and midbrain. IVH is
also associated with elevated intracranial pressure (ICP), which lowers the CPP (by the principle of
the equation, CPP = MAP – ICP) if the mean arterial pressure (MAP) remains constant. Moreover,
IVH has been reported to be an independent risk factor for increased risk of developing symptomatic
vasospasm. The mass effect and cerebral edema may rapidly progress to herniation syndrome and
death. As such, the presence of IVH has been recognized as a significant risk factor for poor outcome
for both ICH and SAH.1-3 Placing an EVD provides two benefits: (1) reliable (as long as the catheter
tip is in the right location to provide appropriate ICP waveforms without obstructing the ventricular
catheter by any blood clot) measurements of the ICP and (2) therapeutic drainage of the CSF in order
to alleviate the intracranial hypertension (Figure 1-2). Placement of an EVD may not be necessary in
a low-grade ([HH] grade 1-2) SAH patient if IVH is not severe and hydrocephalus is not present. In a
high-grade patient, however, even if hydrocephalus is not seen in the first CT scan, if the patient has
bled significantly (ie, a thick basal cistern SAH clot with classic Fisher group 3 and a modified Fisher
grade 3 or 4; more on this below), placement of an EVD is often required.
P1
P2 P
3
P2
P1 P3
B
Figure 1-2. ICP waveforms and compliance. A. ICP waveform with normal compliance. B. ICP waveform with
poor compliance.
Lee_Ch01_p0001-0035.indd 3 5/15/17 7:30 PM

It is important to note that the presence of IVH does not necessarily mean the ICP is abnormally
elevated, and the placement of an EVD alone may not always lead to an improved outcome even if
the high ICP responds favorably to opening and lowering of the drain.4 In the past, there were con-
cerns regarding the potential harmful effect of EVD placement in treating the acute hydrocephalus
in SAH patients. These concerns were mainly focused on the theoretical impact of suddenly lower-
ing the ICP by EVD placement and eliminating the tamponade effect on a ruptured aneurysmal wall,
leading to an increased risk of rebleeding in the acute phase. However, clinical studies have failed
to prove such a hypothesis, and there is not sufficient evidence to believe that the CSF diversion
by an EVD in treating acute hydrocephalus after SAH results in a higher incidence of rerupturing
of the unsecured aneurysms.5,6 It is wise, however, to avoid aggressively lowering the drain level
immediately after placement. For example, leaving the EVD open at about 15 cm above the level of
the external auditory meatus is reasonable before securing the aneurysm. In managing SAH cases,
whether or not to place an EVD is occasionally debatable. For instance, a patient with low-grade
(eg, HH I or II) SAH who is awake, follows commands with normal strength, and has no IVH, no
acute hydrocephalus, and either absent or minimal volume of SAH (eg, classic Fisher groups 1 to 2)
is not a candidate for EVD placement. On the other hand, a patient with a high HH grade and Fisher
group 3 SAH, plus the radiographic evidence of severe IVH and acute hydrocephalus, who exhibits a
progressively worsening level of arousal needs emergent placement of an EVD (classic indication for
ABC and EVD). These are extreme ends of the clinical spectrum of SAH, and the timing and indica-
tion for EVD could be debated for the cases that are somewhere between these two extreme case sce-
narios. Acute hydrocephalus with IVH and clinical signs and symptoms of intracranial hypertension
are all good indications for placing EVDs. It is also important to remember that even if the patient
does not have any of the indications mentioned above, if the treating physician believes that there is
a reasonable probability of developing these signs and symptoms in the near future, EVD placement
should be considered. (Technical details and further management strategies are discussed in Chapter
22.) Despite the lack of “level 1” evidence of randomized data for improved outcomes, the use of
an EVD is important because it can be helpful in managing ICP and CPP and often is lifesaving in
certain SAH patients.
This patient’s level of arousal improves a few minutes after placing

the EVD (opening pressure was 35 mm Hg). He is now able to localize
to painful stimulations. Does the prognosis change with improved
neurological examination after EVD placement?
Changing Neurologic Status After EVD Placement
Placement of an EVD frequently results in a significant improvement in neurologic status. Comatose
patients may start to localize to painful stimulation and may even open their eyes. Although this is not
always seen, when it happens, it may possibly indicate a favorable outlook (eg, a patient who presents
with HH grade V after aneurysmal SAH wakes up after EVD placement and begins to follow verbal
commands: if this patient remains awake and continues to follow commands throughout the course
of his or her illness, then the patient is behaving at a low-grade HH [ie, grades I to III], not like a grade V
patient who presents with and remains in coma).
Patients with HH grade V have extremely poor prognosis. Many physicians and surgeons disclose
such a poor prognosis to the patient’s family, and this disclosure often leads to withdrawal of life-
sustaining care prior to any treatment. Although the decision to treat or not to treat should be made
based on the prognosis and in the best interest of the patient, the initial prognosis is mostly based on
the bedside neurologic assessment. Physicians should be aware that the patient’s clinical status may
dramatically change after placement of an EVD, which has significant implications for the prognosis.7
When a patient with high-grade SAH is stuporous or comatose, it is difficult to determine whether
Lee_Ch01_p0001-0035.indd 4 5/15/17 7:30 PM

Diseases
Neurocritical Care
such exam is due to hydrocephalus and IVH or to the initial injury, which is independent of the
hydrocephalus and/or IVH. Thus, it would be prudent to wait until the initial resuscitation (ABC and
EVD) is completed before making any predictions.
There are several SAH grading systems worth mentioning here. In 1967, Hunt and Hess reported
275 consecutive patients who were treated at the Ohio State University over a 12-year period. They
believed that the intensity of the meningeal inflammatory reaction, the severity of neurologic deficit,
and the presence or absence of significant systemic disease should be taken into account when clas-
sifying SAH patients. From their original manuscript, their grading system (which is now known and
widely used as the Hunt and Hess Grade) was a classification of patients with intracranial aneurysms
according to surgical risk (Table 1-1).8
Higher grades are associated with increased surgical risk for the repair of ruptured intracranial
aneurysms. The Hunt and Hess original report included the presence of significant systemic disease
(such as “hypertension, diabetes, severe arteriosclerosis, chronic pulmonary disease, and severe vaso-
spasm seen on angiography”) as a negative sign, and the presence of such disease resulted in placement
of the patient in the next less favorable (higher surgical risk) grading category.8 This grading system
is not flawless as it can be challenging sometimes to differentiate between categories. For example,
consider a patient with SAH with mild headache and nuchal rigidity compared with another patient
with moderate headache and nuchal rigidity (which means grades I and II, respectively, according
to the original HH grading system). The only differentiating variable here would be the intensity of
the headache, which can be problematic because the intensity of headache is subjective, and patients
often cannot differentiate mild from moderate headache (most people would describe a “very bad”
headache and cannot provide specific details).
This criticism had been actually predicted, and the original authors mentioned it in their jour-
nal article: “It is recognized that such classifications are arbitrary and that the margins between cat-
egories may be ill-defined.”8 For this reason, it has been pointed out that the HH system has poor
interobserver reliability and reproducibility.9 Nevertheless, the HH grading system is widely used, and
numerous studies have shown that the higher grade (or sometimes called poor grade, which usually
refers to HH grades IV and V) is associated with a poor outcome.10-13
Another grading system to consider is the one that is the most universally accepted system for
patients presenting with an altered level of consciousness: the Glasgow Coma Scale (GCS). In 1975,
Jennet and Bond, from the University of Glasgow, reported a scale called Assessment of Outcome
After Severe Brain Damage, a Practical Scale (Table 1-2).14
Table 1-1. Hunt and Hess Grade for SAHa

Criteria Category
Grade I Asymptomatic, or mild headache and slight nuchal rigidity
Grade II Moderate to severe headache, nuchal rigidity, no neurologic deficit other than cranial
nerve palsy
Grade III Drowsiness, confusion, or mild focal deficit
Grade IV Stupor, moderate to severe hemiparesis, possibly early decerebrate rigidity and
vegetative disturbances
Grade V Deep coma, decerebrate rigidity, moribund appearance

a
Classification of patients with intracranial aneurysms according to surgical risk.
(Reproduced with permission from Hunt W, Hess R. Surgical risk as related to time of intervention in the repair of intracranial
aneurysms. J Neurosurg. 1968;28:14-20.)
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Table 1-2. Glasgow Coma Scale

Category Score
Eye opening
Spontaneous 4
To loud voice 3
To pain 2
None 1
Verbal response
Oriented and converses 5
Confused, disoriented 4
Inappropriate words 3
Incomprehensive sounds 2
None 1
Best motor response

Obeys commands 6
Localizes to pain 5
Withdraws (flexion) 4
Abnormal flexion posturing 3
Extension posturing 2
None 1
(From Jennett B, Bond M. Assessment of outcome after severe brain damage. Lancet. 1975;1:480-484.)
The GCS is a more general grading system and was not developed specifically for SAH patients.
However, studies show that for patients with aneurysmal SAH, the initial GCS score has positively
correlated with long-term outcome.15
In 1988, the World Federation of Neurosurgical Societies (WFNS) developed a grading system
that incorporated both the GCS and bedside neurologic assessment focusing on any focal deficit
(Table 1-3).16
The HH and WFNS grading systems are by far the two most commonly used systems for
grading patients with acute aneurysmal SAH. Despite the frequently raised criticisms regarding
the interobserver variability, the HH grade is used even more commonly than the WFNS scale
Table 1-3. World Federation of Neurosurgical Societies Scale for SAH

Grade Criteria
I GCS 15 without focal deficita
II GCS 13-14 without focal deficit
III GCS 13-14 with focal deficit
IV GCS 7-12 with or without focal deficit
V GCS 3-6 with or without focal deficit
Abbreviations: GCS, Glasgow Coma Scale; SAH, subarachnoid hemorrhage.

a
Focal deficit is defined as either aphasia and/or motor deficit.
(From Drake C. Report of World Federation of Neurological Surgeons Committee on a Universal

Subarachnoid Hemorrhage Grading Scale. J Neurosurg. 1988;68:985-986.)
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Neurocritical Care
Table 1-4. Fisher Scale of SAH

Group CT finding description
1 No detectable SAH
2 Diffuse SAH, no localized clot > 3 mm thick or vertical layers > 1 mm thick
3 Localized clot > 5 × 3 mm in subarachnoid space or > 1 mm in vertical thickness
4 Intraparenchymal or intraventricular hemorrhage with either absent or minimal SAH
Abbreviation: SAH, subarachnoid hemorrhage.
(From Fisher CM, Kistler JP, Davis JM. Relation of cerebral vasospasm to subarachnoid hemorrhage visualized by computerized
tomographic scanning. Neurosurgery. 1980;6:1-9.)
(71% of reported studies from 1985 to 1992 used the HH grade compared with 19% that used the
WFNS scale),17,18 and both grading systems have been shown to correlate reasonably well with the
long-term outcome.19
In 1980, Fisher and colleagues reported the relationship between the amount of SAH and the risk
of developing severe vasospasm (defined as delayed clinical symptoms and signs; Table 1-4).20
The Fisher group’s grading system is based on the description of CT findings, mainly focusing
on the actual volume of blood in the subarachnoid space. There is a linear relationship between the
amount of hemorrhage and the rate of developing symptomatic vasospasm.20 This grading system
has been extensively studied and there are numerous clinical studies validating its usefulness.21-25 In
multiple studies, the risk of developing symptomatic cerebral vasospasm appears to increase along
with the increasing amount of acute hemorrhage in the subarachnoid space. Although original report
by Fisher et al does describe the low risk of vasospasm, there is a clearly observed risk of vasospasm
even for patients with minimal blood in the subarachnoid space and for those with intraparenchymal
or intraventricular hemorrhage.20
It is important to understand that the Fisher scale actually did report some incidence of vaso-
spasm in groups 1, 2, and 4. Group 3 had the highest incidence of vasospasm, but other groups also
had vasospasms, just much lower in frequency.20 Like all other grading systems, the Fisher scale is not
without limitations. There have been concerns in the literature reporting a low correlation between
the Fisher grade and the incidence of symptomatic vasospasm (one recent study showed about 50%
correlation between the Fisher grade and vasospasm).26 Another criticism about the Fisher scale is
its inevitable interpersonal variability in assessing the estimated blood volume. Also, according to the
scale, all cases of CT of the head showing SAH with greater than 1 mm of vertical thickness is catego-
rized as grade III, but this includes vast majority of patients with SAH who may not in fact have the
same risk of developing vasospasm.26,27
In light of these concerns, Claassen et al’s group, from Columbia University, proposed another
grading system (Table 1-5): the modified Fisher scale (mFS).28,29
Note that the mFS incorporates the presence or absence of IVH, and if a patient has IVH, even if
there is no blood in the subarachnoid space, the scale is 2 (as opposed to 1 [no blood seen] or 4 [mini-
mal SAH and the presence of intraparenchymal hemorrhage or IVH] in the original Fisher scale).
This scale emphasizes that the presence of IVH increases the risk of developing symptomatic vaso-
spasm. This emphasis is stronger but not completely different from that of the Fisher scale, because
the original Fisher scale does report some incidence (although low) of vasospasm in those with IVH
and absent or minimal SAH. Furthermore, the mFS uses a subjective description and coding of the
hemorrhage by the use of “thick” or “thin” clots in the subarachnoid space, and the description of
IVH does not take the exact amount of IVH into account (this scale takes the “presence” versus the
“absence” of IVH into account, not how much IVH there is). The mFS emphasizes the importance
Lee_Ch01_p0001-0035.indd 7 5/15/17 7:30 PM

Table 1-5. The Modified Fisher Scale

CT finding description IVH Modified Fisher Scale
Diffuse thick SAH Present 4

Absent 3
Localized thick SAH Present 4

Absent 3
Diffuse thin SAH Present 2

Absent 1
Localized thin SAH Present 2

Absent 1
No SAH Present 2
Absent 0
Abbreviations: IVH, intraventricular hemorrhage; SAH, subarachnoid hemorrhage.
(From Claassen J, Bernardini GL, Kreiter KT, et al. Effect of cisternal and ventricular blood on risk of delayed
cerebral ischemia after subarachnoid hemorrhage: the Fisher Scale revisited. Stroke. 2001;32:2012-2020.)
of IVH, and it also highlights how the amount of hemorrhage once again plays an important role. Its
grading system is easy and intuitive (unlike the classic Fisher scale in which group 4 actually has a
lower incidence of vasospasm than lower grades), as the scale goes from 0 to 4, and the higher grade
has the higher risk of developing delayed cerebral ischemia (DCI).
In order to minimize the interobserver variability in assessing the estimated volume of blood in
the subarachnoid space, a volumetric quantification of Fisher grade 3 has been proposed and studied
by Friedman and colleagues from the Mayo Clinic.30 However, although quantification of SAH may
provide a more accurate assessment of the volume of blood in the subarachnoid space, it requires
manual outlining of the hemorrhage volume, which can be time consuming and less reliable.
In 2011, Ko and colleagues, from Columbia University, reported a study of volumetric analysis
of SAH using a MIPAV (Medical Image Processing, Analysis, and Visualization; version 4.3; National
Institutes of Health [NIH]) software package that automatically outlines the hemorrhage on CT at the
click of a button.31 This quantification analysis showed that patients with a higher volume of cisternal
plus IVH clot burden developed a greater risk of developing DCI and poor outcome at 3 months
(Figure 1-3).
It also validated the modified Fisher scale as a reasonable grading system in predicting DCI that
can be done easily at the bedside. However, it is important to note that although both the Fisher scale
and the mFS have demonstrated the association between blood burden and DCI, a question still
remains: Do the location and exact thresholds of blood volume matter? Ko and colleagues reported.31
Our data show that the quantitative blood volume in contact with the cisternal space, whether directly in
the cisternal subarachnoid space or intraventricular space, acts as cumulative blood burden and is associ-
ated with an increased risk of DCI. The quantitative volume scale and the mFS were equivalent in predict-
ing DCI, validating the accuracy of the mFS. However, volumetric analysis had no overlaps in the odds
ratio for DCI in different blood burden groups, which may suggest more robust association between the
total blood burden and DCI.
Klimo and Schmidt have eloquently summarized a historical review of the literature on the rela-
tionship between the CT findings and the rate of developing cerebral vasospasm after aneurysmal
SAH using different scales.32
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Diseases
Neurocritical Care
mRS 0 1 2 3 4 5 6
CIHV
mFS
< 9.6 ml 1.0
0.8
9.6-16.5 ml
Sensitivity
0.6
16.5-31.0 ml
0.4
≥ 31.0 ml 0.2
0.0
0.0% 20.0% 40.0% 60.0% 80.0% 100.0% 0.0 0.2 0.4 0.6 0.8 1.0
A B 1 - Specificity
Figure 1-3. The effect of blood volume on functional outcome at 3 months. A. Using cisternal blood plus intra-
ventricular hemorrhage volume (CIHV) criteria, patients with higher quartiles had higher risk of death or severe
disability at 3 months. B. CIHV was better at predicting 3-months outcome than modified Fisher Scale (B).
(Reproduced with permission from Ko SB, Choi HA, Carpenter AM, et al. Quantitative analysis of hemorrhagic
volume for predicting delayed cerebral ischemia after subarachnoid hemorrhage. Stroke. 2011 Mar;42(3):669-74.
https://doi.org/10.1161/STROKEAHA.110.600775.)
The elucidation of predictive factors of cerebral vasospasm following aneurysmal subarachnoid hemorrhage
is a major area of both clinical and basic science research. It is becoming clear that many factors contribute
to this phenomenon. The most consistent predictor of vasospasm has been the amount of SAH seen on the
postictal CT scan. Over the last 30 years, it has become clear that the greater the amount of blood within the
basal cisterns, the greater the risk of vasospasm. To evaluate this risk, various grading schemes have been
proposed, from simple to elaborate, the most widely known being the Fisher scale. Most recently, volumetric
quantification and clearance models have provided the most detailed analysis. IVH, although not supported
as strongly as cisternal SAH, has also been shown to be a risk factor for vasospasm.
Angiography shows an anterior communicating (A-comm) artery

aneurysm, and coiling was performed to secure the ruptured aneurysm.
The patient returns to the ICU but now has elevated ICP of 50 to 55 mm Hg
with MAP of 100 mm Hg.
What is the stepwise approach for treating high ICP for SAH patients?
The first battle in high-grade SAH: The battle against elevated ICP
The early phase of high-grade SAH is often complicated by the presence of ICP crisis. An ICP value out
of the normal range (0-20 mm Hg) is considered abnormal, but the ICP alone as an absolute value may
not always signify the need for an urgent treatment. A good example would be people with pseudotumor
cerebri and high ICP who perform normal daily activities. ICP also rises when patients cough or are
suctioned. Such an increase, if it is induced and transient, does not necessarily require any treatment. In
the setting of acute, high-grade SAH, however, abnormally elevated ICP is a major concern owing to its
direct, negative impact on the CPP. With persistently low or decreasing CPP, a certain degree of ischemic
insult is inevitable. A step-by-step algorithm for managing refractory ICP crisis is outlined below. This is
a recommendation that reflects the latest medical treatment available in the literature.
Lee_Ch01_p0001-0035.indd 9 5/15/17 7:30 PM

A Step-by-Step Algorithm for Intracranial Hypertension
ICP > 20 mm Hg for > 10 minutes (EVD is functional and draining bloody CSF, and the patient is not coughing, not being suctioned, or being
agitated)
Surgical Decompression
1. Consider placing the second EVD on the opposite side.

2. Decompressive craniectomy/craniotomy is the most effective way of reducing intracranial hypertension. If surgery is not an option,
proceed to the following medical steps.
Step 1: Sedation with Short-Acting Agents

(Patients should be on mechanical ventilation. The very first step in medically addressing an ICP crisis is sedation. LEAVE THE PATIENT ALONE. This
is not the right time to pinch the patient to get the best examination every 10 minutes.)
If hemodynamically stable (no hypotension and euvolemic state):
IV propofol: Repeat propofol, 20 mg IV q20s up to 1 to 2 mg/kg for initial bolus, maintenance 5 to 50 μg/kg/min (0.3-3 mg/kg/h).
*Dose of propofol greater than 50 μg/kg/min IV may be used, but be aware of the rare but potentially fatal propofol infusion syndrome.
Refractory ICP crisis and status epilepticus are two important neuro-emergencies that may require high-dose propofol, often as high as
100 to 150 μg/kg/min.
OR
If hemodynamically unstable (eg, hypotensive, poor cardiac output (CO), intravascular volume depletion):
IV midazolam: Load 0.01 to 0.05 mg/kg over 2 minutes, maintenance 0.02 to 0.2 μg/kg/h.
AND
Consider adding an analgesic agent:
IV fentanyl: IV bolus 25 to 100 μg, followed by maintenance 1 to 3 μg/kg/h.
*Adding an analgesic agent may synergistically lower the ICP more efficiently, but it takes longer for the patient to wake up. This is not
desirable during an active cerebral vasospasm as it is important to be able to follow patient’s clinical examination closely. Analgesia is an
important step in managing intracranial hypertension if pain is suspected as a component of agitation. Analgesia is especially helpful for
SAH in trauma cases, but it may be helpful even for aneurysmal SAH cases. Pain can lead to agitation and agitation worsens ICP. Rarely,
opioids have been associated (case reports) with a paradoxical rise in ICP as a result of an unclear mechanism.
Step 2: Hyperventilation and Order Osmotic Agents

1. Hyperventilation (unless patient is already autohyperventilating above the set rate of mechanical ventilation) induces cerebral
vasoconstriction and reduced cerebral blood flow (CBF), which leads to ICP reduction. Target end-tidal PCO2, 30 mm Hg.
*There are heated debates regarding whether or not to recommend hyperventilation as brain ischemia is a well-documented potential
risk of hyperventilation. In the setting of refractory ICP crisis and brain herniation, hyperventilation is a rapid and effective way of control-
ling high ICP temporarily and should be used only to buy time to initiate further therapies.
2. Mannitol: 1 to 1.5 g/kg 10%-25% solution, IV bag infused over 30 min, q6h. Osm < 360, Osm gap < 10. The Osm limit of “320”
is an arbitrary number.
*Avoid if intravascular volume depletion is present. Avoid underdosing and avoid blind dosing (eg, mannitol IV 25 g q6h round the clock,
for all patients regardless of the body weight without assessing the intravascular volume or ICP). If the patients are showing signs and
symptoms of ICP crisis and/or brain herniation, underdosing is not a good idea.
3. Hypertonic saline (HTS): 30 mL of 23.4% IV push over 5 minutes, q4 to 6h PRN. Avoid serum Na > 155 mEq/L.
*Continuous infusion of 3% HTS all day, every day at high volume (eg, 3% HTS at 150 mL/h continuously for 5 days) frequently
leads to severe pulmonary edema (remember, ICU patients are always receiving other medicine in high volume as well, which
Lee_Ch01_p0001-0035.indd 10 5/15/17 7:30 PM

Diseases
Neurocritical Care
leads to liters of positive input and not enough output), and such blind infusion may not be effective in controlling high ICP as the
intracellular–extracellular osmotic equilibrium occurs. It may be more effective to use the high concentration (23.4% bolus) on
a prn basis. A recent small (N = 34) randomized trial demonstrated hypertonic saline (20% sodium lactate) showing more effective
and longer lasting control of ICP directly compared with an equivalent osmotic dose of mannitol in severe traumatic injury patients.31
Step 3: Barbiturate Coma

entobarbital: Load 10 mg/kg IV infusion over 1 hour, maintenance 1 to 3 mg/kg/h, target 1 to 2 bursts per 10-second suppression
P
on continuous electroencephalogram.
Using pentobarbital is not easy. Pentobarbital is notorious for suppressing the heart function, leading to reduced CO and systemic
hypotension (be prepared to use pressor/inotropes shortly after starting it). Because of its long elimination t1/2 (15-50 h), the loss
of the ability to follow the clinical examination is another serious (especially for high-grade SAH patients) downside. However, pen-
tobarbital is effective in lowering ICP by its potent central nervous system suppression (which likely lowers the cerebral metabolic
demand).
*Avoid prolonged use of pentobarbital. The combination of prolonged use of high-dose pentobarbital and multiple pressors (eg, the
patient receiving both phenylephrine and norepinephrine in order to maintain a certain MAP) is a cocktail for multisystem failure. (Kidneys
will be injured first and then the liver, followed by severe acidosis and irreversible shock, along with dark, necrotic fingers and toes.) Yes,
we are focusing on saving the brain, but the brain also dies if everything else dies.
Step 4: Therapeutic Hypothermia

Target temperature = 32°C to 34°C using either surface cooling or an endovascular cooling device
(IV infusion of cold saline is a cost-effective and efficient induction method)
• Surface devices are noninvasive with fewer complications.
• Endovascular devices are invasive but may achieve the target temperature more rapidly and are associated with less shivering in general.
• Use of an advanced temperature modulation system is recommended over conventional methods (cooling blanket or ice packs) because
temperature must be controlled during cooling and slow, passive rewarming in order to avoid rebound intracranial hypertension.
• A prolonged (> 7 days: the actual days for different devices’ safety may vary) use of endovascular cooling devices increases the risk of
developing thrombotic complication and catheter-related bloodstream infection.
• Hypothermia may be effective in reducing ICP in otherwise refractory intracranial hypertension.
• Shivering needs to be aggressively treated for three reasons:
A. Shivering prevents the core body temperature from falling and leads to prolonged time to achieve the target temperature.
B. Shivering can increase ICP and further worsen the intracranial hypertension.
C. Shivering can increase the brain metabolism and increase the risk of developing brain hypoxia and cellular metabolic distress
(a decrease in the partial pressure of oxygen in brain tissue [Pbto2] tension and an increase in the brain lactate/pyruvate ratio [LPR]).
• Antishivering methods33-38
A. Skin counterwarming: warm, forced-air blankets and mattress
B. IV magnesium (IV bolus 60-80 mg/kg, then maintenance 2 g/h) may reduce the shivering threshold but is not effective as a single
agent to treat the shivering during full hypothermia (ie, 32-34°C).
C. Buspirone, 20 to 30 mg tid, via nasogastric tube after crushing
D. IV dexmedetomidine, 0.4 to 1.5 μg/kg/h
E. IV meperidine, 0.4 mg/kg (usual dose 25-50 mg) IV q4-6h
F. IV propofol, 50 to 100 mg rapid IV push, maintenance 0.3 to 3 mg/kg/h
G. IV clonidine, 1 to 3 μg/kg prn
Targeted temperature management is one of the hot topics in the recent literature. The idea is not that hypothermia necessarily improves
outcome in brain-injured patients, but it may reduce ICP and potentially reduce the length of ICU stay.
Lee_Ch01_p0001-0035.indd 11 5/15/17 7:30 PM

With all other factors that are known to influence the ICP being constant, increas-
ing the MAP leads to increased CPP. Increased CPP and blood flow may result in increased
cerebral blood volume. Increased cerebral blood volume could lead to any one of the following
scenarios:
1. Development of vasoconstriction would occur if autoregulation is intact in response to

increased blood volume delivered. Such vasoconstriction may result in a decrease in ICP.
2. No vasoconstriction would occur if autoregulation is impaired (pressure–volume breakdown).
Because blood volume is increased, there may be a further increase in the ICP.
3. A mixed picture of all of the above as different parts of the brain have either impaired or intact
autoregulation at a point prior to the pressure–volume breakdown.
Intracranial hypertension in SAH (ICP > 20 mm Hg)
Should you increase the MAP?
CPP Optimization
This is important, but simply increasing the BP with phenylephrine or norepinephrine may increase the volume of cerebral edema and may even
worsen the ICP crisis. CPP optimization does not imply simply raising MAP, as CPP can be optimized by either increasing the MAP or reducing
the ICP.
There may be a breakdown of the cerebral autoregulation
Impa
curve (see right: blue curve, intact; red curve, impaired autoregu- ired
lation), where every millimeter of mercury change in MAP leads
to change in CBF. Normally (the blue curve) the brain is able to
self-regulate its vessels so that the CBF remains constant regard-
less of change in MAP. This capability may be impaired in severe
brain injuries. Intact
For example, if a patient with SAH has an ICP, 40 mm Hg;
CBF
a MAP, 90 mm Hg; a CPP, 50 mm Hg, then the immediate next

step is not to start the phenylephrine in order to increase the MAP
to 100 to 120 mm Hg to make the CPP 60 to 80 mm Hg and walk
away. The right step is to focus on reducing the ICP without add-
ing vasopressors, so that the CPP is corrected by improving the
ICP, not by bringing up the BP without lowering the ICP. If the ICP
is controlled, then the CPP must be kept above a certain level (no
class I evidence exists in SAH, but ≥ 50-60 mm Hg). Of course, in
MAP
the event of systemic hypotension + high ICP + low CPP, the first
step is to improve MAP by using pressors. After reducing the MAP > 60 mm Hg, then the next step is to reduce the ICP (as opposed to
continuing to increase the MAP).
Let’s reduce the ICP!
1. Adequate sedation
2. Hyperventilation and osmotic therapy
3. Barbiturate coma
4. Therapeutic hypothermia
Lee_Ch01_p0001-0035.indd 12 5/15/17 7:30 PM

Diseases
Neurocritical Care
It is important to emphasize that increasing the BP with phenylephrine may either increase or
decrease the ICP. Clearly, if the MAP is too low to the point that the patient is in a state of shock, it makes
sense to increase the MAP in order to maintain adequate end-organ perfusion. However, if the MAP is
already 90 mm Hg, then increasing the MAP to 130 mm Hg with phenylephrine may have a deleterious
effect on the ICP. Finally, it is important to remember that every effort needs to be made to avoid the worst
combination that is associated with devastating results: systemic hypotension and uncontrolled ICP.
The Pbto2 tension monitoring system (Licox; Integra LifeSciences,

Plainsboro, NJ) is inserted in order to monitor the brain oxygenation. A
jugular venous oximetry probe is also inserted.
What is the relationship between the delivery of oxygen (Do2), the Pbto2,
and the jugular venous oxygen saturation (Sjvo2) (Figure 1-4)?
The CO, hemoglobin concentration [Hgb], and the arterial saturation of oxygen determine the deliv-
ery of oxygen from the heart to all the end-organ systems, including the brain. The Pbto2 is signifi-
cantly affected by the Do2 and the blood flow to the brain. Flow, by definition, is blood volume per
given time. Therefore, there is a positive correlation between the blood volume reaching the brain
tissue and Pbto2 measurements. Do2 has a linear relationship with the CO and Hgb levels as well as
arterial oxygen saturation (Sao2).
The oxygen content in the venous return from the brain back to the heart (measured by Sjvo2)
depends on the Do2 and oxygen consumption (Vo2). The product of the Do2 and OEF (oxygen extrac-
tion fraction) determines the total Vo2:
Vo2 = Do2 × OEF
Brain Venous return

[PbtO2] is affected by: [SjVO2] is affected by:
1. CBF, CPP 1. OEF driven by
2. O2 content of the brain cellular
blood flow metabolism
3. Brain cellular 2. DO2
metabolism
Heart
DO2 = Q × CO × Hgb × SaO2
Figure 1-4. Do2, Pbto2, Sjvo2 relationship. CBF, cerebral blood flow; CPP, cerebral perfusion pressure; OEF,
oxygen extraction fraction; Do2, delivery of oxygen; CO, cardiac output; Hgb, hemoglobin; Sao2, arterial oxygen
saturation; Q, a constant.
Lee_Ch01_p0001-0035.indd 13 5/15/17 7:30 PM

Therefore, the oxygen extraction fraction is determined by the total consumption divided by the
delivery of oxygen:
OEF = Vo2/Do2
Thus, the oxygen extraction decreases when the delivery increases while the consumption
remains the same. As the consumption of oxygen decreases, the extraction decreases as not as much
oxygen is needed to be extracted from the vasculature into the brain cellular tissues. Understanding
this relationship is crucial in applying this principle to the bedside information. If a patient has Pbto2,
Sjvo2, and CO monitoring, one would observe that by increasing the CO significantly, assuming the
brain cellular metabolism is constant (eg, under pentobarbital coma for ICP control), the OEF will
decrease, and as a result Sjvo2 increases:
↑ CO → ↑ brain Do2 → ↓ brain OEF→ ↑ Sjvo2

(if brain oxygen consumption remains the same)
↑ CO → ↑ brain Do2 → ↑ brain OEF→ ↓ Sjvo2

(if brain oxygen consumption increases more than Do2)
As one can see above, the brain cellular metabolism plays an important role in brain oxygen con-
sumption, and therefore extraction, and affects the Pbto2.
ICP is finally controlled within the range of 5 to 15 mm Hg. MAP,

100 mm Hg, CPP > 85 mm Hg. However, the Pbto2 is decreasing to
< 15 mm Hg, and the LPR is > 50. What could you do to improve the brain
oxygenation and reduce the brain metabolic stress?
There are ongoing debates regarding whether the partial pressure of oxygen tension measured in the
brain means anything in brain-injured patients (or what it means in the short or long term). Fre-
quently encountered criticisms are focused on the fact that the location of the probe may not be in the
perfect location for monitoring the injury. The probe provides direct information, but it only provides
the local information, and the number it gives may not be applicable to the rest of the brain. It is also
criticized that the absolute value of Pbto2 may not always correlate with the long-term outcome, mak-
ing it difficult to determine what the critical or “dangerous” value is. From the traumatic brain injury
(TBI) literature, there are studies that have shown a positive correlation between the Pbto2 level and
mortality39 and the outcome both in the pediatric as well as in the adult population.40 As long as the
probe is not located in the isolated, dead brain tissue (eg, in the middle of a completed infarct, which
will provide very low Pbto2 values, but that does not necessarily mean the rest of the brain is critically
ischemic), it is ununreasonable to believe that persistent, severe (Pbto2 < 15 mm Hg) brain hypoxia
is probably a bad sign.
As described above, significant brain hypoxia and neurochemical metabolic stress (LPR > 40) can
be treated with a number of different methods. The basic mechanism of how these methods improve
the Pbto2 and LPR is by increasing the Do2 and the flow to the brain. Another factor, brain cellular
metabolism, plays a role in determining the Pbto2 as it influences the consumption and extraction of
the delivered oxygen supply. Figure 1-5 illustrates how to address the factors that may contribute to
the brain hypoxia and metabolic stress. A number of factors should be considered for estimating the
brain cellular metabolism: fever, shivering, CO2 calorimetry for energy expenditure, pain/agitation,
sedation/paralysis, and other variables that may affect the basic oxygen consumption and demand.
Lee_Ch01_p0001-0035.indd 14 5/15/17 7:30 PM

Another random document with
no related content on Scribd:
—¡Qué vergüenza! —exclamó la señora sin disimular su enfado—
¿Conque para despachar un pasaporte se ha de gastar más tiempo
que para juzgar y condenar a muerte a un hombre?... ¡Qué tribunales
Santo Dios! ¡Qué Superintendencia y qué Comisión militar! Pongan
todo eso en manos de una mujer, y despachará en dos horas lo que
ustedes no saben hacer en una semana.
—Pero usted, señora —dijo Chaperón en el tono que empleaba
para parecer benévolo—, no tiene en cuenta las circunstancias...
—Veo que aquí las circunstancias lo hacen todo. Invocándolas a
cada paso, se cometen mil torpezas, infamias y atropellos. Si volviera
a nacer, Dios mío, querría que fuese en un país donde no hubiera
circunstancias.
—Si se tratara aquí del pasaporte de una señora —indicó e
Presidente de la Comisión con énfasis, como el que va a desarrolla
una tesis jurídica—, ande con Barrabás... Pero usted lleva dos criados
los cuales es preciso que antes se definan y purifiquen, porque uno de
ellos perteneció en tiempo de la Constitución a la clase de tropa, y e
otro sirvió largos años al ministro Calatrava... Pero nos ocuparemos
del asunto sin levantar mano...
—Yo deseo partir mañana —dijo la señora con displicencia—. Voy
muy lejos, señor Chaperón: voy a Inglaterra.
—Empezaremos, empezaremos ahora mismo. A ver, Lobo...
Al dirigirse a la mesa, Chaperón fijó la vista en la víctima cuyo
proceso verbal había sido suspendido por la entrada de la soberbia
dama.
—¡Ah!... Ya no me acordaba de ti —dijo entre dientes—. Voy a
despacharte.
Soledad miraba a la señora con espanto. Después de observarla
bien, cerciorándose de quién era, bajó los ojos y se quedó como una
muerta. Creeríase que batallaba angustiosamente con su desmayado
espíritu, tratando de infundirle fuerza, y que entre sollozos
imperceptibles le decía: «Levántate, alma mía, que aún falta lo más
espantoso».
—Con el permiso de usted, señora —dijo Chaperón mirando a la
dama—, voy a despachar antes a esta joven. Lobo, extienda usted la
orden de prisión... Llame usted para que la lleven... Orden al alcaide
para que la incomunique...
La víctima dejó caer su cabeza sobre el pecho.
Después miró de nuevo a la dama; pero esta vez encendiose su
rostro, y parecía que sus ojos relampagueaban con viva expresión de
amenaza. Esto duró poco. Fue la sombra del espíritu maligno al pasa
en veloz corrida por delante del ángel oscureciendo su luz.
La señora estaba también pálida y desasosegada. Indudablemente
no gustaba de ver a quien veía, y en presencia de aquella humilde
personilla condenada parecía tener miedo.
—Aquí tienes, mala cabeza —dijo Chaperón dirigiéndose a la
huérfana—, el resultado de tu terquedad. Demasiado bueno he sido
para ti... ¿Qué hemos sacado de tu declaración? Que Cordero es
inocente. ¿Y qué ganamos con eso, qué gana con eso la justicia? Tú y
nosotros adelantamos muy poco... Si hablaras sería distinto... Tú
habrás oído decir aquello de... quien te dio el pico, te hizo rico. ¿Te vas
enterando? Pero ahora, picarona, lo meditarás mejor en la cárcel... All
se aclaran mucho los sentidos..., verás. Esta linda pieza —añadió
señalando a la víctima y mirando a la señora—, es la estafeta de los
emigrados, ¿qué tal? Ella misma lo confiesa, lo cual no deja de tene
mérito; pero nos ha dejado a media miel, porque no quiere decir a
quién entregó las cartas que ha recibido hace unos días.
Soledad se levantó bruscamente.
—Una de las cartas de los emigrados —dijo con tono grave
extendiendo el brazo— la entregué a esta señora.
Después de señalarla con energía, cayó en su asiento con la
cabeza hacia atrás. Breve rato estuvieron mudos y estupefactos los
tres testigos de aquella escena.
—Es verdad —balbució la dama—. He recibido una carta de un
emigrado que está en Inglaterra; no sé quién la llevó a mi casa... ¿qué
mal hay en esto?
Chaperón, que estaba como aturdido, iba a contestar algo muy
importante, cuando la señora corrió hacia la huérfana, gritando:
—Se ha desmayado esta infeliz.
En efecto, rendida Sola a la fuerza superior de las emociones y de
cansancio, había perdido el conocimiento.
La señora sostuvo la cabeza de la víctima, mientras Lobo, cuya
oficiosidad filantrópica no se desmentía un solo momento, acudió
transportando un vaso de agua para rociarle el rostro.
—Eso no es nada —afirmó Chaperón—. Vamos, mujer, ¡qué mimos
gastamos! Todo porque la mandan a la cárcel...
La puerta se abrió dando paso a cuatro hombres de fúnebre
aspecto, que parecían pertenecer al respetable gremio de
enterradores.
—Ea, llevadla de una vez... —dijo don Francisco resueltamente—
El alcaide le dará algún cordial... No quiero desmayitos en m
despacho.
Los cuatro hombres se acercaron a la condenada.
—Un poco de vinagre en las sienes... —añadió el jefe de la
Comisión militar—. Ea, pronto..., quitadme eso de mi despacho.
—¡A la cárcel! —exclamó con lástima la señora, acercándose más a
la víctima como para defenderla.
—Señora, dispense usted —dijo Chaperón apartándola con enfática
severidad—. Deje usted a la justicia cumplir con su deber... Vamos
cargar pronto. No le hagáis daño.
Los cuatro hombres levantaron en sus brazos a la joven y se la
llevaron, siendo entonces perfecta la similitud de todos ellos con la
venerable clase de sepultureros.
La mampara, cerrándose sola con estrépito, produjo un sordo
estampido, como golpe de colosal bombo, que hizo retumbar la sala.
XVII
Aquel mismo día, ¡por vida de la chilindraina!, ¡cuán amargas horas

pasó el pobre don Patricio! Habrían bastado a encanecer su cabeza s
ya no estuviera blanca, y a encorvar su cuerpo si ya no lo estuviera
también. Sus suspiros eran capaces de conmover las paredes de la
casa; sus lágrimas corrían amargas y sin tregua por las
apergaminadas mejillas. No podía permanecer en reposo un solo
instante, ni distraerse con nada, ni comer, ni aposentar en su cerebro
pensamiento alguno, como no fuera el fúnebre pensamiento de su
desamparo y de la gran pena que le desgarraba el corazón. Este
lastimoso estado provenía de que Solita había salido temprano
diciéndole:
—No sé cuándo volveré. Quizás vuelva pronto, quizás mañana
quizás nunca... Escribiré al abuelo diciéndole lo que debe hacer
Adiós...
Y dirigiéndole una mirada cariñosa, se limpió las lágrimas, y bajó
rápidamente la escalera y desapareció, ¡santo Dios!, como un ánge
que se dirige al cielo por el camino del mundo.
«¿Será posible que haya salido hoy para Inglaterra? —se
preguntaba don Patricio, apretándose el cráneo con las manos para
que no se le escapara también—. ¡Pero cómo, si aquí está toda su
ropa, si no ha hecho equipaje, si en la cómoda ha dejado todo su
dinero!... ¿Pues a dónde ha ido entonces?... Quizás vuelva pronto
quizás mañana, quizás nunca... Nunca, nunca».
Y repetía esta desconsoladora palabra como un eco que de su
cerebro a sus labios saliera. Otro motivo de gran confusión para él era
que Soledad había despedido a la criada el día anterior. Estaba, pues
el viejo solo, enteramente solo, encerrado en la espantosa jaula de sus
tristes pensamientos, que era como una jaula de fieras. Pasaba de un
sentimentalismo patético a la desesperación rabiosa, y si a veces
secaba sus lágrimas despaciosamente, otras se mordía los puños y se
golpeaba el cráneo contra la pared. En los momentos de exaltación
recorría la casa desde la sala a la cocina, entraba en todas las piezas
salía para volver a entrar, daba vueltas, y tropezaba y caía y se
levantaba. Como entrara en la alcoba de Sola y viera su ropa, se
abalanzó a ella, hizo con febril precipitación un lío, y oprimiéndolo
contra su pecho cual si fuera el cuerpo mismo de la persona amada y
fugitiva, exclamó así con lastimero acento:
—Ven acá, paloma... Ven acá, niña de mi corazón... ¿Por qué huyes
de mí? ¿Por qué huyes del pobre viejo que te adora? Ángel divino
ángel precioso de mi guarda, cuya hermosura no puedo comparar sino
a la de la diosa de la Libertad, circundada de luz y sonriendo a los
pueblos; adorada hija mía, ¿en dónde estás? ¿No oyes mi voz? ¿No
oyes que te llamo? ¿No ves que me muero sin ti? ¿No te sacrifiqué m
gloria?... ¡Ay!... Mi destino, mi glorioso destino ahora me reclama, y no
puedo ir, porque sin ti soy un miserable y no tengo fuerzas para nada
Contigo al suplicio, a la gloria, a la inmortalidad, a los Elíseos Campos
sin ti a la muerte oscura, a la ignominia. Sola, Sola de mi vida, ¿en
dónde estás? Dímelo, o revolveré toda la tierra por encontrarte.
Esto decía, cuando llamaron fuertemente a la puerta. Más ligero
que una liebre fue y abrió... No era Sola quien llamaba: eran seis
hombres, que sin fórmula alguna de cortesía se metieron dentro. Uno
de ellos soltó de la boca estas palabras:
—¿No es este el viejo Sarmiento que predicaba en las esquinas?..
Echadle mano mientras yo registro.
—¡Ah!... —exclamó don Patricio algo confuso—. ¿Son ustedes de la
policía?... Sí, yo recuerdo..., conozco estas caras.
—Procedamos al registro —dijo solemnemente el que parecía jefe
de los corchetes—. Toda persona que se encuentre en la casa, debe
ser presa. Cuidado no se escape el abuelo.
—Quiere decir —balbució Sarmiento— que estoy preso.
—Ya se lo dirán allá —replicó el polizonte desabridamente—
Andando... Llévenme para allá al vejete, que aquí nos quedamos dos
para despachar esto.
Según la orden terminante del funcionario (que era un funcionario
vaciado en la común turquesa de los cazadores de blancos en aquella
infame y tenebrosa época), Sarmiento fue inmediatamente conducido
a la cárcel, y solo por un exceso de benevolencia, incomprensible y
hasta peligrosa para la reputación de aquella celosa policía, le dieron
tiempo para ponerse el sombrero, recoger el pañuelo y media docena
de cigarrillos.
No se daba cuenta de lo que le pasaba el infeliz maestro, y durante
el trayecto de su casa a la cárcel de Corte, que no era largo, fue con
los ojos bajos, encorvado el cuerpo, las manos a la espalda, en un
estado tal de confusión y aturdimiento, que no veía por dónde pasaba
ni oía las observaciones picarescas de los transeúntes. Cuando
entraron en la cárcel, el anciano se estremeció, revolviendo los ojos en
derredor. Su entrada había sido como el choque del ciego contra un
muro, símil tanto más exacto cuanto que don Patricio no veía nada
dentro de las paredes del lóbrego zaguán por donde se comunicaba
con el mundo aquella mansión de tristeza y dolor.
Lleváronle al registro y del registro a un patio, donde había algunas
personas que imploraban la misericordia de los carceleros para pode
ver a los detenidos. Hiciéronle subir luego más que de prisa po
hedionda escalera que se abría en uno de los ángulos del patio, y
hallose en un largo corredor o galería, que parecía haber sido claustro
pero que tenía entonces tapiadas todas sus ventanas, sin dejar más
entrada a la luz que unos ventanillos bizcos en la parte más alta.
Al entrar en la galería, Sarmiento oyó gritos, lamentos
imprecaciones. Era al caer de la tarde, y como la luz entraba all
avergonzada, al parecer, y temerosa, deteniéndose en los ventanillos
por miedo a que la encerraran también, no era fácil distinguir de lejos
las personas. Veíanse sombrajos movibles, los cuales, al acercarse a
ellos, resultaban ser la simpática humanidad de algún calabocero que
entraba en las celdas o salía de ellas.
Había centinelas de trecho en trecho, cuya vigilancia no podía se
muy grande, porque a cada instante les era forzoso apartar de las
puertas de las celdas a personas importunas que iban a turbar la
tranquilidad de los reos. Las llorosas mujeres, abusando de los
miramientos que se deben a su sexo, molestaban a los señores cabos
pidiéndoles noticias de tal o cual preso, dándoles cualquier recadillo
verbal o encargo enojoso, como llevar pan a alguno de los muchos
hambrientos que se comían los codos dentro de las celdas. En una de
estas debía de estar encerrado un loco furioso, cuya manía era da
golpes en la puerta, con lo cual estaban muy disgustados los
carceleros, hombres celosísimos de la paz de la casa. El dolor y la
desesperación, callado el uno, ruidosa la otra, hacían estremecer las
frágiles paredes, porque el mezquino edificio era indigno de la rabia
que contenía, y a ser tal como a ella cuadraba, hubiera tenido más
piedras que el Escorial y más hondos cimientos que el Alcázar de
Madrid.
Sarmiento fue introducido en una pieza relativamente grande, cuya
suciedad parecía resumen y muestrario de todas las suertes de
inmundicia que los años y la incuria de los hombres habían acumulado
en la indecorosa cárcel de Corte. En la zona más baja, una especie de
faja mugrienta marcaba el roce de muchas generaciones de presos, de
muchas generaciones de alguaciles, de muchas generaciones de
jueces y curiales. Alumbrábala el afligido resplandor de un quinqué
colgado del techo, que parecía acababa de oír leer su sentencia de
muerte, y se disponía con semblante contrito a hacer confesión de sus
pecados. Como el techo era muy bajo, y los allí presentes se movían
de un lado para otro en torno al ajusticiado quinqué, las sombras
bailaban en las paredes haciendo caprichosos juegos y cabriolas. En
el fondo había la indispensable estampa de Su Majestad, y sobre ella
un crucifijo cuya presencia no se comprendía bien, como no tuviera
por objeto el recordar que los hombres son tan malos después como
antes de la Redención.
Delante de Su Majestad en efigie y de la imagen de Cristo
crucificado, estaba en pie, apoyándose en una mesa, no fingido, sino
de carne y hueso, horriblemente tieso y horriblemente satisfecho de su
papel, el representante de la justicia, el apóstol del absolutismo, don
Francisco Chaperón, siempre negro, siempre de uniforme, siempre
atento al crimen para confundirlo donde quiera que estuviese, en
honra y gloria del trono, del orden y de la fe católica. Pocas veces se le
había visto tan fieramente investigador como aquella noche. Parecía
que el tal personaje acababa de llegar del Gólgota, y que aún le dolían
las manos de clavar el último clavo en las manos del otro, del que
estaba detrás y en la cruz, sirviendo de sarcástico coronamiento a
retrato del señor don Fernando.
A la derecha estaban junto a una mesa media docena de diablejos
vestidos con el uniforme de voluntario realista, y acompañados por e
licenciado Lobo, prestos todos a sumergir las plumas dentro de los
tinteros. La izquierda era ocupada por un banquillo pintado de color de
sangre de vaca: en él se sentaba alguien a quien don Patricio no vio
en el primer momento. El anciano no había salido aún de aque
estupor que le acometió al ser conducido fuera de su casa; miró con
cierta estupidez al tremendo fantasma; miró después a toda la chusma
curialesca que le rodeaba, al licenciado Lobo; miró al santo Cristo, a
rey pintado, y por fin, clavando los ojos en el banco de color de sangre
vio a su adorada hija y compañera.
—¡Sola!... ¡Hija de mi alma!... —gritó con alegría—. ¡Tú aquí..., yo
también..., parece que esto es la cárcel..., el suplicio..., la gloria..., m
destino!...
XVIII
Clarísima luz entró de improviso en la mente del afligido viejo

desaparecieron las percepciones vagas, las ideas confusas, para da
paso a aquella siempre fija, inmutable y luminosa, que había dirigido
su voluntad durante tanto tiempo, llenando toda su vida moral.
—Ya estoy en mí —dijo en tono de seguridad y convicción—
Soledad..., ¡tú y yo en este sitio! Al fin, al fin Dios ha señalado mi día
¿No lo decía yo?... ¿No decía yo que al fin vendría la hora sublime?
¡Destino honroso el nuestro, hija mía! He aquí que no solo heredas m
gloria, sino que la compartes, y los dos juntamente, unidos aquí como
lo estuvimos allá, somos llamados...
—Silencio —gritó Chaperón bruscamente—. Responda usted a lo
que le pregunto: ¿cómo se llama usted?
—Excusada pregunta es esa —repuso con aplomo y dignidad don
Patricio—, pues todo el mundo sabe en Madrid y fuera de él que soy
Patricio Sarmiento, adalid incansable de la idea liberal, compañero de
Riego, amigo de todos los patriotas, defensor de todas las
constituciones, amparo de la democracia, terror del despotismo. Soy e
que jamás tembló delante de los tiranos, el que no tiene en su corazón
una sola fibra que no grite libertad, y el que aun después de muerto
sacará la cabeza de la sepultura para gritar...
—Basta —dijo Chaperón, notando que las palabras del reo
provocaban murmullos—. Charlatán es el viejo... Responda usted
¿Conoce a esta joven?
—¿Que si la conozco? ¡Que si conozco a Sola...! Si no temiera
faltar al respeto que debo a todo juez, quienquiera que sea, diría que
es necia pregunta la que vuecencia acaba de hacerme. Esta es mi hija
adoptiva, mi ángel de la guarda, mi amparo, mi compañera de vida, de
muerte, de cielo y de inmortalidad. Dios, que dispone todas las
grandezas, así como el hombre es autor de todas las pequeñeces, ha
dispuesto que este ángel divino me acompañe también ahora
¡Admirable solución de la Providencia! Yo creí haberla perdido, y la
encuentro junto a mí en la hora culminante de mi vida, cuando se
cumple mi destino; aparece a mi lado, no para darme esos triviales
consuelos que no necesita mi corazón magnánimo, sino para
compartir mi sacrificio, y con mi sacrificio, mi gloria. Adelante, señores
jueces, adelante. Acaben ustedes. Soledad y yo nos declaramos reos
de amor a la libertad, nos declaramos dignos de caer bajo vuestras
manos, y confesamos haber trabajado por el triunfo del santo principio
ahora y antes y siempre, porque para ello nacimos y por ello morimos.
Causaba diversión a los diablillos menores y aun al diablazo grande
el desenfado del buen viejo, por lo cual no habían puesto tasa a la
charla de este. Mas Chaperón, que deseaba concluir pronto, dijo a
reo:
—¿Es cierto que esta joven recibió un paquete de cartas de los
emigrados para repartirlas a varias personas de Madrid?
—¿Y eso se pregunta? —replicó Sarmiento como si admirara la
candidez del vestiglo—. ¿Pues qué había de hacer sino trabajar noche
y día por el triunfo de la sagrada causa?... ¿No he dicho que para eso
nacimos y por eso morimos?
Soledad miraba con ojos muy compasivos a su amigo y al juez
alternativamente. Mas pronto dejó de mirarlos y se reconcentró en s
misma, mostrando estoica indiferencia hacia aquel lúgubre diálogo
entre un insensato y un verdugo. Había hecho ya con Dios pacto de
resignación absoluta, y se entregaba a la voluntad divina, prometiendo
no oponer ninguna resistencia a los accidentes humanos, ni acepta
otro papel que el de víctima callada y tranquila. Entre el instante en
que la sacaron desmayada de la caverna del gran esbirro, hasta aque
en que le pusieron delante a su compañero de infortunio, habían
pasado para ella horas muy angustiosas. Pero su espíritu se había
rendido al fin, aceptando la fórmula esencial del cristiano, que es
rendirse para vencer y perderse absolutamente para absolutamente
salvarse. Si algún combate sostenía aún su alma, era porque e
propósito de pensar solamente en Dios no podía cumplirse aún con
rigurosa exactitud. Pensaba en algo que no era Dios; pero aun así, iba
conquistando la tranquilidad y un pasmoso equilibrio moral, porque
había arrojado fuera de sí valerosamente toda esperanza.
—Usted sabrá sin duda a quién venían dirigidas esas cartas —
preguntó Chaperón a Sarmiento.
—¿Pues qué?... ¿Ella no lo ha dicho?... —repuso el anciano
nuevamente admirado de la ignorancia del tribunal—. Esto no puede
considerarse como delación, porque esas personas son leales
patricios que también anhelan llegue la coyuntura de sacrificarse por la
libertad. Nosotros no tenemos secretos; nosotros, como los héroes de
la antigüedad, lo hacemos todo a la luz del día. Fue preciso prestar un
servicio a la santa causa, facilitando las comunicaciones entre todos
los que conspiran dentro y fuera por hacerla triunfar, y lo prestamos, sí
señor, lo prestamos a la clarísima luz del sol, coram populo. Las cartas
eran cuatro.
—Atención —dijo don Francisco acercándose a la mesa de los
escribanos.
—Una era para don Antonio Campos, ese gran patriota que acaba
de llegar de Tarifa y Almería; otra para un oficial de la antigua guardia
que se llama Ramalejo; la tercera venía dirigida a don Roque Sáez y
Onís, y la cuarta a doña Jenara de Baraona.
—Muy bien —gruñó Chaperón, asemejándose mucho en su gruñido
al perro que acaba de encontrar un hueso perdido—. Veo que el viejo
y la niña son la peor casta de conspiradores que se conoce en Madrid.
—Sí —dijo Sarmiento con exaltación—, insúltenos usted... Eso nos
agrada. Los insultos son coronas inmarcesibles en la frente del justo
Mire usted las espinas que lleva en su cabeza aquel que está en la
cruz.
—Silencio —gritó Chaperón—. Veo que él es tan parlanchín como
ella hipocritona. Ya sabemos lo de las cartas, linda pieza... Ahora e
buen viejo nos informará de todas las particularidades que hayan
ocurrido en la casa. ¿Tiene noticia de que entrara en estos líos don
Benigno Cordero?
—¡Cordero! —exclamó Sarmiento con asombro—. Cordero es un
hombre vulgar, un tendero, un quídam... ¿Cómo puede ser capaz
semejante hombre de intervenir en un complot de esos que solo
acometen las almas grandes y valerosas?
—¿Seudoquis fue muchas veces a la casa?
—Dos veces, dos. Para nada hay que mentar a Cordero. Nuestra
gloria es nuestra, señor mío, y de nadie más. ¡Ay de aquel que intente
quitarnos una partícula de ella, siquiera sea del tamaño de un grano de
alpiste! Nosotros, nosotros solos somos los héroes, nosotros las
víctimas sublimes. Fuera intrusos y gentezuela que se presenta en e
festín de la gloria con sus manos lavadas, reclamando lo que no les
pertenece ni han sabido ganar con su abnegación. ¡Nosotros solos
ella y yo, nadie más que ella y yo!
—El que enviaba las cartas —añadió don Francisco dando un paso
hacia Sarmiento— ¿no hablaba de lo de Almería y Tarifa, ni de la
revolución que estaban preparando?
—Nosotros —repuso Sarmiento con desdén—, no nos ocupamos
de frívolos detalles. ¡Almería, Tarifa! ¿Qué vale eso ni qué significa?
Hechos aislados que ni precipitan ni detienen el hecho principal, que
es la victoria de la libertad. ¡Si al fin tiene que ser, si ha de venir tan de
seguro como saldrá el sol mañana!... Que se frustre una intentona, que
salga mal un desembarco, que fusiléis a trescientos o a mil o a un
millón de patriotas..., nada importa, señores. Lo que ha de venir
vendrá. Si pretendéis atajarlo con patíbulos, vendrá más pronto. Los
patíbulos son árboles fecundos, que con el riego de la sangre dan
frutos preciosísimos. Echad sangre, más sangre; eso es lo que hace
falta. Las venas de los patriotas son el filón de donde mana la nueva
vida.
»No me habléis de conspiraciones parciales: yo no entiendo de eso
El que escribió las cartas, lo mismo que mi hija, lo mismo que yo
cooperamos con nuestra voluntad y nuestros deseos más íntimos y
más ardientes en ese gran complot moral, cuyas ramificaciones se
extienden por todo el mundo. ¡Ah!, señores, no conocéis la gran
conspiración del tiempo. A ella pertenezco, a ella pertenecen todas
vuestras víctimas... Ea, despachemos pronto. Basta de fórmulas y de
procedimientos necios. El patíbulo, el patíbulo, señores, esa es
nuestra jurisprudencia. De él hemos de salir triunfantes, trocados de
humanos miserables en inmaculados espíritus. Lo mismo nos da que
nos ahorquéis de esta o de la otra manera, más o menos noblemente
¿A los mártires del circo romano les importaba que el tigre que se los
comía tuviera la oreja negra o amarilla? No, porque no atendían más
que a la sublime idea; lo mismo nosotros no atendemos más que a
esta idea que nos lleva en pos del suplicio, la cual es como un fuego
sacrosanto que nos embelesa y nos purifica. No tenemos ya sentidos
no sabemos lo que es dolor... ¡La carne!... ¡Ah!, no nos merece más
interés que el despreciable polvo de nuestros zapatos. Adelante, pues
Cumpla cada uno con su deber: el vuestro es matar, el nuestro
sucumbir carnalmente, para vivir después la excelsa, la inacabable y
deliciosa vida del espíritu... Vamos allá: ¿en dónde, en dónde está esa
bendita horca?
Había tanta naturalidad en las entusiastas expresiones del exaltado
viejo patriota, y al propio tiempo un tono de dignidad tan majestuoso
que los empleados de la Comisión, así militares como civiles, no
podían resistir al deseo de oírle. Aunque el sentimiento que a la
mayoría dominaba era de burla con cierta tendencia a la compasión
no faltaba quien oyese al estrafalario viejo con un interés distinto de
que comúnmente inspiran las palabras de los tontos. El mismo
Chaperón se mostraba complacido, sin duda porque le divertía su
víctima, haciéndolo mucho más barato que el célebre gracioso
Guzmán, que empezaba su carrera en el teatro del Príncipe. Poro
como la dignidad del tribunal no permitía tales comedias, don
Francisco mandó al reo que diese por terminada la representación.
Los polizontes que se quedaron registrando la casa de Sola
aparecieron. Habían encontrado alguna cosa de gran valor jurídico
habían hecho provisión de pedacitos de papel, fragmentos de cartas
sin olvidar un polvoriento retrato de Riego, hallado entre los bártulos
de don Patricio; dos o tres documentos masónicos o comuneros, y una
carta dirigida al maestro de escuela. Examinolo todo ávidamente
Chaperón, y lo entregó después a Lobo para que constase en e
proceso. En tanto, don Patricio se acercaba a su compañera de
infortunio y en voz baja le decía:
—Ánimo, ángel de mi vida, cordera mía. Que en esta ocasión
solemne no deje de subir tu espíritu a la altura del mío. Inspírate en mí
Reflexiona en la gloria que nos espera y en el eco que tendrán
nuestros sonorosos nombres en los siglos futuros, perpetuándose de
generación en generación. ¿Por qué estás triste, y no alegre como
unas castañuelas? ¿Por qué bajas los ojos en vez de alzarlos como
yo, para tratar de ver en el cielo el esplendoroso asiento que nos está
destinado? Tu destino es mi destino. Ambos están escritos en e
mismo renglón. Hay gemelos del morir como los hay del nacer: tú y yo
somos mellizos, y juntos saldremos del vientre de este miserable
mundo a la inmensa vida del otro... Posible es que no lo
comprendieras antes, niña de mis ojos; yo tampoco lo creía, y era
engañado por hechos mentirosos. Tu proyecto de abandonarme era
una ficción del destino para sorprenderme después con esta unión
celestial. Mi entrada en tu casa, el amparo que me diste, ¿qué
significan sino la preparación para estas nuestras bodas mortuorias
de las cuales saldremos unidos por siempre ante el altar de la
glorificación eterna? Tú necesitas de mí para este santo objeto, as
como yo necesito de ti... Bien sabía yo que conspirabas... ¡Y
conspirabas por la santa libertad! Bendita seas... Serás condenada y
yo también. ¡Seremos condenados!... ¿Ves cómo no es posible la
separación? ¿Ves cómo lo ha dispuesto Dios así? Viviremos juntos
eternamente. ¡Qué inefable dicha!... Solilla de mi vida, ten ánimo; que
la flaca naturaleza corporal no soborne con sus halagos tu alma de
patriota. Vive como yo la excelsa vida del espíritu. Desprécialo todo
mira al cielo, nada más que al cielo y a mí, que soy tu compañero de
gloria, tu gemelo, tu segundo tú, a quien has de estar unida por los
siglos de los siglos.
Soledad miró a su amigo. La serenidad, que en él provenía de un
loco entusiasmo, provenía en ella de la resignación, ese heroísmo más
sublime que todas las exaltaciones del valor, y al cual damos un
nombre oscuro: lo llamamos paciencia, y germina como flor invisible y
modesta en el alma de los que parecen débiles.
—Veo que no lloras —dijo don Patricio observando aquel semblante
plácidamente tranquilo, a quien la virtud mencionada daba angelica
hermosura—. No lloras, no estás demudada...
—¿Yo llorar? ¿Por qué?
—Así me gusta —exclamó Sarmiento con entusiasmo—. ¡Oh almas
sublimes! ¡Oh almas escogidas! ¡Y pensar que os han de intimida
horcas y suplicios!... Señores jueces, aquí aguardamos la hora de
holocausto. Llevadnos ya; subidnos a esos gallardos maderos que
llamáis infamantes. Mientras más altos, mejor. Así alumbraremos más
Somos los fanales del género humano.
Chaperón mandó que los dos reos fuesen conducidos cada cual a
su calabozo; mas como el alcaide manifestase la imposibilidad de
ocupar dos departamentos, se dispuso que ambos gemelos de la
muerte fuesen encerrados en un solo cuarto.
—Vamos —dijo don Patricio enlazando con su brazo la cintura de
Sola.
Esta se dejó llevar. Cuando iban por la oscura galería, la joven
huérfana oyó claramente en su oído estas palabras, dichas en voz
muy baja, como un silbido:
—Señora, no se sofoque usted... Se hará un esfuercito po
salvarla... Una persona que se interesa por usted..., que se interesa
sí..., me encarga de advertírselo.
Soledad volviose prontamente y vio unos ojos verdes y grandes, de
tamaño de huevos. Estos ojos brillaban, reflejando la claridad del faro
de los carceleros, en un semblante amojamado y partido en dos por la
hendidura sonriente de la prolongada boca, casi vacía. En vez de
tranquilizarse, Soledad tuvo miedo.
XIX
El licenciado Lobo, asesor privado del señor Chaperón, tenía su

oficina en el ángulo más oscuro y apartado de la planta baja de la
Comisión militar. Cubría el piso la estera más vieja, servíale de
escritorio la mesa más rota que contaba entre sus propiedades e
Estado, y el pupitre, el tintero, la estantería, denotaban con honrosa
vejez haber acompañado en toda su larga vida a las antiguas
covachuelas. Hasta el retrato de Fernando VII que decoraba la pared
era el más feo de toda la casa, y comido de polilla, no presentaba a la
admiración del espectador más que los ojos y parte del cuerpo. Lo
demás era una mancha irregular con grandes brazos al modo de
tentáculos. Parecía un gran cefalópodo que estaba contemplando a su
víctima antes de chupársela.
En el centro de este mueblaje, y encorvado sobre una mesa llena
de descoloridos papeles, aparecía el leguleyo, cuya figura encajaba en
tal marco como el cernícalo en su nido. La diestra pluma rasgueaba
sin cesar, cual si fuera absolutamente imprescindible su actividad para
la existencia de todo aquello, o como si fuera la clave cabalística de
que dependían las imágenes del despacho, del retrato, de los muebles
y del licenciado mismo. Cuando la pluma paraba, creyérase que todo
iba a desvanecerse. A no ser porque en los ratos de descanso e
asesor se ponía a tararear alguna tonadilla trasnochada de las de
tiempo de la Briones y de Manolo García, se le hubiera tenido po
momia automática, o por alma en pena a quien se había impuesto la
tarea de escribir mil millones de causas para poderse redimir.
Al día siguiente de la prisión de Sarmiento, y cuando aún no había
despachado regular porción de su faena de la mañana, una señora se
presentó sin anunciarse en el escondrijo del asesor.
—¡Oh! señora... —exclamó Lobo suspendiendo la escritura—. No
esperaba a usted tan tempranito. Hágame el obsequio de toma
asiento.
Ya la señora lo había hecho en la única silla que servía para e
caso. Era la misma dama a quien vimos en el despacho de Chaperón
guapa si las hay, seductora de cara, cuerpo y apostura, tota totalitate
hermosa. Envolvíase en un rico chal blanco, que a Lobo le pareció
sobre los lindos hombros y entre los brazos de verde vestidos, como e
más gracioso capricho de la nieve entre las plantas de un jardín. Como
a los viejos feos se les permite ser galantes, Lobo dijo que la cara de
la señora era una rosa con la cual no se había atrevido la nieve
temiendo que una mirada la derritiera.
—Déjese usted de sandeces —dijo ella—. Yo vengo a salir de
dudas.
—¿Respecto a esa jovenzuela que se delató a sí misma?..
Confieso que es el primer caso que he visto desde que tengo esta
nobilísima pluma en la mano. Por ella se interesa la señora.
—Mucho, muchísimo —repuso la dama con pena—. Anoche he
tenido una pesadilla... No es la primera vez que sueño con ella..
¿Pues no he dado en soñar que soy verdugo y que la estoy
ahorcando?
—Graciosísimo, señora mía, graciosísimo. ¿La conoce usted hace
tiempo? ¿De qué procede ese interés tan vivo? Ella no demuestra
tenerla a usted grabada en las telas de su corazón. Recordemos cómo
declaró haberle entregado una de las cartas. Sin duda quería perderla
a usted. ¡Infame víbora! ¡Y usted quiere favorecerla! ¡Oh generosidad
inaudita!
—¡Ella me aborrece!
—Se conoce, sí, porque lo de la carta es una calumnia.
—No es una calumnia, no. Recibí la carta —dijo la señora
suspirando—. Pero Chaperón me ha dicho que no seré molestada po
ello. Mostraré la carta, si es preciso. No contiene nada que transcienda
a conspirar.
—Todo sea por Dios —dijo Lobo con ademán distraído—. Pues se
arreglará. Basta que usted se interese por ella, para que don Francisco
sea benigno. Para él no hay más Dios que Calomarde, y como m
señora tiene felizmente todo el favor de nuestro querido ministro y
también el de Quesada...
—No me fío yo del ministro —dijo la dama nublando su hermoso
semblante con las sombras de la duda—. Muy amigo mío era don
Víctor Sáez, y en Cádiz me prendió, como usted sabe. Aquello duró
poco; pero fui maltratada del modo más grosero. En estos tiempos no
hay que fiar de las amistades.
—No, no hay que fiar, señora mía —repitió Lobo riendo y bajando la
voz como el que va a decir un secreto peligroso—. ¡Estamos en los
tiempos más perros que se han visto desde que hay tiempos, y
bregamos con la gente más mala que se ha visto desde que e
hombre, esa infame bestia inteligente, apareció sobre la tierra! Empero
usted conseguirá lo que desea. ¿Es cuestión de gratitud? ¿Ha recibido
usted favores de esa infeliz o de su familia?
—No, no es eso —dijo la dama, mostrando que le importunaba la
curiosidad del hombre de leyes—. Es cuestión de conciencia.
—¿Debe usted favores a esa desgraciada?
—No, ella me debe a mí un disfavor muy grande. Yo he sido mala
señor Lobo..., pero no, no soy tan mala como yo misma creo. No faltan
voces en mi conciencia... Verdad es que tengo un genio arrebatado
que soy capaz en ciertos momentos... Vamos, lo diré: soy capaz hasta
de coger un puñal...
La hermosa dama, moviendo su brazo como para matar, convirtiose
por breve momento en una figura trágica de extraordinaria belleza.
—Pero estos furores me pasan —añadió pasándose la mano po
los ojos—. Pasan, sí, y como Dios castiga y advierte... Yo he sido
mala; pero no he cerrado mis ojos a las advertencias de Dios. No es
posible siempre reparar el mal que se ha causado... Pero se me
presenta ahora ocasión de hacer un bien, y he de hacerlo: quiero
sacar de la prisión a esa joven.
—El señor don Francisco...
—No me fío yo del señor don Francisco. Es demasiado amigo de m
esposo para que yo haga caso de sus palabrejas corteses. Usted
usted puede arreglarlo fácilmente.
—¿Cómo?
—Componiendo la causa de modo que aparezca la reo tan inocente
de conspiración como los ángeles del cielo, aunque no sé yo s
Chaperón y Calomarde podrán convencerse de que los ángeles no
conspiran.
—¡La causa, señora! —exclamó Lobo sonriendo con malicia.
—Sí; componer la causa, hombre de Dios; poner lo blanco negro y
lo negro blanco.
—Pero, señora doña Jenara de mis pecados, si aquí no hay
causas, ni jurisprudencia, ni ley, ni sentencia, ni testimonio, ni pruebas
ni nada más que el capricho de la Comisión militar y de la
Superintendencia, sometidas, como usted sabe, al capricho más
bárbaro aún de los voluntarios realistas. Si todo este fárrago de
papeles que usted ve aquí es tan inútil para la suerte de los presos
como los guijarros de que está empedrada la calle... ¡Si todo esto es
vana fórmula; si yo escribo porque me pagan para que escriba; si esto
es puramente lo que yo llamo pan de archivo, porque no sirve más que
para llenar esa gran boca que está siempre abierta y nunca se sacia!..
¡Oh inocencia, oh candor pastoril! No hable usted de causas ni de
procedimientos, porque si todo esto (señaló los legajos que en
grandes pilas le rodeaban) se escribiera en griego, serviría para lo
mismo que en castellano sirve: para nada... ¡Pobres ratones! ¡Y es tan
inhumana la Sala que manda poner ratoneras para impedirles que se
coman esto!
El licenciado, después que concluyó de hablar, siguió riendo un
buen rato.
—En ese caso, emprenderemos la conquista de Chaperón.
—Cosa muy fácil, pero facilísima... Tenga usted de su parte a
Calomarde y a Quesada, y échese a dormir, señora.
—Es que ahora —repuso la dama muy preocupada— dicen que
apretarán mucho la cuerda y que no perdonarán a nadie.
—Sí; el gobierno necesita ahora más que nunca demostrar gran
celo para perseguir a los liberales. Los voluntarios realistas le acusan
de que ahorca poco.
—¡Qué horror!
—De que ahorca poco. Pues bien: el gobierno se verá en el caso de
ahorcar mucho.
—¡Y a esa pobre joven...!
—Esa pobre joven... La verdad es que la causa, como causa de
conspiración, es de las que más alto piden un desenlace trágico
Ahora me acuerdo de una circunstancia que favorece mucho su deseo
de usted.
—¿Qué?
—Anoche nos han traído al que figura como cómplice de la
tunantuela.
—¿Sarmiento?... Le conozco —dijo la señora desanimándose—. Es
un pobre tonto, a quien la Comisión no puede considerar como reo.
—Poquito a poco. La ley está de tal modo redactada, que yo no me
atrevería a absolverle. Puesto que la señora quiere que yo dé unos
cuantos toques a la causa, se hará. Nada se pierde en ello. Verá usted
cómo resulta que el culpable de todo es Sarmiento, y que la joven
jamás ha roto un plato.
—Buena idea, si ese infeliz estuviese en su claro juicio, si tuviera
responsabilidad...
—Allí está el quid. Anoche dijo Chaperón que iba a mandarle a
Nuncio de Toledo. Puede que persista en esta humanitaria idea. Allá
veremos... Ya sabe usted que la cabeza de mi jefe es una piedra
berroqueña.
—Puede sostenerse —dijo la dama en tono humorístico— que su
jefe de usted es uno de los hombres más brutos que han comido pan
en el mundo.
—Señora —replicó Lobo como quien da expansión a un sentimiento
contenido por el deber—, yo le aseguro a usted que no come cebada
por no dar qué decir. Así anda el reino en manos de esta gente
Malaventurados los que se ven en la dura necesidad de servirle, como
yo, por ejemplo, que pudiendo estar pavoneándome en una Sala de
Consejo, cual lo piden mis merecimientos y servicios, me hallo
reducido a la triste condición en que usted me ve. ¡Ay, señora de m
vida! —añadió haciendo pucheros—. Esto me pasa por haber sido una
mala cabeza, por haber fluctuado entre los dos partidos sin decidirme
por ninguno. Desde la guerra vengo haciendo quiebros como un
bailarín, sin saber a qué faldón agarrarme. Mis vacilaciones, mi timidez
natural, y, ¿por qué no decirlo?, mi honradez me han traído al estado
en que me veo, simple secretario de un Chaperón, yo que llegué a
posarme en la sala de Mil y Quinientas... ¡Y que no he pasado yo
congojas en gracia de Dios!... (Al decir esto movía la cabeza como los
muñecos que la tienen pegada al cuerpo por una espiral de alambre)
¡Sin destino, y teniendo que mantener esposa, dos suegras y once
becerros mamones! Es verdad que Dios se llevó de mi casa a la gente
mayor; pero vinieron nietecillos..., ¡y qué casorios los de mis hijas!..
En fin, señora, me callo, porque si sigo hablando de mis lástimas ha de

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Lee-FM_pi-xxx.indd 1 5/15/17 8:01 PM

Lee-FM_pi-xxx.indd 2 5/15/17 8:01 PM

Kiwon Lee, MD, FACP, FAHA, FCCM

New York Chicago San Francisco Athens London Madrid

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eBook conversion by codeMantra

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Section 1 Neurocritical Care Diseases................................................................ 1

5.  Acute Ischemic Stroke................................................................................................... 93

7.  Paroxysmal Sympathetic Hyperactivity.................................................................147

9.  ICU Management of Brain Tumors...........................................................................174

10.  Inflammatory and Demyelinating CNS Diseases................................................203

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11.  Cardiac Arrest and Anoxic Brain Injury...................................................................214

12.  Fulminant Hepatic Failure...........................................................................................230

13.  Encephalopathy and Delirium..................................................................................239

Section 2 Neurocritical Care Monitoring.................................................. 249

14.  Management of Increased Intracranial Pressure................................................249

15.  Continuous Electroencephalogram Monitoring in the ICU............................262

16.  Multimodality Neuromonitoring..............................................................................289

17.  Advanced Hemodynamic Monitoring....................................................................325

18.  Evoked Potentials in the Operating Room and ICU...........................................338

19.  Neurophysiologic Decision Support Systems.....................................................351

20.  Sedation ............................................................................................................................361

21.  Fever and Temperature Modulation........................................................................378

22. External Ventricular Drain Management and

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23.  Endovascular Surgical Neuroradiology..................................................................416

24.  Brain Aneurysm, AVM, and Bypass Surgery..........................................................460

25.  Carotid Endarterectomy and Extracranial-Intracranial Bypass......................473

26.  Postcraniotomy Complication Management............................................................ 482

27.  Spine Trauma...................................................................................................................505

28.  Pediatric Neurosurgery................................................................................................520

Section 4 Trauma and Surgical Intensive Care................................547

29. Thoracic Trauma and Cardiothoracic Intensive Care Unit Management........547

30.  Abdominal Trauma........................................................................................................560

31.  Traumatic Vascular Injuries.........................................................................................575

32.  Abdominal Emergencies.............................................................................................586

33.  Genitourinary Emergencies........................................................................................609

34.  Critical Care Ultrasound...............................................................................................622

Section 5 Cardiovascular Section..........................................................................645

35.  Acute Coronary Syndrome.........................................................................................645

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36.  Rhythm Disturbances in Critically Ill Patients......................................................660

37.  Acute Decompensated Heart Failure......................................................................680

38.  Cardiogenic Shock and Intraaortic Balloon Pump.............................................696

39.  Management of Cardiopulmonary Devices at the End of Life......................709

40.  The Role of ECMO in Cardiopulmonary Failure in Adults................................722

Section 6 Pulmonary Diseases....................................................................................739

41.  The Neurocritical Care Airway...................................................................................739

42.  Mechanical Ventilation.................................................................................................757

43.  Acute Respiratory Distress Syndrome....................................................................786

44.  Deep Vein Thrombosis and Pulmonary Embolism.............................................799

45.  Percutaneous Tracheostomy......................................................................................814

46.  Bronchoscopy in the NeuroICU.................................................................................826

Section 7 Renal and Electrolyte Disorders.............................................841

47.  Acute Kidney Injury.......................................................................................................841

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48.  Renal Replacement Therapies...................................................................................857

49 Disorders of Water Homeostasis: Hypo- and Hypernatremia........................869

5. Acute Ischemic Stroke................................................................................................... 93

7. Paroxysmal Sympathetic Hyperactivity.................................................................147

9. ICU Management of Brain Tumors...........................................................................174

10. Inflammatory and Demyelinating CNS Diseases................................................203

11. Cardiac Arrest and Anoxic Brain Injury...................................................................214

12. Fulminant Hepatic Failure...........................................................................................230

13. Encephalopathy and Delirium..................................................................................239

14. Management of Increased Intracranial Pressure................................................249

15. Continuous Electroencephalogram Monitoring in the ICU............................262

16. Multimodality Neuromonitoring..............................................................................289

17. Advanced Hemodynamic Monitoring....................................................................325

18. Evoked Potentials in the Operating Room and ICU...........................................338

19. Neurophysiologic Decision Support Systems.....................................................351

20. Sedation ............................................................................................................................361

21. Fever and Temperature Modulation........................................................................378

22. External Ventricular Drain Management and

23. Endovascular Surgical Neuroradiology..................................................................416

24. Brain Aneurysm, AVM, and Bypass Surgery..........................................................460

25. Carotid Endarterectomy and Extracranial-Intracranial Bypass......................473

26. Postcraniotomy Complication Management............................................................ 482

27. Spine Trauma...................................................................................................................505

28. Pediatric Neurosurgery................................................................................................520

29. Thoracic Trauma and Cardiothoracic Intensive Care Unit Management........547

30. Abdominal Trauma........................................................................................................560

31. Traumatic Vascular Injuries.........................................................................................575

32. Abdominal Emergencies.............................................................................................586

33. Genitourinary Emergencies........................................................................................609

34. Critical Care Ultrasound...............................................................................................622

35. Acute Coronary Syndrome.........................................................................................645

36. Rhythm Disturbances in Critically Ill Patients......................................................660

37. Acute Decompensated Heart Failure......................................................................680

38. Cardiogenic Shock and Intraaortic Balloon Pump.............................................696

39. Management of Cardiopulmonary Devices at the End of Life......................709

40. The Role of ECMO in Cardiopulmonary Failure in Adults................................722

41. The Neurocritical Care Airway...................................................................................739

42. Mechanical Ventilation.................................................................................................757

43. Acute Respiratory Distress Syndrome....................................................................786

44. Deep Vein Thrombosis and Pulmonary Embolism.............................................799

45. Percutaneous Tracheostomy......................................................................................814

46. Bronchoscopy in the NeuroICU.................................................................................826

47. Acute Kidney Injury.......................................................................................................841

48. Renal Replacement Therapies...................................................................................857

50. Management of Systemic Blood Pressure in the NeuroICU...........................889

51. Disseminated Intravascular Coagulation..............................................................901

52. Bleeding Disorders and Coagulopathy Reversal................................................906

53. Sepsis and Septic Shock..............................................................................................919

54. Antimicrobial Therapies in the ICU..........................................................................935

55. Catheter-Related Bloodstream Infections.............................................................952

56. Common Infections in the ICU..................................................................................960

57. Nutrition and Metabolic Support.............................................................................975

58. Endocrine Disorders in Critical Illness.....................................................................988

59. Brain Death and Organ Donation............................................................................993