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Essentials of

General Surgery

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About the Cover:

Portrait of Dr. Samuel D. Gross (The Gross Clinic)

Thomas Eakins
Oil on canvas, 1875
8 feet 6 feet 6 inches (243.8 198.1 cm)
Philadelphia Museum of Art: Gift of the Alumni Association to Jefferson Medical College in 1878 and purchased
by the Pennsylvania Academy of the Fine Arts and the Philadelphia Museum of Art in 2007 with the generous
support of more than 3,600 donors, 2007

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Essentials of
General Surgery

Senior Editor
Peter F. Lawrence, MD
Wiley Barker Endowed Chair in Vascular Surgery
Director, Gonda (Goldschmied) Vascular Center
David Geffen School of Medicine at UCLA
Los Angeles, California

Richard M. Bell, MD
Professor of Surgery
University of South Carolina School of Medicine
Columbia, South Carolina

Merril T. Dayton, MD
Professor and Chairman
Department of Surgery
State University of New York at Buffalo
Buffalo, New York

Questions Editor
James C. Hebert, MD
Albert G. Mackay and H. Gordon Page Professor of Surgery
University of Vermont College of Medicine
Burlington, Vermont

Content Editor
Mohammed I. Ahmed, MBBS, MS (Surgery)
Department of Surgery
Affiliated Institute for Medical Education
Chicago, Illinois

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Acquisitions Editor: Susan Rhyner
Product Manager: Angela Collins
Freelance Editor: Catherine Council
Marketing Manager: Joy Fisher-Williams
Vendor Manager: Bridgett Dougherty
Design & Art Direction: Teresa Mallon, Doug Smock
Compositor: SPi Global

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Library of Congress Cataloging-in-Publication Data

Essentials of general surgery / [edited by] Peter F. Lawrence. 5th ed.
p. ; cm.
Includes bibliographical references and index.
ISBN 978-0-7817-8495-5
I. Lawrence, Peter F.
[DNLM: 1. Surgical Procedures, Operative. WO 500]

Care has been taken to confirm the accuracy of the information present and to describe generally accepted practices. However, the
authors, editors, and publisher are not responsible for errors or omissions or for any consequences from application of the informa-
tion in this book and make no warranty, expressed or implied, with respect to the currency, completeness, or accuracy of the contents
of the publication. Application of this information in a particular situation remains the professional responsibility of the practitioner;
the clinical treatments described and recommended may not be considered absolute and universal recommendations.
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What do all medical students need to know about surgery to research process also identified technical skills, such as sutur-
be effective clinicians in their chosen fields? ing skin, that should be mastered by all physicians and that are
The primary responsibility of medical schools is to educate best taught by surgeons.
medical students to become competent clinicians. Because
most physicians practice medicine in a nonacademic setting,
clinical training is paramount. The 3rd year of medical school, FIFTH EDITION ENHANCEMENTS
which focuses on basic clinical training, is the foundation
The fifth edition of this textbook has continued the approach
for most physicians clinical training. These realities do not
that has resulted in its use by many medical students in the
diminish the other critical functions of medical school, includ-
United States, in Canada, and throughout the world:
ing basic science education for MD and PhD candidates, basic
and clinical research, and the education of residents and prac- 1. This edition has been extensively revised to provide the
ticing physicians. However, the central role of providing clini- most current and up-to-date information on general sur-
cal education for medical students cannot be overemphasized. gery. Additionally, the entire interior has been refreshed
The education of students, residents, and practicing sur- and is now full-color for an even more enjoyable reading
geons should be a continuum, although it may seem frag- experience.
mented at times to students. Because of the length of time 2. Our authors are surgeons devoted to teaching medical stu-
needed to completely train surgeons, surgical residents remain dents and understand the appropriate depth of knowledge
students for 3 to 9 years beyond medical school. As a result for a 3rd-year student to master.
of this extensive training period, most medical schools have 3. We do not attempt to provide an encyclopedia of surgery.
large numbers of surgical residents, and resident training We include only information that 3rd- and 4th-year stu-
makes up the bulk of their educational efforts. Student educa- dents need to knowand explain it well.
tion is part of the continuum that starts in the 1st or 2nd year of 4. We intentionally limit the length of each section, so that it
medical school, continues through residency, and never ends, can reasonably be read during the clerkship.
because continuing education and lifelong learning are essen- 5. Through problem solving, clinical cases, and sample exam
tial for all physicians. questions, we provide numerous opportunities to practice
and test new knowledge and skills, as well as features to aid
in review and retention. We believe that this approach best
NOT JUST FOR SURGEONS prepares students to score high on the National Board of
Medical Examiners surgery shelf exam and also prepares
This textbook and its companion volume, Essentials of Sur- them for residency training.
gical Specialties, were produced to start that continuum of
education for medical students, and to focus on medical stu-
dents who are not planning a surgical career. We believe that PEDAGOGICAL FEATURES
all physicians need to have a fundamental understanding of
Learning objectives
the options provided by surgery to be competent, so the book
Full-color art program
asks the question, What do all medical students need to know
New and updated tables, algorithms, and charts
about surgery to be effective clinicians in their chosen field?
New Appendix including 40 four-color burn figures
Rather than using traditional textbook-writing techniques to
Sample questions, answers, and rationales for every chapter
address this question, members of the Association for Surgi-
cal Education (ASE), an organization of surgeons dedicated to
undergraduate surgical education, have conducted extensive MORE TOOLS ONLINE
research to define the content and skills needed for an opti-
mal medical education program in surgery. Somewhat surpris- Bonus chapters
ingly, there has been consensus among practicing surgeons, Question bank
internists, and even psychiatrists about the knowledge and Patient management problems and oral exam questions
skills in surgery needed by all physicians. The information Glossary
from this research has become the basis for this textbook. The Fully searchable e-book

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Chapter outlines and specialty programs and practice oral and multiple-choice
Image bank questions will acquire the essential surgical knowledge and
problem-solving skills that all physicians need.

A companion textbook on the surgical specialties, Essentials
of Surgical Specialties, is based on an approach similar to that You are entering the most exciting and dynamic phase of your
of Essentials of General Surgery and trains you in specialty professional life. This educational package is designed to help
and subspecialty fields of surgery. This text is separate from you achieve your goal of becoming an adept clinician and
Essentials of General Surgery because some medical schools developing lifelong learning skills. It will also help you get
teach the specialties in the 3rd year and others teach them in into the residency of your choice. Best wishes for success in
the 4th year. Students who complete both the general surgery your endeavor.

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Many members of the Association for Surgical Education We would like to thank our student editors, Tamera Beam
(ASE) provided advice and expertise in starting the first edi- and Jason Rogers, who reviewed many of the chapters and pro-
tion of this project nearly 25 years ago. Since that time, ASE vided valuable student perspective on the material presented.
members have volunteered to assist in writing chapters and We would like to extend our thanks to Cathy Council, our edi-
editing the textbook. At its annual meetings, the ASE provides tor in Salt Lake City, who coordinated all components of this
an excellent forum to discuss and test ideas about the content project. I also would like to thank our editors at Lippincott
of the surgical curriculum and methods to teach and evaluate Williams & Wilkins, Susan Rhyner, Jennifer Verbiar, and
what has been learned. Angela Collins.


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Lawrence_FM.indd viii 7/21/2012 6:20:15 PM
Mohammed I. Ahmed, MBBS, MS (Surgery) Richard M. Bell, MD
Clinical Instructor in Surgery Professor of Surgery
Affiliated Institute for Medical Education University of South Carolina School of Medicine
Chicago, Illinois Columbia, South Carolina

James Alexander, MD Juliane Bingener, MD

Associate Professor of Surgery Associate Professor of Surgery
Vice Chief for Education Mayo Clinic
Cooper Medical School of Rowan University Rochester, Minnesota
Camden, New Jersey
H. Scott Bjerke, MD
Adnan A. Alseidi, MD Clinical Professor of Surgery
Program Director Surgery Residents Kansas City University of Medicine and Biosciences
Co-Director HPB Fellowship Program Clinical Associate Professor of Surgery at UMKC
Hepato-Pancreato-Biliary Surgery Division Kansas City, Missouri
Virginia Mason Medical Center
Seattle, Washington Karen R. Borman, MD
Clinical Professor (Adjunct), Surgery
Gina L. Andrales, MD Temple University School of Medicine
Associate Professor of Surgery Senior Associate Program Director, General Surgery Residency
Dartmouth Medical School Abington Memorial Hospital
Lebanon, New Hampshire Abington, Pennsylvania

David Antonenko, MD Mary-Margaret Brandt, MD

Professor of Surgery Trauma Director and Surgical Intensivist
University of North Dakota School of Medicine and Health St. Joseph Mercy Hospital
Sciences Ann Arbor, Michigan
Grand Forks, North Dakota
Karen Brasel, MD, MPH
Lecia Apantaku, MD Professor of Surgery, Bioethics and Medical Humanities
Associate Professor of Surgery Medical College of Wisconsin
Chicago Medical School Milwaukee, Wisconsin
Rosalind Franklin University of Medicine and Science
North Chicago, Illinois Melissa Brunsvold, MD
Assistant Professor of Surgery
Tracey D. Arnell, MD University of Minnesota
Assistant Professor of Surgery Minneapolis, Minnesota
Columbia University College of Physicians & Surgeons
Memorial Sloan-Kettering Cancer Center Kenneth W. Burchard, MD
New York, New York Professor of Surgery
Dartmouth-Hitchcock Medical Center
Dimitrios Avgerinos, MD Lebanon, New Hampshire
Clinical Fellow
Department of Cardiothoracic Surgery Arnold Byer, MD
New York Presbyterian Weill Cornell Medical Center Clinical Professor of Surgery
New York, New York UMDNJNew Jersey Medical School
Newark, New Jersey
Melinda Banister, MD
General Surgeon
Lubbock, Texas


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Michael Cahalane, MD Gail Cresci, PhD, RD

Associate Professor of Surgery Research Staff
Harvard Medical School Digestive Disease and Lerner Research Institutes
Acting Chief, Division of Acute Care Surgery Departments of Gastroenterology and Pathobiology
Beth Israel Deaconess Medical Center The Cleveland Clinic
Boston, Massachusetts Cleveland, Ohio

Jeannette Capella, MD Brian J. Daley, MD

Medical Director, Trauma/Surgical ICU Professor, Department of Surgery
Assistant Medical Director, Trauma University of Tennessee Medical Center at Knoxville
Altoona Regional Medical Center Knoxville, Tennessee
Altoona, Pennsylvania
Dale A. Dangleben, MD
Frederick D. Cason, MD Associate Surgery Residency Program Director
Associate Professor Lehigh Valley Health Network
Residency Program Director Allentown, Pennsylvania
Section of Gastrointestinal and Minimally Invasive Surgery
Department of Surgery Debra A. DaRosa, PhD
The University of Toledo College of Medicine Professor of Surgery
Toledo, Ohio Vice Chair for Education
Northwestern University Feinberg School of Medicine
William C. Chapman, MD Chicago, Illinois
Professor and Chief, Section of Transplantation
Chief, Division of General Surgery Merril T. Dayton, MD
Washington University in St. Louis Professor and Chairman
St. Louis, Missouri Department of Surgery
State University of New York at Buffalo
Gregory S. Cherr, MD Buffalo, New York
Associate Professor of Surgery
Chief of Vascular Surgery, Buffalo General Hospital Chris de Gara, MBBS, MS
Director, Medical Student Surgical Education Professor of Surgery
Associate Program Directory, General Surgery Program Director, Division of General Surgery
State University of New York at Buffalo Department of Surgery, University of Alberta
Buffalo, New York Director, Department of Surgical Oncology
Cross Cancer Institute, Alberta Cancer Board
Jeffrey G. Chipman, MD Edmonton, Alberta, Canada
Associate Professor of Surgery
University of Minnesota Medical School Matthew O. Dolich, MD
Minneapolis, Minnesota Professor and Director, General Surgery Residency Program
University of California, Irvine
Nicholas P.W. Coe, MD Orange, California
Professor of Surgery
Tufts University School of Medicine Serge Dub, MD
Department of Surgery Professor of Surgery
Baystate Medical Center Faculty of Medicine
Springfield, Massachusetts University of Montreal
Montreal, Quebec, Canada
Annesley W. Copeland, MD
Assistant Professor of Surgery Gary L. Dunnington, MD
Uniformed Services University of the Health Sciences J. Roland Folse Professor and Chair of Surgery
Bethesda, Maryland Southern Illinois University School of Medicine
Springfield, Illinois
Julia Corcoran, MD
Associate Professor of Surgery Virginia A. Eddy, MD
Feinberg School of Medicine Director, Undergraduate Surgical Education
Northwestern University Maine Medical Center
Chicago, Illinois Portland, Maine

Wendy R. Cornett, MD Michael Edwards, MD

Associate Professor of Clinical Surgery Associate Professor of Surgery
University of South Carolina School of MedicineGreenville Georgia Health Sciences University
Greenville, South Carolina Augusta, Georgia

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Timothy M. Farrell, MD Mitchell H. Goldman, MD

Professor of Surgery Professor and Chairman
University of North Carolina at Chapel Hill Department of Surgery
Chapel Hill, North Carolina Assistant Dean for Research
University of Tennessee Graduate School of Medicine
Patrick Forgione, MD Knoxville, Tennessee
Associate Professor of Surgery
University of Vermont College of Medicine Oscar H. Grandas, MD
Fletcher Allen Healthcare Associate Professor of Surgery
Burlington, Vermont University of Tennessee at Knoxville
Surgical Director
Kevin N. Foster, MD Transplant Surgery Service and Vascular Access Center
Vice Chair for Education and Research University of Tennessee Medical Center at Knoxville
Director Arizona Burn Center Knoxville, Tennessee
Program Director, General Surgery residency
Department of Surgery James S. Gregory, MD
Maricopa Integrated Health Systems Director Intensive Care Services
Phoenix, Arizona Department of Surgery
Conemaugh Memorial Hospital
Glen A. Franklin, MD Johnstown, Pennsylvania
Associate Professor of Surgery
University of Louisville School of Medicine Oscar D. Guillamondegui, MD, MPH
Louisville, Kentucky Assistant Professor of Surgery
Vanderbilt University Medical Center
Shannon Fraser, MD, MSc Medical Director, Surgical Intensive Care
Assistant Professor Department of Surgery
McGill University Tennessee Valley Healthcare System, Veterans Affairs
Chief General Surgery Nashville, Tennessee
Jewish General Hospital
Montreal, Quebec, Canada Kenneth A. Harris, MD
Director of Education
Charles M. Friel, MD Royal College of Physicians and Surgeons of Canada
Associate Professor of Surgery Ottawa, Ontario, Canada
University of Virginia
Charlottesville, Virginia Alan E. Harzman, MD
Assistant Professor of Surgery
Gregory J. Gallina, MD The Ohio State University
Associate Director of Surgical Education Columbus, Ohio
Hackensack University Medical Center
Hackensack, New Jersey Imran Hassan, MD
Assistant Professor of Surgery
R. Neal Garrison, MD Southern Illinois University School of Medicine
Professor of Surgery Springfield, Illinois
University of Louisville School of Medicine
Louisville, Kentucky James C. Hebert, MD
Albert G. Mackay and H. Gordon Page Professor of Surgery
Jonathan Gefen, MD University of Vermont College of Medicine
Clinical Assistant Professor of Surgery Burlington, Vermont
Jefferson Medical College
Wynnewood, Pennsylvania Jonathan R. Hiatt, MD
Professor and Chief
Bruce L. Gewertz, MD Division of General Surgery
Surgeon-in-Chief Vice Chair for Education
Chair, Department of Surgery Department of Surgery
Cedars-Sinai Health System David Geffen School of Medicine at UCLA
Los Angeles, California Los Angeles, California

Steven B. Goldin, MD, PhD O. Joe Hines, MD

Associate Professor of Surgery Assistant Professor
Vice Chairman of Surgical Education Director, Surgery Residency Program
University of South Florida Department of Surgery
Tampa, Florida David Geffen School of Medicine at UCLA
Los Angeles, California

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Mary Ann Hopkins, MD D. Scott Lind, MD

Associate Professor of Surgery Professor and Chairman
Director of Education for the Clinical Sciences Department of Surgery
NYU School of Medicine Drexel University College of Medicine
New York, New York Philadelphia, Pennsylvania

Hwei-Kang Hsu, MD Kimberly D. Lomis, MD

Assistant Professor of Surgery Associate Professor of Surgery
State University of New York at Buffalo Associate Dean for Undergraduate Medical Education
Buffalo, New York Vanderbilt University School of Medicine
Nashville, Tennessee
Gerald A. Isenberg, MD
Professor of Surgery Fred A. Luchette, MD
Director, Surgical Undergraduate Education The Ambrose and Gladys Bowyer Professor of Surgery
Jefferson Medical College Medical Director, Cardiothoracic Critical Care Services
Program Director, Colorectal Residency, TJUH Department of Surgery
Philadelphia, Pennsylvania Stritch School of Medicine
Maywood, Illinois
Ted A. James, MD
Associate Professor of Surgery John Maa, MD
Division of Surgical Oncology Assistant Professor of Surgery
Director of Surgery Clerkship and Student Education University of California, San Francisco
University of Vermont College of Medicine San Francisco, California
Burlington, Vermont
Bruce V. MacFadyen Jr, MD
Daniel B. Jones, MD Moretz-Mansberger Professor of Surgery
Professor, Harvard Medical School Department of Surgery
Chief, Section of Minimally Invasive Surgery Georgia Health Sciences University
Beth Israel Deaconess Medical Center Augusta, Georgia
Boston, Massachusetts
Barry D. Mann, MD
Susan Kaiser, MD, PhD Chief Academic Officer, Main Line Health
Division of General Surgery Program Director, The Lankenau Surgical Residency Program
Jersey City Medical Center Professor of Surgery, Jefferson Medical College
Jersey City, New Jersey Wynnewood, Pennsylvania

Lewis J. Kaplan, MD Alan B. Marr, MD

Associate Professor of Surgery Professor of Surgery
Yale University School of Medicine Vice Chairman of Education
New Haven, Connecticut Department of Surgery
Louisiana State University Health Science Center
Alysandra Lal, MD New Orleans, Louisiana
Clinical Assistant Professor
Medical College of Wisconsin James A. McCoy, MD, PhD
Columbia St. Marys Hospital Professor of Surgery
Milwaukee, Wisconsin Morehouse School of Medicine
Atlanta, Georgia
Peter F. Lawrence, MD
Wiley Barker Endowed Chair in Vascular Surgery James F. McKinsey, MD
Director, Gonda (Goldschmied) Vascular Center Associate Professor and Chief
David Geffen School of Medicine at UCLA Division of Vascular Surgery
Los Angeles, California Columbia University
New York, New York
Jong O. Lee, MD
Assistant Professor of Surgery John D. Mellinger, MD
University of Texas Medical Branch Professor and Chair of General Surgery
Galveston, Texas Department of Surgery
Southern Illinois University School of Medicine
Susan Lerner, MD Springfield, Illinois
Assistant Professor of Surgery
The Mount Sinai Medical Center David W. Mercer, MD
New York, New York McLaughlin Professor and Chairman
Department of Surgery
Carlos M. Li, MD University of Nebraska Medical Center
Assistant Professor of Surgery Omaha, Nebraska
State University of New York at Buffalo
Buffalo, New York

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Hollis W. Merrick III, MD Jan Rakinic, MD

Professor, Surgery Associate Professor of Surgery
Chief, Division of General Surgery Chief, Section of Colorectal Surgery
Director, Undergraduate Surgical Education Program Director, SIU Program in Colorectal Surgery
The University of Toledo Vice Chair for Clinical Operations, Department of Surgery
Toledo, Ohio Southern Illinois University School of Medicine
Springfield, Illinois
James E. Morrison, MD
Assistant Professor of Surgery H. David Reines, MD
University of South Carolina School of Medicine Professor of Surgery
Columbia, South Carolina Virginia Commonwealth University
Vice Chair Surgery
Russell J. Nauta, MD InovaFairfax Hospital
Professor of Surgery Falls Church, Virginia
Harvard Medical School
Chairman, Department of Surgery Melanie L. Richards, MD
Mt. Auburn Hospital Professor of Surgery
Cambridge, Massachusetts Associate Dean of Graduate Medical Education
Mayo Clinic
Peter R. Nelson, MD Rochester, Minnesota
Assistant Professor of Surgery
Director, Surgery Clerkship Jeffrey R. Saffle, MD
University of Florida College of Medicine Professor of Surgery
Gainesville, Florida Director, Burn-Trauma ICU
University of Utah Health Sciences Center
Leigh Neumayer, MD, MS Salt Lake City, Utah
Professor of Surgery
University of Utah Health Sciences Center Hilary Sanfey, MD
Salt Lake City, Utah Professor of Surgery
Vice Chair for Education
John T. Paige, MD Southern Illinois University School of Medicine
Associate Professor of Clinical Surgery Springfield, Illinois
Louisiana State University School of Medicine
New Orleans, Louisiana Kennith H. Sartorelli, MD
Professor of Surgery
Tina L. Palmieri, MD The University of Vermont College of Medicine
Associate Professor and Director Burlington, Vermont
University of California Davis Regional Burn Center
Assistant Chief of Burns Kimberly D. Schenarts, PhD
Shriners Hospital for Children Northern California Affiliate Professor of Surgery
Sacramento, California Brody School of Medicine at East Carolina University
Greenville, North Carolina
Alexander A. Parikh, MD
Assistant Professor Paul J. Schenarts, MD
Division of Surgical Oncology Vice Chair, Department of Surgery
Vanderbilt University Medical Center University of Nebraska Medical Center
Nashville, Tennessee Omaha, Nebraska

Lisa A. Patterson, MD Mohsen Shabahang, MD, PhD

Associate Professor of Surgery Director, General Surgery
Tufts University School of Medicine Geisinger Medical Center
Trauma Director Danville, Pennsylvania
Department of Surgery
Baystate Health Saad Shebrain, MD
Springfield, Massachusetts Assistant Professor of Surgery
Michigan State University/Kalamazoo Center for Medical Studies
Elizabeth Peralta, MD Kalamazoo, Michigan
Associate Professor of Surgery
Southern Illinois University School of Medicine Timothy R. Shope, MD
Springfield, Illinois General Surgery
Hershey, Pennsylvania
Timothy A. Pritts, MD, PhD
Associate Professor of Surgery Ravi S. Sidhu, MD, PhD
Division of Trauma and Critical Care Assistant Professor
Department of Surgery Department of Surgery
University of Cincinnati College of Medicine University of British Columbia
Cincinnati, Ohio Vancouver, British Columbia, Canada

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Mary R. Smith, MD Samuel A. Tisherman, MD

Professor of Medicine and Pathology Professor
Associate Dean for Graduate Medical Education Departments of Critical Care Medicine and Surgery
The University of Toledo College of Medicine University of Pittsburgh
Toledo, Ohio Pittsburgh, Pennsylvania

David A. Spain, MD Judith L. Trudel, MD

Professor of Surgery Clinical Professor of Surgery
Chief, Trauma/Critical Care Surgery Division of Colon and Rectal Surgery
Stanford University School of Medicine Department of Surgery
Stanford, California University of Minnesota Medical School
St. Paul, Minnesota
Kimberley E. Steele, MD
Assistant Professor of Surgery Richard B. Wait, MD, PhD
Director of Adolescent Bariatric Surgery Professor of Surgery
The Johns Hopkins Center for Bariatric Surgery Tufts University School of Medicine
Baltimore, Maryland Chairman, Department of Surgery
Baystate Medical Center
Michael D. Stone, MD Springfield, Massachusetts
Professor of Surgery
Boston University School of Medicine James Warneke, MD
Chief of the Section of Surgical Oncology Associate Professor of Surgery
Boston Medical Center University of Arizona College of Medicine
Boston, Massachusetts Tucson, Arizona

John P. Sutyak, MD Jeremy Warren, MD

Associate Professor of Surgery Instructor
Director, Southern Illinois Trauma Center Department of Surgery
Southern Illinois University School of Medicine Georgia Health Sciences University
Springfield, Illinois Augusta, Georgia

Glenn E. Talboy Jr, MD Warren D. Widmann, MD

Professor of Surgery Associate Chair, Education and Training
Program Director, General Surgery Residency Program Director, Department of Surgery
University of MissouriKansas City School of Medicine Staten Island University Hospital
Kansas City, Missouri Clinical Professor of Surgery
State of New York Downstate Medical Center
J. Scott Thomas, MD New York, New York
Assistant Professor of Surgery
Program Director, General Surgery Residency Christopher Wohltmann, MD
Texas A&M Health Science Center Clinical Associate Professor of Surgery
Scott & White Memorial Hospital Southern Illinois University School of Medicine
Temple, Texas Springfield, Illinois

Areti Tillou, MD
Associate Professor
Associate Program Director
Department of Surgery
David Geffen School of Medicine at UCLA
Los Angeles, California

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Preface ...................................................................................v CHAPTER 5 90
Acknowledgments ............................................................... vii
Shock: Cell Metabolic Failure in Critical Illness
Contributors ......................................................................... ix
Kenneth W. Burchard, M.D.
Introduction .......................................................................xviii Karen Brasel, M.D., M.P.H.
Jeannette Capella, M.D.
CHAPTER 1 1 Timothy A. Pritts, M.D., Ph.D.

Perioperative Evaluation and Management

of Surgical Patients CHAPTER 6 110
Virginia A. Eddy, M.D. Surgical Critical Care
Tracey D. Arnell, M.D. Samuel A. Tisherman, M.D.
Kenneth A. Harris, M.D. Melissa Brunsvold, M.D.
Imran Hassan, M.D. Brian J. Daley, M.D.
James E. Morrison, M.D. James E. Morrison, M.D.
Paul J. Schenarts, M.D.
CHAPTER 2 33 Christopher Wohltmann, M.D.

Fluids, Electrolytes, and Acid-Base Balance

David Antonenko, M.D.
Mary-Margaret Brandt, M.D. Wounds and Wound Healing
H. David Reines, M.D. Glenn E. Talboy, Jr., M.D.
Hilary Sanfey, M.D. Annesley W. Copeland, M.D.
Areti Tillou, M.D. Gregory J. Gallina, M.D.


Nutrition Surgical Infections
Gail Cresci, Ph.D., R.D. R. Neal Garrison, M.D.
Bruce V. MacFadyen, Jr., M.D. Glen A. Franklin, M.D.
James S. Gregory, M.D. Oscar D. Guillamondegui, M.D., M.P.H.
Alan B. Marr, M.D. Lewis J. Kaplan, M.D.
Jeremy Warren, M.D. David A. Spain, M.D.


Surgical Bleeding: Bleeding Disorders, Hypercoagulable States, Trauma
and Replacement Therapy in the Surgical Patient Matthew O. Dolich, M.D.
Hollis W. Merrick III, M.D. H. Scott Bjerke, M.D.
Kevin N. Foster, M.D. Jeffrey G. Chipman, M.D.
Timothy R. Shope, M.D. Fred A. Luchette, M.D.
Ravi S. Sidhu, M.D. Lisa A. Patterson, M.D.
Mary R. Smith, M.D.
John P. Sutyak, M.D.


Lawrence_FM.indd xv 7/21/2012 6:20:15 PM


CHAPTER 10 187 CHAPTER 17 344

Burns Pancreas
Jeffrey R. Saffle, M.D. Steven B. Goldin, M.D., Ph.D.
Melinda Banister, M.D. Dimitrios Avgerinos, M.D.
Michael Cahalane, M.D. Alexander A. Parikh, M.D.
Jong O. Lee, M.D. Mohsen Shabahang, M.D., Ph.D.
Tina L. Palmieri, M.D.
CHAPTER 18 367
CHAPTER 11 202
Abdominal Wall, Including Hernia William C. Chapman, M.D.
Leigh Neumayer, M.D., M.S. Adnan A. Alseidi, M.D.
Dale A. Dangleben, M.D. Jonathan R. Hiatt, M.D.
Shannon Fraser, M.D., M.SC. Russell J. Nauta, M.D.
Jonathan Gefen, M.D. Michael D. Stone, M.D.
John Maa, M.D.
Barry D. Mann, M.D.
CHAPTER 19 390
CHAPTER 12 218 Breast
Gary L. Dunnington, M.D.
Esophagus Lecia Apantaku, M.D.
Carlos M. Li, M.D. Ted A. James, M.D.
James A. McCoy, M.D., Ph.D. Susan Kaiser, M.D., Ph.D.
Hwei-Kang Hsu, M.D. Elizabeth Peralta, M.D.

CHAPTER 13 244 CHAPTER 20 406

Stomach and Duodenum Surgical Endocrinology
John T. Paige, M.D. Thyroid Gland: Nicholas P.W. Coe, M.D. and Wendy R. Cornett, M.D.
Timothy M. Farrell, M.D. Parathyroid Glands: Karen R. Borman, M.D. and Melanie L. Richards, M.D.
Daniel B. Jones, M.D. Adrenal Glands: Richard B. Wait, M.D., Ph.D. and Alysandra Lal, M.D.
Saad Shebrain, M.D. Multiple Endocrine Neoplasia Syndromes: Karen R. Borman, M.D.
Kimberley E. Steele, M.D.
CHAPTER 21 429
CHAPTER 14 274
Spleen and Lymph Nodes
Small Intestine and Appendix James C. Hebert, M.D.
John D. Mellinger, M.D. Gina L. Andrales, M.D.
Serge Dub, M.D. Patrick Forgione, M.D.
Charles M. Friel, M.D. Kennith H. Sartorelli, M.D.
Alan E. Harzman, M.D. Warren D. Widmann, M.D.
David W. Mercer, M.D.
CHAPTER 22 450
CHAPTER 15 300
Diseases of the Vascular System
Colon, Rectum, and Anus James F. McKinsey, M.D.
Merril T. Dayton, M.D. James Alexander, M.D.
Gerald A. Isenberg, M.D. Arnold Byer, M.D.
Jan Rakinic, M.D. Gregory S. Cherr, M.D.
J. Scott Thomas, M.D. Bruce L. Gewertz, M.D.
Judith L. Trudel, M.D. Peter F. Lawrence, M.D.
Peter R. Nelson, M.D.
CHAPTER 16 327
CHAPTER 23 486
Biliary Tract
O. Joe Hines, M.D. Transplantation
Juliane Bingener, M.D. Hilary Sanfey, M.D., B.CH.
Frederick D. Cason, M.D. Mitchell H. Goldman, M.D.
Michael Edwards, M.D. Oscar H. Grandas, M.D.
Mary Ann Hopkins, M.D. Susan Lerner, M.D.

Lawrence_FM.indd xvi 7/21/2012 6:20:15 PM


CHAPTER 24 505 Appendix ........................................................................... 534

Glossary............................................................................. 547
Surgical Oncology: Malignant Diseases of the Skin Index .................................................................................. 561
and Soft Tissue
D. Scott Lind, M.D.
Mohammed I. Ahmed, M.B.B.S., M.S. (Surgery)
Chris de Gara, M.B.B.S., M.S.
James Warneke, M.D.

Lawrence_FM.indd xvii 7/21/2012 6:20:15 PM

Introduction: Transitioning to the
Role as a Junior Member of the
Surgical Health Care Team

You are about to embark on an immersive clinical experience 2. Quality of study methodsactive learning requires stu-
in surgery. It does not matter if you plan to be a surgeon; your dents to take responsibility for their learning. Disciplined
surgery clerkship will provide you with learning opportunities students recognize how they best learn and maintain an
that will help you hone clinical skills important to a physi- ongoing study plan that meets their learning style and
cian, regardless of chosen specialty. During your career as a needs.
doctor, you will undoubtedly encounter patients and family 3. Organizational skillssuccessful lifelong learners know
members who require surgical intervention, and the surgery how to arrange their time and priorities so as to avoid
clerkship can equip you with the knowledge and skills neces- stressful situations such as last-minute cramming.
sary to identify surgical diseases, recognize the type of surgi- 4. Motivation and emotionstudents enthusiasm and feel-
cal consult needed, and position yourself to better understand ings about the content to be learned, the people involved,
and empathize with the emotional, physiological, and logisti- and the learning environment can have a significant effect
cal experiences they will have, should an operation or consult on how a student experiences a clerkship and how their
be required. How you approach your role and responsibili- patients and team experiences and perceives them.
ties as a junior member of the surgical health care team will 5. Physical healththere is an undeniable link between how
determine the extent to which you enjoy and benefit from this a person feels physically and how well he or she learns.
incredible educational experience. Students need to pay attention to their own health needs.
You are already a well-seasoned learner or you would not 6. Distractibility and concentration skillsstudents must be
be in medical school. But the first day as a junior member on a active learners. Whether reading or listening to a lecture,
health care team, typically begun in your 3rd year of medical students who cant be fully attentive and engaged will have
school, is a profound transition and requires rethinking how difficulties deeply processing information and translating it
you approach learning and studying. It is no longer just about into useful knowledge. Its hard to learn when you are not
memorizing facts and then repeating them on a test. You now cognitively present or are sleeping!
have real patients who need your understanding of their pre- Your aim should be to take full advantage of every teachable
senting complaints and disease entities. You also have serious moment in your surgery clerkship. Here is how:
time constraints on reading, voluminous information needing
to be learned, and the challenge of determining the scope and
detail level of information needed to help your patients. These MAXIMIZE YOUR INTELLECTUAL CAPABILITIES
challenges are not insurmountable. Variables that typically
affect clinical performance include Prepare, practice, and review
Organize your knowledge
1. Preparatory coursework and experiencenew knowledge Know expectations and thyself
is constructed from existing knowledge. Learning is about Ask! Ask! Ask! Ask! Ask! Ask!
linking new information with what you already know. Stu-
dents who worked hard to do more than just memorize and
accomplished a deep knowledge of anatomy, for example, Prepare, Practice, and Review
will more easily associate what they are hearing, feeling, You need to prepare for your clinical and didactic learning
or seeing for the first time with this prior knowledge, to experiences by activating prior knowledge. This can be done
further form solidly constructed understanding. Remem- by prereading about the topics youll be exposed to the next
bering follows understanding. day, for example in a lecture session, in the operating room,


Lawrence_FM.indd xviii 7/21/2012 6:20:15 PM


or on rounds. Although few students read textual material Know Expectations and Thyself
before a lecture, empirical evidence shows that prereading Read the provided syllabus or Web site provided from the
increases comprehension and puts information into longer- clerkship director and carefully listen at orientation. Be crystal
term memory. It is somewhat akin to looking at a map before clear as to your role and responsibilities. If this cant be ascer-
going on a trip. You will know ahead of time where the route tained using the syllabus materials, then talk with students
changes and landmarks along the way. Just as looking at a who did well in prior clerkships, residents, or faculty. Most
map before a trip is an advanced organizer for your journey, surgeons value commitment, timeliness, and work ethic as
prereading is an advanced organizer for the topic to be learned highly as intelligence. Once you know what you are expected
or the operation to be seen. Youll glean the most from seeing to do and what you expect from yourself, you are set up to
a thyroid nodule or acute cholecystitis if youve read about it succeed. Secondly, think about what you want to glean from
beforehandmake the most of these learning opportunities this clerkship and outline your own learning goals. Dont be a
by preparing for them. reactive learner; instead be an active adult learner and have a
Practice is applied thinking and requires engaged learners. learning agenda in mind. For example, if assigned to attend
Be an active listener, carry an electronic or paper notebook, a breast surgeons clinic, reflect in advance and write what
and jot down one or two learning issues or questions that youd like to learn from that experience. Lastly, know your
surface during the day and then read about them with a pur- learning style. For example, if you are someone who learns
pose that evening. Note taking doesnt mean the transfer of better by talking through topics and issues, find a like-minded
the attendings lecture to your notebook without its passing study partner and do it. On the other hand, if you are a learner
through your brain! Studies have demonstrated that students who does best by sequestering yourself somewhere with no
who make their own notes have better retention than students distractions, find study spaces inside and outside the hospital
who do not. Jotting notes and self-generating questions about to accommodate yourself. The point is to be reflective about
the topic being addressed in a lecture or whatever learning this and plan your study approaches in advance.
environment embeds information into memory.
Reviewing information on an ongoing basis is critical to
retention. Use the test questions and patient management prob- Ask! Ask! Ask!
lems provided in this book to assess your understanding of Persistence and assertiveness are necessary in all clerkships
the material read. It is also helpful to create your own tests by including surgery. If you have a question, need performance
listing open-ended questions or copying charts or tables and feedback, or have unresolved learning issues, ask someone.
then blanking out portions to see if you can fill in the blanks. Most faculty and residents are happy to help a medical stu-
Review notes, flowcharts, tables and diagrams, and test ques- dent who shows interest and is invested in their learning. And
tions while looking for patterns. Re-review throughout the if they are too busy at the time and you happen to be told
clerkship. Spending as little as 30 minutes per day can help no just say to yourself next and go to someone else. It
reinforce information and significantly affect recall capabilities. is not personal. Everyone who works with you knows things
you dont know. If you are wise, youll learn from everyone
Organize Your Knowledge on or near the surgery team including nurses, physician assis-
tants, pharmacists, social workers, and technicians. They cant
You can organize your knowledge by taking three steps to read your mind though, so even timid individuals will need to
studying. reach out and ask for feedback, for assistance, or for answers
1. Get the big picture first. Prior to reading a book chapter, as needed.
review the learning objectives listed at the start of the chap-
ter. Review the headings and subheadings to get a sense of
how the author organized the information presented and MAXIMIZE YOUR EMOTIONAL INTELLIGENCE
what s/he thinks is important for you to learn. Also, review
the questions before you read to get an additional sense of Focus forward with a positive attitude
what the author finds important. You can also list questions Set goals and celebrate successes
you have about the topic and then read the chapter with this Promote a supportive learning environment
purpose in mind.
2. Review the charts, tables, and diagrams. Authors emphasize Focus Forward with a Positive Attitude
key information in these and are an excellent source for It is not what happens to you in the clerkship that matters, it
study. As noted above, it is excellent practice to eliminate is how you respond to it that determines the outcome. Make
parts of the table, chart, and diagram and test yourself to decisions about how you respond to situations or challenges
see if you know the missing information. with the end in mind. You cant always control situations,
3. Emphasize integration. As you read each chapter, exam- but you can control your response to them. If a resident or
ine the information to see how it relates to a patient you faculty member is having a bad or overly intense day, seek
may have seen, a lecture you attended, an image you may to have enough situational awareness to maintain a positive
have reviewed, etc. Create your own mind maps or concept perspective. Anticipate in the operating room when questions
maps that help to organize the information in your mind might be welcome and when a surgeon needs to concentrate.
and create patterns where appropriate. Many senior faculty A student with high emotional intelligence maintains an open
use memories of former patients to fix surgical principles mind, approaches responsibilities with positive energy and
in their minds. enthusiasm, and seeks to make a constructive difference in his
Search for relationships between ideas and concepts, and note or her patients and team members days. This doesnt mean
anything confusing or difficult to comprehend for follow-up we should maintain an artificial positive attitude when things
through reading or discussions with peers, residents, or faculty. are going awry, because focus forward is not about denying

Lawrence_FM.indd xix 7/21/2012 6:20:16 PM


what we feel. Forward focus is about managing energy and negative attitudes and behaviors. They constantly are com-
focusing on solutions and not just problems. We go toward plaining about someone or something, and can suck the pos-
what we focus on. itive energy out of anyone or team. They are rigid in their
thinking and highly judgmental. If their negativity is fed, it
Set Goals and Celebrate Successes becomes contagious and results in reduced productivity, lower
morale, and frustration. Negaholism creates a pessimistic
Mature-minded learners are specific about what they want to learning environment and is damaging to the teams esprit de
achieve. They dream big dreams and are committed to achiev- corps and functionality. It is important to not get caught up in
ing them. Surgery clerks should start their clerkship by defining their negativity netavoiding these individuals helps neutral-
goals of what they desire to glean from the clerkship experience ize their effect.
and how achievement of these goals will move them toward An important element to creating a supportive learning
their long-range mission. I encourage all students to document environment is to take care of those learners behind you,
their short- and long-range goalsgoals that are achievable, beside you, and in front of you. This establishes trust among
believable, conceivable, desirable, measurable, growth facili- team members, which is what makes a team productive and
tating, and life enhancing! What we write tends to manifest effective and the learning environment supportive.
itself internally rather than serving as passing thoughts. Goals The electronic portion of this book includes a chapter enti-
should address what one wants to accomplish as a learner, but tled Maximally Invasive Learning that includes specific
can also include financial goals, relationship goals, as well as suggestions on how to address five common questions faced
goals about the values you want to reflect and practice. Goals by students in the surgery clerkship including
set directionif you dont know where you are going, you are
not likely to get there! The notebook should also include a sec- Problem One: What exactly is my role? What are the expecta-
tion for documenting successeslarge and small. Overachiev- tions?
ers and leaders tend to meet a goal and simply move to the next Problem Two: There is not enough time to read.
one without taking the time to appreciate and honor what they Problem Three: I am getting little or no feedback.
accomplished. Being able to reread written accomplishments Problem Four: How can I do well on examinations?
serves as a useful reminder of all youve done well, which can Problem Five: What does it take to be an honors student?
be especially lifting and reinforcing to ones self-confidence Although there is overlap between this Introduction and the
and sense of accomplishments when needed. electronic chapter, since they are mutually based on learning
principles, Id encourage students who want to do well in their
surgery clerkship to read both for a more comprehensive over-
Promote a Positive Learning Environment view on successful learner practices.
You are going to make mistakes. A good thing about being the In summary, approach the surgery clerkship with a fire in
junior member of a patient care team is that you have many your belly! Do all you can to earn your credibility as a junior
layers of expertise to help defray them. Your team mem- member of the surgery health care team by taking measures
bers will have made mistakes themselves. The key is to take to maximize your intellectual capabilities and advance your
responsibility for mistakes by owning up to them, and learn- emotional intelligence. Lastly, keep in mind John Woodens
ing from them so they arent repeated. sage advice. He advised that although tempting when you are
Avoid keeping company with negative people or nega- in a competitive, busy, and complex environment, never try to
holics. These individuals are not unique to surgery, and are be better than anyone else, but never cease to be the best you
important to be aware of, as they can create serious chaos can be. That is all you need to be successful in the surgery
for the team. Negaholics are individuals who are beset with clerkship, and frankly, in life as well.

Lawrence_FM.indd xx 7/21/2012 6:20:16 PM

Perioperative Evaluation and
Management of Surgical Patients

1. Describe the value of the preoperative history, physical 7. Discuss the effect of renal dysfunction, hepatic dysfunction,
examination, and selected diagnostic and screening tests. diabetes, adrenal insufficiency, pregnancy, and advanced age
2. Describe the important aspects of communication skills. on preoperative preparation and postoperative management.

3. Discuss the role of outside consultation in evaluating a 8. Describe the documentation required in the medical record
patient undergoing an elective surgical procedure. of a surgical patient, including physicians orders and daily
progress notes.
4. Discuss the elements of a patients history that are essential
in the preoperative evaluation of surgical emergencies. 9. Describe the most commonly used surgical tubes and
5. Discuss the appropriate preoperative screening tests.
10. Discuss common postoperative complications and their
6. Discuss the assessment of cardiac and pulmonary risk. treatment.

PREOPERATIVE EVALUATION patient should be established, maintained, and valued. Good

interviewing techniques are fundamental in establishing a
Surgery and anesthesia profoundly alter the normal physi- good relationship. The basis for good interviewing comes from
ologic and metabolic states. Estimating the patients ability a genuine concern about people, although there are interview-
to respond to these stresses in the postoperative period is ing skills that can be learned and that can improve the quality
the task of the preoperative evaluation. Perioperative com- of the interaction. Medical students should also acknowledge
plications are often the result of failure, in the preoperative their own special role in the patients care. Students should
period, to identify underlying medical conditions, maximize not be ashamed of their status, or feel that they are ineffec-
the patients preoperative health, or accurately assess periop- tive members of the team. Patients commonly view medical
erative risk. Sophisticated laboratory studies and specialized students as more accessible and will often share details with
testing are no substitute for a thoughtful and careful history them that they might withhold from the more senior mem-
and physical examination. Sophisticated technology has merit bers of the team. Also, the intensity and enthusiasm of the
primarily in confirming clinical suspicion. intelligent novice is a definite asset that can be brought to the
This chapter is not a review of how to perform a history patients great advantage. The role of the student is to dis-
and physical examination. Instead, this discussion is a review cover the patients chief medical complaint, perform a focused
of the elements in the patients history or findings on physi- history and physical examination, and present the findings to
cal examination that may suggest the need to modify care in the resident or faculty member. Interviewing a patient well
the perioperative period. Other chapters discuss the signs and requires communicating to the patient who you are and how
symptoms of specific surgical diagnoses. you fit into the team.
Effective interviewing can be challenging because of the
PHYSICIANPATIENT COMMUNICATION variety of settings in which interviews occur. These set-
tings include the operating room, the intensive care unit,
a private office, a hospital bedside, the emergency room,
Interviewing Techniques and an outpatient clinic. Each setting presents its own chal-
The physicianpatient relationship is an essential part of lenges to effective communication. To achieve good phy-
surgical care. The relationship between the surgeon and sicianpatient relationships, surgeons adjust their styles to

Lawrence_Chap01.indd 1 7/21/2012 5:56:58 PM


the environment and to each patients personality and needs. she is in a state of total helplessness. There is an immense duty
Some basic rules are common to all professional interviews. on the part of the surgeon to merit this level of trust. Part of
The first rule is to make clear to the patient that during the earning this trust involves honest discussions with patients and
history and examination, nothing short of a life-or-death their families about available choices (including the choice to
emergency will assume greater importance than the interac- not operate) and their consequences.
tion between the surgeon and the patient at that moment. Once the surgeon has gathered information sufficient to
This is our first, and best, chance to connect with the patient. identify the likely problem and its contributory factors, the
The patient must come to understand that a caring, knowl- surgeon then identifies a number of reasonable courses of
edgeable, and dedicated surgeon will be the patients part- action to pursue the evaluation or treatment of the patients
ner on the journey through the treatment of surgical disease. problem. These strategies are discussed in laymans terms
The surgeon should observe certain other rules, including with the patient (and family where appropriate). Together, the
giving adequate attention to personal appearance to present patient and the surgeon select the course of action that seems
a professional image that inspires confidence; establishing best. This is what is meant by informed consent. Informed
eye contact; communicating interest, warmth, and under- consent is a process, not an event, and not a form. It is the
standing; listening nonjudgmentally; accepting the patient process wherein the patient and surgeon together decide on
as a person; listening to the patients description of his or a plan. Informed consent is different from a consent form. A
her problem; and helping the patient feel comfortable in consent form is intended to serve as legal documentation of
communicating. these discussions between the physician and the patient. It
When the patient is seen in an ambulatory setting, the first is an unfortunate reality that consent forms must serve as a
few minutes are spent greeting the patient (using the patients shield behind which care providers may take shelter should
formal name); shaking hands with the patient; introducing a tort claim be filed against them. The process of informed
himself or herself and explaining the surgeons role; attending consent serves the more noble cause; consent forms serve
to patient privacy; adjusting his or her conversational style and the more mundane cause. Informed consent often takes place
level of vocabulary to meet the patients needs; eliciting the not just in one session, but over time, in multiple sessions, as
patients attitude about coming to the clinic; finding out the the patient has time to digest the information and formulate
patients occupation; and determining what the patient knows further questions.
about the nature of his or her problem. Sometimes, patients cannot speak for themselves. In these
The next step involves exploring the problem. To focus the situations, the health care team will turn to those who might
interview, one moves from open-ended to closed-ended ques- reasonably be thought to be able to speak on behalf of the
tions. Important techniques include using transitions; asking patient. Usually, but not always, this is the next of kin. (The
specific, clear questions; and restating the problem for verifi- reader is strongly encouraged to become familiar with perti-
cation. At this point, it is important to determine whether the nent state law on this matter.) These individuals are known
patient has any questions. Near the end of the interview, the as surrogate decision makers. Another concept that arises
surgeon explains what the next steps will be and that he or she in this context is advance directives. Advance directives are
will examine the patient. Last, the surgeon should verify that legal documents that inform care providers about the general
the patient is comfortable. wishes of the patient regarding level of care to be delivered
Most of the techniques used in the ambulatory setting are should the patient not be able to speak for himself or herself.
also appropriate for inpatient and Emergency Department Most people wish to receive enough medical care to allevi-
encounters. Often, more time is spent with the patient in the ate their suffering and to give them a reasonable chance of
initial and subsequent interviews than in an outpatient set- being able to enjoy the remainder of their life in a functional
ting. At the initial interview, patients are likely to be in pain, manner. The definitions of reasonable and functional will
worried about financial problems, and concerned about lack vary among individuals, but these are the causes that advance
of privacy or unpleasant diets. They may also have difficulty directive documents are intended to serve.
sleeping, be fearful about treatment, or feel helpless. It is Finally, there will be times when there is nobody present
important to gently and confidently communicate the purpose who can speak for the patient in a time frame that per-
of the interview and how long it will take. mits acceptable medical care. In these circumstances, the
The patient is not only listening, but also is observing the physician must remember that the first duty is to the patient,
physicians behavior and even attire. The setting also affects and that duty is to improve the patients life. Improving life
the interview. For example, a cramped, noisy, crowded envi- is not always the same thing as prolonging life. It is the duty
ronment can affect the quality of communication. Patients of the physician to manage this aspect of the patients care
may have negative feelings because of insensitivities on the in a reverential and respectful manner. There will be times
part of the physician or others. Examples include speaking when Physicians must make difficult judgments about mat-
to the patient from the doorway, giving or taking personal ters of life and death. The responsible physician does so,
information in a crowded room, speaking about a patient in expeditiously and thoughtfully, without attempting to evade
an elevator or another public space, or speaking to a patient the painful dilemmas that arise.
without drawing the curtain in a ward. It is important to begin to address the issues of informed
consent and end-of-life care early on in the relationship
Informed Consent between surgeon and patient. This is not so much a legal issue
The relationship between a patient and his or her surgeon is as one of matching the care offered to the specific situation
one of the strongest in any professional endeavor. The patient of the patient. For example, if a patient with end-stage car-
comes to the surgeon with a problem, the solution to which diomyopathy is felt to be too fragile for elective aortic
may include alteration of the patients anatomy while he or aneurysmorrhaphy, that patient is almost certainly a terrible

Lawrence_Chap01.indd 2 7/21/2012 5:56:58 PM


candidate for emergent repair of a ruptured aneurysm. Con- cardiorespiratory, renal, hematologic, nutritional, and endo-
versely, an otherwise healthy 18-year-old patient who comes crine systems. Within the nutritional review is sought infor-
in for an elective herniorrhaphy will not require the same mation about appetite and weight change, which can impact
degree of delicate issue exploration as the first patient men- healing. Further, information about the timing of the patients
tioned. However, they should be informed that unexpected last meal can affect the timing of urgent (but not emergent)
complications could sometimes arise, including death. They operations. A full stomach predisposes the patient to aspira-
should also be informed that the treating team will manage tion of gastric contents during the induction of anesthesia. If
any unusual events to the best of their ability. In all cases, the the patients disease process permits, it is generally best to
surgeon must be careful to explain that while they are compe- allow gastric emptying to occur as much as possible prior to
tent and compassionate, they are also human. induction of anesthesia. This usually takes about 6 hours of
The student is referred to any number of excellent sources strict nil per os status. If anesthesia must be induced emer-
for further information on the subject of medical ethics. (See gently, the rapid sequence induction technique is used to
bonus chapter on medical ethics at http://thepoint.lww.com). optimize the chances for safe endotracheal intubation without
Another example is The Hastings Center Report, a journal aspiration.
devoted to ethical issues. Family history likewise should record the specific ques-
tions asked and the patients actual responses. For example,
family histories of bleeding diatheses, or bad reactions to gen-
History eral anesthesia, are of obvious interest to the surgical team, as
A careful history is fundamental to the preoperative evaluation would a history of myocardial infarction or malignancy in all
of the surgical patient, whether for an elective or emergent of the patients first-degree relatives.
operation. It is here that the doctor learns about comorbidi- Determining allergies and drug sensitivities is important
ties that will influence the patients ability to withstand and and will influence selection of such critical interventions as
recover from the operation. This understanding begins with perioperative antibiotics and anesthetic technique.
a careful review of systems intended to elicit problems that, A medication history should also be taken. This history
although perhaps not the focus of the patients surgical experi- includes prescription drugs, over-the-counter agents, and
ence, are nonetheless important to his or her ability to recover herbal remedies (nutraceuticals). Many prescription drugs
from the operation. The following sections will consider have important implications in perioperative patient manage-
the ways in which certain historical findings can influence ment and are detailed in Table 1-1. Some drugs adversely
a patients perioperative risk, and what further evaluation interact with anesthetic agents or alter the normal physiologic
should be prompted by the discovery of certain aspects of the response to illness, injury, or the stress of surgery. For example,
patients history. patients who take -blocking agents cannot mount the usual
The history of the present illness (HPI) will obviously chronotropic response to infection or blood loss. Anticoagu-
direct the lines of inquiry. Within the context of the HPI, a his- lants such as warfarin compounds or antiplatelet agents can
tory of the events that preceded the accident or onset of illness carry specific risks, both if they are continued in the surgical
may give important clues about the etiology of the problem period and if they are discontinued perioperatively. Patients
or may help to uncover occult injury or disease. For example, and/or families should also be questioned about the use of
the onset of severe substernal chest pain before the driver of a dietary supplements and over-the-counter medications. The
vehicle struck a bridge abutment may suggest that the hypo- popularity of complementary and alternative medicines and
tension that the driver exhibited in the emergency department the use of nutraceuticals have dramatically increased world-
may be related to acute cardiac decompensation from a myo- wide. Patients should be asked specifically about these, as
cardial infarction as well as from blood loss associated with a many do not regard them as medicines. Many of these nutra-
pelvic fracture. Such a situation might require modification of ceuticals have the potential to adversely affect the administra-
hemodynamic monitoring and volume restoration. Although tion of anesthetic agents, hypnotics, sedatives, and a variety of
such scenarios sound extreme, they are encountered in emer- other medications. Some are thought to interfere with platelet
gency departments on a daily basis. These historical elements function and coagulation, and others to potentiate or reduce
add significantly to the physicians ability to provide optimal the activity of anticoagulants and some immunosuppressants.
patient care. These products have been classified as supplements and are
Most clinical situations provide an adequate opportunity not regulated by the Food and Drug Administration. As a con-
for a careful review of systems. Occasionally, patients cannot sequence, robust scientific studies concerning their mecha-
provide details of their illness, and then available resources, nism of action, herbdrug interactions, active drug content,
including family, friends, previous medical records, and effectiveness, and potential side effects are difficult to iden-
emergency medical personnel, will be used to glean what tify. Further, reliable information regarding these products is
information is available. A review of systems, with emphasis difficult to obtain. The sheer number of preparations available
on estimating the patients ability to respond to the stress of makes it difficult, if not impossible, to compile detailed infor-
surgery, is imperative. It is sometimes tempting to attempt to mation on all of them.
summarize a lengthy review of systems with statements such Common nutraceuticals are listed in Table 1-2, along with
as review of systems is negative. This terminology should their indications for use and potential adverse side effects. The
be avoided. It is often important to know exactly what the American Society of Anesthesiologists (ASA) recommends
patient was asked, what they affirmed, and what symptoms discontinuation of these supplements for 2 to 3 weeks prior to
they denied experiencing. Therefore, specific questions an operative procedure, but this recommendation is not based
should be asked and specific answers documented. Areas of on sound scientific evidence. The hospital pharmacist or Doctor
focus, explored more fully below, include in particular the of Pharmacy is an excellent resource for questions in this area.

Lawrence_Chap01.indd 3 7/21/2012 5:56:58 PM


TABLE 1-1 Perioperative Medication Management

Drug Type Comment Preoperative Management Postoperative Management

-blockers Abrupt discontinuation can increase With a sip of water a few hours Parenteral agent until taking p.o.
risk of MI before operation
Atrial antiarrhythmics With a sip of water a few hours IV -blockers, diltiazem or digoxin until
before operation p.o. intake resumed
Ventricular Monitor Mg, K, and Ca levels periop- With a sip of water a few hours Parenteral amiodarone or procainamide
antiarrhythmics eratively before operation
Nitrates Transdermal (paste, patch) may be With a sip of water a few hours Intravenous (most reliable) or transdermal
poorly absorbed intraoperatively before operation until p.o. intake resumed
Antihypertensives Abrupt discontinuation of clonidine can With a sip of water a few hours Parenteral antihypertensives; if on
cause rebound hypertension before operation clonidine, consider clonidine patch or
alternative antihypertensive agents
Inhalers No modification necessary Can use nebulized or metered dose
Leukotriene inhibitors With a sip of water a few hours
before operation
Insulin 5% dextrose solutions should be given dose usual long-acting agent SSI until p.o. intake back to baseline
intravenously intra- and postopera- at the usual time preoperatively
tively in patients receiving insulin
Oral agents (except Hold AM of operation SSI until p.o. intake back to baseline
Metformin Can produce lactic acidosis, particularly Hold for at least 1 day preop- Monitor renal function closely. Resume
in the setting of renal dysfunction or eratively metformin when renal function normal-
with administration of IV radio- izes, usually 23 days postoperatively.
graphic contrast agents SSI until then.
Antiplatelet agents/anticoagulants
Aspirin, clopidogrel, D/C 7 days preoperatively Resume when diet resumed
Warfarin Hold until INR normalizes, usually Resume when diet resumed
35 days. If anticoagulation
critical, maintain anticoagula-
tion with heparin
Heparin Discontinue 4 hr preoperatively Resume 612 hr postoperatively, pro-
vided no increased risk of hemorrhage
thought to exist
Osteoporosis agents
SERMs Associated with increased risk of DVT Hold 1 week preoperatively for
procedures with moderate to
high risk DVT
HIV agents With a sip of water a few hours Resume when taking p.o.
before operation
Antiparkinson agents
Carbidopa/levodopa Prolonged cessation of levodopa can With a sip of water a few hours
lead to syndrome similar to neuro- before operation
leptic malignant syndrome
Seligilene Life-threatening syndrome similar to Avoid use with meperidine Avoid use with meperidine
neuroleptic malignant syndrome
reported when used with meperidine
Antiseizure medications With a sip of water a few hours Parenteral agents until p.o. intake
before operation resumed

Lawrence_Chap01.indd 4 7/21/2012 5:56:58 PM


TABLE 1-1 Perioperative Medication Management (continued)

Drug Type Comment Preoperative Management Postoperative Management

Tricyclic Anticholinergic effects and conduction Monitor for anticholinergic side effects
antidepressants abnormalities can be seen
Monoamine oxidase Life-threatening hypertension reported Stop 2 weeks preoperatively
inhibitors when used with certain sympatho-
mimetics; life-threatening syndrome
similar to neuroleptic malignant
syndrome reported when used with
SSRIs Serotonin syndrome reported With a sip of water a few hours Resume as soon as possible
when used with tramodol; some before operation postoperatively
agents have associated withdrawal
Antipsychotics Can cause ECG abnormalities (pro- Resume as soon as possible
longed QT interval) postoperatively
Lithium Monitor levels perioperatively Resume when p.o. intake resumes
Benzodiazepines Abrupt cessation can cause withdrawal Parenterally until diet resumed
Levothyroxine Can be held for a few days if Parenterally until diet resumed
needed without adverse effect
Propylthiouracil Preoperative blockade for Parenteral blockers; resume PTU when
hyperthyroid patients; preop- medications can be given via NG tube
erative potassium iodide
Estrogen Can increase risk of postoperative DVT Consider stopping for 4 weeks
prior to cases with high risk
of DVT
Methotrexate Does not interfere with wound healing Continue usual regimen Resume when taking p.o.
or increase wound infection rate
COX-2 inhibitors Can impair renal function Hold 23 days preoperatively Resume when taking p.o.
SSI, sliding scale insulin; SERM, selective estrogen receptor modulator; SSRI, selective serotonin reuptake inhibitors.
From Mercado DL. Perioperative medication management. Med Clin North Am 2003;87(1):4157.

Even in a surgical emergency, serious efforts must be made practice is expensive and unwarranted. In fact, the potential
to acquire essential historical information about the patient. harm caused by the routine screening of asymptomatic
An emergency situation does force the physician to focus on patients is greater than any benefit derived from uncover-
the critical aspects of the patients history. The mnemonic ing occult abnormalities. The time and resources necessary
AMPLE history (Allergies, Medications, Past medical his- to chase unanticipated results, the occasional performance of
tory, Last meal, Events preceding the emergency) is a con- additional invasive (and risky) secondary procedures, and the
venient way to remember the essential elements during a very fact that 60% of these abnormal results are ignored are argu-
time-pressured encounter. ments against unselected screening. If there is a legal liability
issue surrounding preoperative screening, the latter is the most
significant one. Obtaining data to establish a baseline is not
PREOPERATIVE SCREENING TESTS AND recommended for the asymptomatic patient. Normal labora-
CONSULTATIONS tory results obtained within 4 months of an elective operative
procedure need not be repeated, since abnormalities could be
predicted based on the patients history. Preoperative screen-
Interpretation of Laboratory and Diagnostic Data ing tests are not a substitute for a comprehensive history and
It is standard practice in most North American hospitals for physical examination focused to identify comorbidities that
doctors to order a battery of routine preoperative screening may influence perioperative management. The need for emer-
tests on otherwise asymptomatic patients under the mistaken gency surgery, especially for patients who cannot provide his-
belief that this practice improves patient safety, and outcome, torical data, obviously alters these recommendations.
by identifying unsuspected conditions that could contribute Routine screening of hemoglobin concentration is per-
to perioperative morbidity and mortality. This indiscriminate formed only in individuals who are undergoing procedures that

Lawrence_Chap01.indd 5 7/21/2012 5:56:59 PM


TABLE 1-2 Nutraceuticals: Proposed Use and Adverse Effectsa

Product Use Potential Side Effects

Echinacea (Echinacea species) Prevent and treat upper respiratory infections Immunosuppression (?)
Ephedra Sympathomimetic Vasoconstriction, MI, CVA, herb-drug interaction with MAO-inhibitors
Feverfew (Tanacetum parthenium) Anti-inflammatory, arthritis, migraine headache Oral ulcers, abdominal pain, bleeding
Garlic (Allium sativum) Cholesterol reduction, anticoagulant, Irreversible antiplatelet activity (?)
antihypertensive, antimicrobial (?)
Excessive bleeding
Ginger (Zingiber officinale) Digestive aide, diuretic, antiemetic, stimulant Thromboxane synthetase inhibitor
Ginkgo (Ginkgo Biloba) Anticoagulant Increased anticoagulant effects, bleeding
Ginseng (Panax Ginseng) Lowers blood sugar, inhibits platelet aggregation Hypoglycemia, bleeding, potentiates warfarin
Glucosamine Inhibits DNA synthesis (?)
Kava (Piper methysticum) Sedation, anxiolytic Addiction, withdrawal, increased sedative effects, extrapyramidal
effects, (?) hepatitis, GI discomfort, false-negative PSA, hyperten-
sion, urinary retention
Saw Palmetto (Serenoa repens) Prostatic health (BPH) Contraindication in women
Saint Johns wort (Hypericum perforatum) Cerebral failure Inhibition of neurotransmitter uptake, multiple herbdrug interactions
including cyclosporin, warfarin, steroids, calcium-channel blockers,
and others.
Valerian (Valeriana officinalis, vandal root) Sedative Withdrawal, enhanced sedative effects of hypnotics, sedatives,
This table of commonly used supplements is neither all-inclusive nor comprehensive. Many of the potential adverse effects and herbdrug interactions are based on anecdotal reports or small,
uncontrolled case studies.

are associated with an extensive amount of blood loss, or who and electrolytes, including those receiving long-term diuretic
may be harboring anemia unbeknownst to the treating team. therapy, and those with intractable vomiting, should also have
Patients with a history of anemia, malignant disease, renal preoperative determination of serum electrolytes. The elderly
insufficiency, cardiac disease, diabetes mellitus, or pregnancy are at substantial risk for chronic dehydration, and testing is
should have baseline determinations of serum hemoglobin appropriate in these patients as well. Although there is no
concentration. Individuals who cannot provide a history or specific age that mandates automatic electrolyte screening,
who have physical findings that suggest anemia should have knowledge of the patients medical history, medications, and
preoperative baseline hemoglobin determinations. The precise systems review should guide decision making about testing.
definition of extensive blood loss will vary depending on the Preoperative urinalysis is recommended only for patients
patients age and comorbidities. For example, patients with who have urinary tract symptoms or a history of chronic uri-
known coronary artery disease should not be allowed to have a nary tract disease, or in those who are undergoing urologic
postoperative hemoglobin level below 7 g/dL. If such a patient procedures.
is scheduled to undergo a breast biopsy or a hernia repair, and Screening chest radiography is rarely indicated. Despite
they are not known to be anemic, it is unlikely that the blood loss the occasional incidental abnormality that is detected with
associated would precipitate an acute cardiac event. In general, a screening radiograph, these findings rarely receive further
major vascular or musculoskeletal operations on the extremi- investigation and generally do not alter the surgical plans.
ties or operations in the chest or abdomen carry enough risk of Screening chest radiography in asymptomatic elderly patients
severe (>500 mL) blood loss to justify a demonstration before- is also controversial because the usefulness of this diagnos-
hand that the patient has sufficient oxygen-carrying capacity tic study in this population is unclear. Chest radiography is
to withstand the stress of the planned procedure, particularly if recommended for patients who are undergoing intrathoracic
there are significant comorbidities (e.g., cardiac failure, chronic procedures and for those who have signs and symptoms of
obstructive pulmonary disease [COPD], end-stage renal disease active pulmonary disease.
[ESRD]). The groups of patients in whom anemia is suspected Recommendations for screening electrocardiography are
preoperatively would include patients with a history of anemia, more firm. Men who are older than 40 years of age and
malignant disease, renal insufficiency, cardiac disease, diabe- women who are older than 50 years of age should have a
tes mellitus, or pregnancy, or patients whose cardiorespiratory baseline recording. Patients with symptomatic cardiovascular
review of systems suggests exertional dyspnea. disease, hypertension, or diabetes are candidates for preopera-
Evaluation of baseline serum electrolyte concentrations, tive electrocardiography screening. Patients who are under-
including serum creatinine, is appropriate in individuals going thoracic, intraperitoneal, aortic, or emergency surgery
whose history or physical examination suggests chronic medi- are also candidates for screening examinations. In summary,
cal disease (e.g., diabetes, hypertension, cardiovascular, renal, laboratory and other diagnostic screening tests should be per-
or hepatic disease). Patients with the potential for loss of fluids formed only on those patients found to be at risk for specific

Lawrence_Chap01.indd 6 7/21/2012 5:56:59 PM


TABLE 1-3 Recommendations for Laboratory Testing before Elective Surgery

Incidence of Abnormalities
Test That Change Management LR+ LR Indications

Hemoglobin 0.1% 3.3 0.90 Anticipated major blood loss or symptoms/history of anemia
White blood count 0.0% 0.0 1.0 Symptoms suggestive of infection, myeloproliferative disease,
myelotoxic medications
Platelet count 0.0% 0.0 1.0 History of bleeding disorder/bruising, myeloproliferative
disease, myelotoxic medications, splenomegaly
Prothrombin time 0.0% 0.0 1.0 History of bleeding disorder/bruising, chronic liver disease,
malnutrition, recent or long-term antibiotic/warfarin use
Partial thromboplastin time 0.1% 1.7 0.86 History of bleeding diathesis, anticoagulant medication
Electrolytes 1.8% 4.3 0.80 Chronic renal insufficiency, CHF, diuretic use, other meds that
affect electrolytes
Renal function tests 2.6% 3.3 0.81 Age 50, hypertension, cardiac disease, major surgery, medica-
tions that may alter renal function
Glucose 0.5% 1.6 0.85 Obesity, known diabetes or symptoms thereof
Liver function tests 0.1% No indication, consider albumin measurement for major
surgery or chronic illness
Urinalysis 1.4% 1.7 0.97 No indication
Electrocardiogram 2.6% 1.6 0.96 Men > 40, women > 50, known coronary artery disease,
diabetes or hypertension
Chest x-ray 3.0% 2.5 0.72 Age > 50, known cardiac or pulmonary disease or symptoms
or exam findings suggesting cardiac or pulmonary disease
LR+, Likelihood ratio that a test will be abnormal in the absence of symptoms or signs; LR, Likelihood ratio that a test will be normal in the absence of symptoms or signs; CHF, congestive heart failure.
Adapted and used with permission from Smetana GW, Macpherson DS. The case against routine preoperative laboratory testing. Med Clin North Am 2003;87(1):740.

comorbidities identified during the preoperative clinical eval- stress response involves a catecholamine surge in response
uation. Table 1-3 is a guide to studies that may be appropriate to the pain and anxiety associated with the operative proce-
in the preoperative screening phase. dure or the disease process itself. The result is an increase
Specialty consultation may be required to optimize the in the myocardial oxygen requirement. A second alteration
patients chance for a successful operation. Medical consult- suppresses the fibrinolytic system, predisposing the patient
ants should not be asked to clear patients for a surgical pro- to thrombosis. Myocardial ischemia secondary to coronary
cedure; their primary value is in helping to define the degree artery disease can result in cardiac segments in which blood
of perioperative risk and making recommendations about how flow is reduced further by occlusive disease putting these seg-
best to prepare the patient to successfully undergo his or her ments at risk during time of additional stress. In a study of
operation and postoperative course. Once this risk is deter- unselected patients over the age of 40, the estimated periop-
mined, the surgical team, in conjunction with the patient or erative MI rate was 2.5%, and this increased with the type of
the patients family, may discuss the advisability of a planned procedure and selected subsets of patients. A useful approach
surgical approach to the patients illness. Postoperative con- to the consideration of cardiac risk is to consider:
sultation should be sought when the patient has unexpected 1. The clinical characteristics of the patient
complications or does not respond to initial maneuvers that 2. The inherent risk of the surgical procedure
are commonly employed to address a specific problem. For 3. The patients functional capacity
example, a nephrology consultation is in order for a patient
who remains oliguric despite appropriate intravascular vol-
ume repletion, particularly if the creatinine level is rising. Evaluation of Patients Asymptomatic for Heart Disease
All evaluations start with an assessment of baseline cardiac
Likewise, consultation should be obtained from specialists
function. Historical aspects should include any congenital or
who have expertise in areas that the treating physician does
acquired cardiac pathology or interventions including valvular
not have. For example, a general surgeon would be well
and ischemic heart disease as well as a list of all drugs. Special
advised to obtain consultation from a cardiologist for a patient
note is taken of the patients overall status during the physical
who had a postoperative myocardial infarction, no matter how
examination. Vital signs can give important clues about the
benign the myocardial infarction appears.
status of the cardiovascular system (i.e., tachycardia, tachyp-
nea, postural changes in blood pressure). Jugular venous dis-
Cardiac Evaluation tension at 30, slow carotid pulse upstroke, bruits, edema, and
Alterations in physiology occurring in the perioperative period a laterally displaced point of maximum cardiac impulse all
impose significant stress on the myocardium. The surgical suggest some type of cardiac disease. Auscultatory findings

Lawrence_Chap01.indd 7 7/21/2012 5:56:59 PM


that suggest cardiac problems include rubs, third heart sounds, myocardial infarction, the risk of an additional acute cardiac
and systolic murmurs. event or death is approximately 30% within the first 3 months.
Determining which murmurs are clinically significant and The risk declines with time and reaches a plateau of approxi-
which are innocent is perplexing for most medical students. mately 5% at 6 months. If possible, elective surgery should be
Most innocent murmurs are apical. Innocent murmurs are postponed for 6 months after a myocardial infarction.
never associated with a palpable thrill, and there are no inno- With the exception of coronary artery bypass grafting, the
cent diastolic murmurs. Maneuvers that change blood flow (i.e., patient who has unstable angina should avoid surgery, and
Valsalva) generally do not change the character or the pitch of undergo further investigation and intervention prior to an elec-
innocent murmurs. A patient who has hemodynamically signif- tive procedure. Although the patient with stable angina is the-
icant aortic stenosis usually has a characteristically harsh holo- oretically at increased risk, no clear answer about the extent
systolic murmur, a slow carotid pulse upstroke, and a displaced of increased postoperative risk is available for this group. In
primary myocardial impulse that is secondary to left ventricular contrast, patients who have undergone coronary artery bypass
hypertrophy. This latter finding, as well as poststenotic aortic have a significantly reduced danger of postoperative infarct
dilation, may be seen on chest radiograph. Patients who have compared with those who have angina. The risk is estimated
a history of mitral insufficiency also have an increased risk of at slightly more than 1%, with a similar mortality rate. Percu-
postoperative congestive heart failure and arrhythmia. taneous angioplasty may confer myocardial protection in the
Preoperative electrocardiogram (EKG) is appropriate postoperative period, but studies confirming the value of this
in those patients with one or more risk factors (history of procedure indicate that it is beneficial only in selected lesions.
ischemic heart disease, history or presence of congestive heart The use of various and at times multiple antiplatelet agents
failure, history of cerebrovascular disease, diabetes or renal in the poststent insertion phase may complicate the planned
impairment). Preoperative EKG is not indicated for asymp- surgical procedure. Patients with any cardiac history must
tomatic patients undergoing a low-risk procedure. Although be evaluated carefully, and the severity of their disease must
any abnormality seen on routine electrocardiography implies be documented. If possible, maximum myocardial perfor-
increased risk to the adult patient, other than acute myocardial mance should be achieved before any operative procedure is
infarction or complete heart block, abnormalities rarely require undertaken.
postponement of surgery, especially in asymptomatic patients. A history of diabetes increases the index of suspicion for
Mild, chronic congestive heart failure is not associated with occult cardiac pathology. Of patients with a documented his-
an increased occurrence of perioperative infarction. Patients tory of diabetes for 5 to 10 years, 60% have diffuse vascular
with cardiomegaly on chest radiograph and even those whose pathology. After 20 years, nearly all patients with diabetes
clinical course is effectively managed medically do not repre- have some type of vascular abnormality. In addition, the risk
sent high-risk groups. However, abnormal third heart sounds of mortality after a cardiac ischemic event for the patient
or signs of jugular venous distension indicate decompensation with diabetes is higher than that for people without diabetes.
of cardiac function. These patients are in jeopardy of serious Silent infarctions or ischemic events without symptoms may
cardiac complications. The perioperative phase of the patients be discovered during investigation. Therefore, patients with
experience is associated with alterations in fluid and electro- diabetes, especially those with a long-standing history of the
lyte control. Patients may be kept fasting for several days and disease, should be viewed with suspicion and presumed to
blood loss and drains deplete fluid and electrolytes. The endo- have some degree of cardiovascular abnormality.
crine response to surgery will also alter flux of fluids across Discussion and close collaboration with the anesthesia
the various body fluid compartments. This may cause addi- team is vital to ensure the safety and optimal management
tional stress if the patient has underlying cardiac compromise. of patients in the perioperative period. Different monitoring
The urgency of the required surgery may alter the risk/ techniques may identify instability before clinical manifesta-
benefit ratio and determine how complete the preoperative tions are apparent and allow for preventative intervention in
cardiac evaluation will be. This segment will focus on the the operative and postoperative phases.
elective workup of a required but nonurgent procedure.
Cardiac Medications
Evaluation of Patients With Known Heart Disease The issue of perioperative medication and cardiac protection
The patient who is scheduled to undergo elective surgery is not totally resolved. It is recommended that patients who
should be questioned carefully about the nature, severity, and are currently on -blockers remain on them, including taking
location of chest pain. Dates and details about infarctions, them the day of surgery. Similarly, statins should be continued
documented or suspected, should be noted, as should coro- as they have been shown to reduce the risk of perioperative
nary artery bypass graft or revascularization procedures, valve cardiac events. If absolute postoperative hemostasis is not a
replacements, and pacemaker insertions. Additional histori- requirement (as it may be in certain neurosurgical or ophthal-
cal elements of significance include a history of dyspnea on mic procedures), then single-agent antiplatelet agents should
exertion (which may signify underlying cardiac or pulmonary be continued.
pathology). Other clues to the possibility of coexisting heart Previous recommendations for the antibiotic prophylaxis
disease include syncope, palpitations, arrhythmia, and a his- of endocarditis following invasive surgery have been altered
tory of either cerebrovascular or peripheral vascular surgery. within the past years. The most recent are presented by the
In the patient with previous infarction, the risk of clinical American Heart Association (Circulation 2007;116:1736
postoperative myocardial ischemia is between 5% and 10% 1754) and currently do not support routine use of antibiotics
overall, with an attendant mortality rate of 50%. This figure to prevent infective endocarditis for gastrointestinal or geni-
contrasts with a risk of <0.5% in patients with no history tourinary procedures. In selected patients undergoing respira-
of infarct or clinically evident heart disease. If an elective tory system procedures, prophylaxis is recommended as well
operative procedure is performed immediately after a recent as for those having invasive dental work.

Lawrence_Chap01.indd 8 7/21/2012 5:57:00 PM


TABLE 1-4 Dripps-American Surgical Classification TABLE 1-6 Energy Expenditure and METs

Class I Healthy patient: limited procedure Class Tasks Patient Can Perform to Completion

Class II Mild to moderate systemic disturbance I Activity requiring >6 METs

Class III Severe systemic disturbance Carrying 24 lb up eight steps
Class IV Life-threatening disturbance Carrying objects that weigh 80 lb
Class V Not expected to survive, with or without surgery Performing outdoor work (shoveling snow, spading soil)
Participating in recreation (skiing, basketball, squash, handball,
jogging/walking at 5 mph)
II Activities requiring >4 but not >6 METs
Quantification of Surgical Risk Having sexual intercourse without stopping
Based on the history, physical findings, and a few simple lab- Walking at 4 mph on level ground
oratory studies, efforts have been made to quantify surgical
Performing outdoor work (gardening, raking, weeding)
risk. The most commonly used system, the Dripps-American
Surgical Association Classification, categorizes patients Participating in recreation (roller-skating, dancing fox trot)
into five groups (Table 1-4). The system offers little guidance, III Activity requiring >1 but not >4 METs
however, for identifying patients who are at risk for postop- Showering, dressing without stopping, stripping, and making bed
erative myocardial ischemia.
Walking at 2.5 mph on level ground
The revised cardiac risk index developed by Lee (Circu-
lation 1999;100:1043) is the most commonly used index of Performing outdoor work (cleaning windows)
cardiac risk and attributes increased risk to: Participating in recreation (golfing, bowling)
High-risk type of surgery IV No activity requiring >1 MET
History of ischemic heart disease Cannot carry out any of the above activities
History of congestive heart failure
METs, metabolic equivalents.
History of cerebrovascular disease Source: American Heart Association, Inc. ACC/AHA 2007 guidelines on perioperative
Preoperative treatment with insulin cardiovascular evaluation and care for noncardiac surgery: a report of the American College
Preoperative serum creatinine >2.0 mg/dL (177 mol/L). of Cardiology/American Heart Association Task Force on Practice Guidelines. Circulation
Based on the number of factors present, the patient is assigned
to class I to IV and estimated for cardiac risk accordingly
(Table 1-5). A reliable indicator of hemodynamic reserve is
made by a quantitative estimate of the patients cardiovascular
functional class. A useful scale is outlined in Table 1-6.
who are undergoing noncardiac surgery. The general recom-
Activity is expressed in metabolic equivalents (METs).
mendation is that preoperative testing should be limited to
One MET represents an oxygen consumption of 3.5 mL/kg/
the small subset of patients who are at very high risk, when
minute, the average for a resting 70-kg man. Achieving a heart
results will affect patient treatment and, most important, out-
rate of more than 100 beats/minute during cardiac stress is
come. The algorithm developed by the Task Force on Practice
roughly equivalent to 4 METs.
Guidelines (Figure 1-1) shows a simplified five-step approach
A useful bedside/clinic assessment question is to enquire
to preoperative cardiac assessment. Patients who need emer-
about exercise tolerance. A patient who can walk four blocks
gency noncardiac surgery require operative intervention
or ascend two flights of stairs without stopping or getting
without extensive preoperative testing. Postoperatively, these
short of breath has reasonable exercise capacity.
patients may require further cardiac evaluation. Step two iden-
The American College of Cardiology and the Ameri-
tifies patients who have active cardiac conditions. Patients
can Heart Association Task Forces have outlined a logical
who are undergoing low-risk surgery (Table 1-7) may proceed
approach to the preoperative cardiac evaluation of patients
with the planned procedure. A patient with a good functional
capacity and no symptoms, even with a history of cardiac dis-
ease, may proceed with planned surgery. Patients with major
clinical predictors (i.e., unstable coronary syndrome, decom-
TABLE 1-5 Revised Cardiac Risk Index pensated congestive heart failure, significant arrhythmia,
severe valvular disease) should be evaluated by noninvasive
Number of Risk Factors Percentage Rate Major tests of myocardial perfusion. The objective of these nonin-
Class Present Myocardial Complications vasive assessments is to identify patients who would benefit
from coronary angiography and subsequent cardiac interven-
I 0 0.40.5 tion before elective surgery. If the patient has only interme-
II 1 0.91.03 diate predictors or if no clinical predictors are present, then
III 2 3.66.6 assessment for functional capacity can be estimated. Individu-
IV More 9.111.0 als who cannot meet a 4-MET demand are at increased risk
for perioperative cardiac ischemia and long-term complica-
Source: American Heart Association, Inc. Lee TH, Marcantonio ER, Mangione CM, et al. tions. Individuals who are at high risk should undergo non-
Derivation and prospective validation of a simple index for prediction of cardiac risk of major
noncardiac surgery. Circulation 1999;100:1043. invasive testing and consideration for coronary angiography.
Patients who show abnormalities by noninvasive testing and

Lawrence_Chap01.indd 9 7/21/2012 5:57:00 PM


are considered candidates for coronary artery revasculariza- tolerance, general health, and the type and urgency of the
tion should undergo coronary angiography and subsequent planned procedure. Symptoms such as coughing, wheezing,
intervention, as determined by the results of those studies. sputum production, dyspnea, snoring, and orthopnea should
be noted. The physical examination should be focused on the
cardiopulmonary and respiratory system. In general, there is
Pulmonary Evaluation no role for routine pulmonary function test. Specialized test-
The reported incidence of postoperative pulmonary compli- ing is reserved for patients who have significant risk factors or
cations is between 2% and 19% depending on the definition who are expected to undergo an operation that carries a rela-
of postoperative pulmonary complications. This incidence is tively high intrinsic risk of pulmonary complications.
comparable to the incidence of postoperative cardiac com- Preoperative pulmonary assessment determines not only
plications and has a similar adverse impact on morbidity, factors that can lead to increased risk but also identification
mortality, and length of stay. The purpose of a preoperative of modifiable factors that can reduce the risk of pulmonary
pulmonary evaluation is to identify patients at risk for perio- complications. Preoperative interventions that may decrease
perative complications and long-term disability. A careful postoperative pulmonary complications include smoking ces-
history and physical examination will usually indicate which sation, inspiratory muscle training, bronchodilator therapy,
patients are most at risk. Important elements of this history antibiotic therapy for preexisting infection, and pretreatment
should include age, a history of smoking, presence of asthma, of asthmatic patients with steroids.
COPD, sleep apnea, and congestive heart failure, previous The most important and morbid postoperative pulmo-
pulmonary complications during or after surgery, exercise nary complications are atelectasis, pneumonia, respiratory

Step 1: Are there active cardiac conditions?

Condition Examples
Unstable coronary syndromes Unstable or severe angina
MI within 30 days
Decompensated HG (NYHA functional class IV; worsening or new-onset HF)
Significant arrhythmias High-grade atrioventricular block
Mobitz II atrioventricular block
Third-degree atrioventricular heart block
Symptomatic ventricular arrhythmias
Supraventricular arrhythmias (including atrial fibrillation) with uncontrolled ventricular rate (HR
greater than 100 beats per minute at rest)
Newly recognized ventricular tachycardia
Symptomatic bradycardia
Severe valvular disease Severe aortic stenosis (mean pressure gradient greater than 40 mm Hg, aortic valve area less
than 1.0 cm2, or symptomatic)
Symptomatic mitral stenosis (progressive dyspnea on exertion, exertional presyncope, or HF)
Step 2: What is their functional capacity? MET 4 = Light housework (dusting, washing dishes); climb a flight of stairs; walk on level ground at 4 mph
Step 3: What is the risk level of the planned operation?
Vascular (reported cardiac risk often more than 5%) Aortic and other major vascular surgery
Peripheral vascular surgery
Intermediate (reported cardiac risk generally 1% to 5%) Intraperitoneal and intrathoracic surgery
Carotid endarterectomy
Head and neck surgery
Orthopedic surgery
Prostate surgery
Low (reported cardiac risk generally less than 1%) Endoscopic procedures
Superficial procedure
Cataract surgery
Breast surgery
Ambulatory surgery
Step 4: Are there clinical risk factors? Ischemic heart disease, heart failure, diabetes mellitus, renal insufficiency, cerebrovascular disease

FIGURE 1-1. Cardiac evaluation for noncardiac surgery based on active clinical conditions (Adapted with permission from Fletcher LA, et al., ACC/AHA 2007
Perioperative guidelines. JACC 2007;50(17):17071732.)

Lawrence_Chap01.indd 10 7/21/2012 5:57:00 PM


Perioperative surveillance
Need for emergency and postoperative risk
Operating Room stratification and risk factor
noncardiac surgery YES management

Active cardiac Evaluate and treat per Consider operating

conditions? (See Table X) YES ACC/AHA guidelines room


Proceed with
Low risk surgery?
planned surgery


Good functional capacity Proceed with

(MET4) without symptoms? YES planned surgery


3 or more clinical 1 or 2 risk factors No clinical

risk factors risk factors

Vascular Surgery Intermediate Vascular Surgery Intermediate

risk surgery risk surgery

Consider testing if
it will change Proceed with surgery with HR control, or consider Proceed with
management noninvasive testing if it will change management planned surgery

FIGURE 1-1. (continued) Cardiac evaluation algorithm for noncardiac surgery, based on patient and procedural risk factors, for patients age 50.

failure or prolonged mechanical ventilation, pulmonary pulmonary care for prophylaxis. The section on pulmonary
embolism, and exacerbation of underlying chronic lung evaluation for nonpulmonary operations describes the spe-
disease. Potential risk factors for postoperative pulmonary cific tests.
complications can be either related to the patient or the There is controversy about whether age itself is a risk fac-
procedure and are shown in Table 1-8. While there is a tor for pulmonary complications. With increasing age, there
significant body of scientific evidence supporting the asso- is a progressive decline in static lung volume, maximum
ciation of most of these risk factors with postoperative expiratory flow, and elastic recoil as well as a decrease in PaO2
pulmonary complications, the evidence for others is not as because of an increase in the alveolararterial oxygen gradient.
convincing. The net effect is a loss of pulmonary reserve. The confounding
factor is that many older persons also have independent risk
Patient-Related Risk Factors factors for pulmonary complications. Age itself is not a con-
Patient-related risk factors include age, chronic lung dis- traindication to surgical intervention, but the normal changes
ease, tobacco abuse, congestive heart failure, functional that occur with the aging process should be kept in mind. Pul-
dependence, and the American Society of Anesthesiologist monary disease is a risk factor and COPD increases periopera-
classification. In general, patients who have an obstruction tive risk for several reasons. Increased pulmonary secretions,
to expiration flow for any reason are in greatest jeopardy. small airway obstruction secondary to mucous plugging, inef-
They may need specialized pulmonary function studies pre- ficient clearing of secretions, and a general lack of pulmonary
operatively and vigorous preoperative and postoperative reserve predispose the patient to atelectasis and superimposed

Lawrence_Chap01.indd 11 7/21/2012 5:57:01 PM


TABLE 1-7 Cardiac Riska Stratification for TABLE 1-9 American Society of Anesthesiologists
Noncardiac Surgical Procedures Classification and Association
with Postoperative Pulmonary
Risk Stratification Procedure Examples Complications

Vascular (reported cardiac Aortic and other major vascular surgery Rates of Postoperative
risk often more than 5%) Peripheral vascular surgery Pulmonary
Intermediate (reported Intraperitoneal and intrathoracic surgery Complications
ASA class Class Definition by Class (%)
cardiac risk generally Carotid endarterectomy
1%5%) I Normal healthy patient 1.2
Head and neck surgery
Orthopedic surgery II Patient with mild systemic disease 5.4
Prostate surgery III Patient with systemic disease that 11.4
Lowb (reported cardiac Endoscopic procedures is not incapacitating
risk generally <1%) Superficial procedure IV Patient with an incapacitating sys- 10.9
temic disease that is a constant
Cataract surgery
threat to life
Breast Surgery
V Moribund patient who is not NA
Ambulatory surgery expected to survive for 24 hr
Combined incidence of cardiac death and nonfatal myocardial infarction. with or without operation
These procedures do not generally require further preoperative cardiac testing.
Adapted with permission from Fleisher J, et al. ACC/AHA 2007 Guidelines on Perioperative
Cardiovascular Evaluation and Care for Noncardiac Surgery. J Am Col Cardiol 2007;50:1717.

volume of secretions, increased carboxyhemoglobin levels,

infection. Patients who have a history of occupational exposure and a predisposition to atelectasis. Smokers should be asked
to known irritants (e.g., silicone, asbestos, textile components) to stop smoking at least 6 weeks before the procedure; how-
may have significant restrictive disease and a noticeable reduc- ever, compliance with this request is rare.
tion in respiratory reserve. Also at high risk are patients who Functional dependence is an important predictor of postop-
cannot cough or breathe deeply for any reason, such as those erative pulmonary complications. Total dependence is defined
with an altered level of consciousness, neuromuscular disease, as the inability to perform any activities of daily living and
paraplegia, or weakness as a result of malnutrition. partial dependence is the need for equipment or devices and
In smokers, the relative risk of pulmonary complications assistance from another person for some activities of daily
is two to six times greater than that in nonsmokers. Smok- life. The ASA classification, while originally designed to help
ers have abnormalities in mucociliary clearance, increased in predicting perioperative mortality rates, has been proven
to predict postoperative pulmonary complications (Table 1-9).
Higher ASA class is associated with a substantial increase risk
in complications, with patients who are higher than ASA class
TABLE 1-8 Risk Factors for Postoperative II having a twofold to threefold increased risk of postopera-
Pulmonary Complications tive complications compared to patients with ASA class of II
or lower.
Patient-Related Factors Low serum albumin level (<3.5 g/dL) has been associated
Advanced age with an increased risk of pulmonary complications and should
ASA class >II be measured in all patients who may be at risk for malnutrition
or in whom there is a clinical suspicion of hypoalbuminemia.
Congestive heart failure
Serum albumin levels should also be evaluated in patients
Functionally dependent with one or more risk factors for postoperative pulmonary
Chronic obstructive pulmonary disease complications.
Impaired sensorium Asthma used to be considered a risk factor for postoperative
Cigarette use pulmonary complications; however, recent evidence suggests
Nutritional status
that this is not necessarily the case. Regardless, it is impor-
tant that patients be compliant with prescribed antiasthma
medications and good pulmonary toilet in the preoperative
Obstructive sleep apnea phase. Perioperative stress and many medications, including
Cerebrovascular accident anesthetic agents, can provoke bronchospasm. Similarly, while
Procedure-Related Factors intuitively it may seem that obesity and obstructive sleep apnea
Site of surgery (chest, upper abdomen, neurosurgery, neck, vascular) would also be a risk factor for pulmonary complications, cur-
Duration of surgery (>3 hr)
rent scientific evidence does not support this contention.
General anesthesia Procedure-Related Risk Factors
Emergency surgery Contrary to the case of cardiac risk assessment, procedure-related
ASA, American Society of Anesthesiologists. risk factors are more important than patient-related factors in
estimating the risk for postoperative pulmonary complications.

Lawrence_Chap01.indd 12 7/21/2012 5:57:01 PM


They include surgery site, duration of surgery, anesthetic tech- whether the patient has a history of occupational exposure to
nique, and type of surgery (elective vs. emergency) known pulmonary irritants. The patient should be asked about
his or her smoking history, sputum production, wheezing, and
Surgical Site exertional dyspnea. Physical examination should begin with a
Patients undergoing thoracic surgery, especially if they general assessment of the patients habitus. Are there signs of
require a lung resection, are at increased risk for pulmonary wasting or morbid obesity? Does the patient exhibit pursed-lip
complications and are discussed separately. Among nonpul- breathing? Does he or she have clubbing or cyanosis? What
monary operations, the risk of pulmonary complications can is the patients respiratory pattern? Is there a prolonged expir-
be stratified by the type of operation. Abdominal operations atory phase, as in obstructive airways disease? What is the
that require an upper midline incision or involve dissection anteroposterior dimension of the chest? On auscultation, does
in the upper abdomen are associated with a much higher the patient wheeze? A patient who cannot climb one flight of
pulmonary complication rate than those that are restricted steps without dyspnea or blow out a match at 8 inches from
to the lower abdomen. Abdominal incisions are painful and the mouth without pursing the lips is a candidate for more
are associated with diminished functional residual capacity sophisticated pulmonary function screening. Another useful
(FRC). These problems contribute to the higher pulmonary bedside test is the loose cough test. A rattle heard through
complication rate. Any thoracotomy incision predisposes the the stethoscope when the patient forcibly coughs is a reliable
patient to pulmonary complications. Interestingly, the median indicator of underlying pulmonary pathology and warrants
sternotomy incision is associated with a low incidence of pul- investigation, beginning with a chest radiograph, with further
monary complications, probably because it is associated with studies ordered as appropriate to the patients history, physical
minimal discomfort during quiet breathing. Neurosurgical, examination findings, and radiographic results.
vascular procedures and neck surgery are also associated with Before the specific elements of pulmonary function tests
a higher risk of pulmonary complications. are discussed, it is useful to review the physiologic definitions
of standard lung volumes and capacities. Figure 1-2 shows a
Duration of Surgery standard spirometry curve. Normal tidal ventilation is shown
Prolonged surgery duration ranging from 3 to 4 hours is by A. At the end of passive tidal exhalation, the patient is said
associated with a higher risk of postoperative pulmonary to be at FRC (shown by B in Figure 1-2). FRC is equal to the
complications. sum of expiratory reserve volume (the amount of air that can
Anesthesia Technique be expelled with a forced expiratory maneuver) and residual
General anesthesia carries a greater risk of postoperative volume (the volume of air left in the lung after a forced expi-
pulmonary complications than peripheral nerve conduction ration). This volume cannot be exhaled under normal circum-
blocks also known as regional anesthesia. Whether spinal or stances. Closing volume (CV) is the volume below which the
epidural anesthesia is less risky is a matter of debate. General alveoli become so structurally unstable that they cannot remain
anesthesia produces an 11% reduction in FRC. Patients do not open, even with the benefit of surfactant. In Figure 1-2, normal
cough under anesthesia, and postoperative sedation depresses CV is shown as being slightly lower than residual volume.
respiratory drive and inhibits coughing. The lasting effects In a smoker, however, CV requires a much higher volume of
of neuromuscular blockade can also weaken the coughing air. Consequently, patients with lung pathology tend to have
effort. Mucociliary clearance is also depressed by anesthetic spontaneous atelectasis at much higher volumes than they would
agents. Anticholinergic drugs commonly thicken the patients otherwise have. CV is actually greater than FRC in smokers
mucus and make it more difficult to mobilize. Tracheal intu- and obese patients, whereas it is much lower than FRC in nor-
bation promotes direct colonization of the upper airway by mal patients. Because FRC is the volume left in the lung after
Gram-negative organisms and sets the stage for infection. A a passive tidal expiration, it is important to understand that cer-
significant portion of hospital-acquired infections is caused tain lung diseases predispose the patient to atelectasis because
by iatrogenic introduction of nosocomial organisms into the
tracheobronchial tree by suction catheters that are passed
without attention to aseptic technique.
It is tempting to assume that regional anesthesia would
obviate these problems. In fact, this assumption may be true
for procedures on extremities or procedures that can be done
with a very specific regional blockade (e.g., axillary block).
However, spinal and epidural anesthesia are also associated
with postoperative pulmonary problems. As a rule, the impor-

tant factor is not the type of anesthetic agent employed, but the
circumstances to which the patient is exposed (e.g., abdomi-
nal procedures, loss of periodic hyperinflation by sighing). *Closing volume
C (smoker/obesity)
Pulmonary Evaluation for Nonpulmonary Operations
The pulmonary evaluation of the patient for nonpulmo- B
D Closing volume (normal)
nary operations begins with a thorough history and physical
examination as mentioned above along with an assessment
of his or her functional status. Questions about activities in
daily life should also be asked. For example, can the patient FIGURE 1-2. Spirometry. A, Tidal volume. B, Functional residual capacity. C,
shovel snow (or rake the yard)? Is he or she out of breath after Expiratory reserve volume. D, Residual volume. *Closing volume for smoker/obese
walking up a flight of stairs? Another important question is patient. Closing volume for normal patient.

Lawrence_Chap01.indd 13 7/21/2012 5:57:01 PM


CV is actually greater than FRC. The most commonly used pul- tolerate a lobectomy. Patients with asthma and COPD should
monary function test (PFT) is the FEV1. During the forced vital be particularly careful to be compliant with their medication
capacity maneuver (part of obtaining the FEV1), the patient is regimen preoperatively.
evaluated for intrinsic lung disease and also for problems with
the ventilatory pump that moves air into and out of the lungs. The Patient with Renal Dysfunction
Any patient who has significant abnormalities in respira-
tory function on routine history or physical examination may Traditionally, patients with renal dysfunction were classified
benefit from formal pulmonary function studies. In some under the broad categories of chronic renal failure (CRF) or
patients, such information leads to a decision to postpone or acute renal failure (ARF). However, in order to standardize
modify the course of therapy. Pulmonary function studies that the definitions and better evaluate these patients, it has been
can potentially uncover or quantitate a condition that can be recommended that the term chronic kidney disease (CKD) or
improved in the preoperative period (thereby lessening the risk acute kidney injury (AKI) be used. CKD is defined as either
of postoperative problems) are cost effective and justifiable. kidney damage or decreased kidney function for three or more
PFTs are often used in combination with arterial blood gas months. Proteinuria or abnormalities in imaging are markers
analysis to study the patient who is thought to be at high risk. for kidney damage, and a reduction in glomerular filtration
There is no evaluation strategy that precisely defines the rate (GFR) is a marker for decreased kidney function. ESRD,
pulmonary risk of a given patient. Although it is possible to which is a commonly used term, indicates chronic treatment
indicate which patients are likely to fare extremely well or by dialysis or transplantation and does not refer to a specific
extremely poorly, the middle groups are difficult to stratify. degree of kidney function. A GFR of <60 mL/minute/1.73 m2
At a minimum, a patient with a preoperative FEV1 of <1 L is considered the threshold for CKD. GFR can vary with age,
(the amount of air that can be exhaled in 1 second during a gender, ethnicity, and body mass and is typically estimated
forced expiration after the patient inhales to total lung capac- with calculations based on serum creatinine level. Kidney
ity), a PaO2 of <50 mm Hg, or a PaCO2 of >45 mm Hg should failure is defined as either a GFR of <15 mL/minute/1.73 m2
have the risks of operation explained in clear terms. These or a need for dialysis or renal transplantation. AKI encom-
risks include not only death and pneumonia, but also the pos- passes the entire range of ARF from small changes in serum
sibility of long-term ventilator dependence. Because of this creatinine to loss of function requiring dialysis. AKI can be
possibility, some patients decide against proceeding with the classified according to prerenal, renal, and postrenal causes.
operation. Perioperatively, the most common cause of AKI is secondary
to acute tubular necrosis (ATN). The risk of AKI in surgical
Pulmonary Evaluation for Pulmonary Operations patients has been estimated to be approximately 1%. Factors
Pulmonary resections present the special problem of removal associated with increased risk of AKI include age, past history
of lung tissue in a patient who is already at risk for postop- of kidney disease, left ventricular ejection fraction of <35%,
erative pulmonary complications. These patients are likely cardiac index <1.7 L/minute/m2, hypertension, peripheral vas-
to have a significant smoking history. Patients who have a cular disease, diabetes mellitus, emergency surgery, and type
greater than a 10 pack-year smoking history are at particu- of surgery. The highest risk surgeries include coronary artery
lar risk for chronic bronchitis. In general, the goal is to leave surgery, cardiac valve surgery, aortic aneurysm surgery, and
the patient with an FEV1 of at least 800 mL postoperatively. liver transplant surgery.
If the predicted postoperative FEV1 is <800 mL, the chances It is estimated that approximately 15% of the general popu-
are significant that the patient will never wean from the ven- lation in the United States has CKD. Surgery presents signifi-
tilator postoperatively. The predicted postoperative FEV1 is cant risks to patients with CKD or those with, or at risk of,
estimated by a variety of methods, ranging from simple to AKI. The metabolic consequences of renal dysfunction fre-
complex. One of the easiest ways to estimate quickly whether quently require special preparation of the patient for an elec-
the postoperative FEV1 will be low is to multiply the preop- tive surgical procedure. Meticulous attention to perioperative
erative FEV1 by the percentage of lung tissue that will be left care can reduce the complication rate in patients with acute
after resection. For example, consider a patient with an FEV1 or chronic renal impairment. The extent of preoperative test-
of 1.8 L who is scheduled to undergo a right upper lobectomy. ing depends on the patients comorbid conditions and should
The percentage of pulmonary tissue to be removed is one of include an electrocardiogram and chest radiograph. Renal
five total lobes (20% of the total lung tissue). This patients function should be assessed by accurate assessment of the
predicted postoperative FEV1 is 1.8 L80% lung remaining fluid balance and measurement of makers of renal function
postoperatively equals 1.4 L. including serum creatinine and blood urea nitrogen (BUN)
In the very high-risk patient who is to undergo pulmonary as well as urinary electrolytes. Cardiovascular disease is the
resection and whose predicted postoperative FEV1 is <1 L, main cause of mortality in patients with CKD and therefore
split perfusion radionuclide lung scanning is helpful in pre- these patients warrant a thorough perioperative cardiovascular
dicting the amount of functioning lung that will remain post- evaluation. Given the diverse nature of diseases that can affect
operatively. If, after careful study, the patients predicted kidney function, patients with kidney dysfunction requiring
postoperative FEV1 is <800 mL, the risk that the patient will surgery should undergo a thorough evaluation that should
not get off the ventilator is such that the patient is considered include the following:
inoperable. Exercise testing is also useful in the evaluation of Diagnosis (type of kidney disease)
these patients and does not require a sophisticated pulmonary Comorbid conditions
laboratory. The stair climb is a simple and reproducible Severity of renal dysfunction as assessed by level of kidney
method of assessing pulmonary function. The interested med- function
ical student can walk with the patient up stairs. A patient Complications related to the level of kidney function
who can climb five flights of stairs can tolerate a pneumo- Risk for loss of kidney function
nectomy, and one who can climb three flights can usually Risk for cardiovascular disease

Lawrence_Chap01.indd 14 7/21/2012 5:57:02 PM


In CKD, the ability to excrete water and sodium and maintain uremic state. Immune responses are deficient, and, as a result,
homeostasis of the intravascular volume is impaired. Exces- the potential for infectious complications may be enhanced.
sive preload usually does not appear, however, until renal Many patients with CKD are carriers of blood-borne patho-
function deteriorates to <10% of normal. Chronic volume gens and also develop antibodies because of multiple transfu-
depletion is encountered in these patients as frequently as sions, which can significantly delay typing and screening of
volume overload. These patients often receive potent diuretic blood products. Chronic coagulopathy secondary to heparini-
agents or have chronic volume contraction associated with zation during dialysis, or the coagulopathy associated with
hypertension. Maintenance of euvolemia and renal perfusion uremia, may exaggerate blood loss during surgery or in the
is the goal in the perioperative management of patients with perioperative period. A coagulation profile may help to iden-
CKD or AKI. For this reason, fluid management is dictated by tify intrinsic deficiencies. d-desamino arginine vasopressin
the patients history and disease process, not by the fact that (DDAVP) promotes the release of von Willebrands multimers
he or she has renal impairment. For example, a patient who from endothelial cells. Thus, a dose of DDAVP may be of use
has ESRD and is in septic shock because of perforated sig- preoperatively in addressing the thrombocytopathy of CKD.
moid diverticulitis requires crystalloid resuscitation to correct Daily weighing and accurate intake and output records are
the relative volume deficit, even though he or she is depend- essential. Exacerbation of renal failure is prevented if hypo-
ent on dialysis. This patient should not be fluid restricted. tension is avoided and medications are carefully administered.
Invasive hemodynamic monitoring can be helpful in this Most drugs can be nephrotoxic, and doses must be adjusted
patient group and allows precision in volume replacement. frequently based on an estimation of the degree of renal func-
The ability to excrete potassium is also impaired, and patients tion. Angiotensin-converting enzyme inhibitors (ACEI) and
with impaired renal function do not tolerate sudden changes angiotensin II antagonist (ARA) should be discontinued for
in potassium level. The risk of malignant hyperkalemia is at least 10 hours before general anesthesia to reduce the risk
directly proportional to the serum potassium level before the of postinduction hypotension. Analgesic requirements in the
last dialysis. Serum potassium levels should be <5 mEq/L perioperative period are an important consideration in patients
before surgery. Achieving this level may require dialysis or with AKI or CKD as opioids may accumulate in patients with
the use of ion exchange resins. CKD is usually accompanied CKD placing them at a higher risk of respiratory depres-
by chronic metabolic acidosis because excretion of fixed acids sion. Nonsteroidal anti-inflammatory drugs are generally not
is reduced. These acids are the byproducts of metabolism and recommended because of their nephrotoxic side effects.
include sulfates, phosphates, and lactate. Postoperatively, the Patients with renal failure may require modifications in anes-
acid load can further increase as hydrogen ions are released thetic techniques. For example, succinylcholine is generally
from damaged cells in which case respiratory compensation avoided because it may promote or exacerbate hyperkalemia.
by hyperventilation can maintain the serum pH at an accept- Also, nondepolarizing neuromuscular blockage agents that are
able level that is slightly below normal. However, if PaCO2 not renally metabolized and excreted should be selected. Cisa-
increases even slightly, a profound exacerbation of acido- tracurium undergoes Hoffman degradation and is often used in
sis may occur. This situation is seen in patients who cannot the anesthetic management of patients with renal failure. To
increase minute ventilation, who have increased dead space, minimize the risks of volume overload, electrolyte imbalances,
or who are receiving an excessive carbohydrate caloric load. and uremic bleeding, patients on dialysis should be dialyzed
Another electrolyte abnormality that is often seen in within 24 hours of surgery. Despite the formidable spectrum of
patients with CKD is hvypocalcemia secondary to hyperphos- potential problems faced by the surgical patient who has CKD,
phatemia. Ionized calcium should be followed in these patients elective surgery can be performed safely in this patient group.
and supplemented as needed in the perioperative period. Oral Precise fluid management may be assisted in these patients with
phosphate binders and dietary restriction of phosphates may the judicious use of invasive monitoring (e.g., central venous
be required as well. Hypermagnesemia is also common; there- pressure monitoring or esophageal Doppler monitoring) as the
fore, magnesium-containing antacids should be avoided in situation dictates. Electrolytes, particularly potassium, mag-
these patients. nesium, and phosphorous, must be followed carefully. The
Most patients with long-standing CKD are malnourished. assistance of a clinical pharmacist is indispensable in provid-
Anorexia, which results from azotemia and the inability to ing advice regarding how to adjust the dosage and scheduled
handle the accumulation of nitrogenous end products, pro- administration of medications to these patients. Renal function
motes depletion of both skeletal muscle and visceral protein is monitored by accurate assessment of the fluid balance and
stores. Malabsorption syndromes are common, as are overt periodic measurements of the markers of renal function (creati-
vitamin deficiencies. Patients who receive long-term perito- nine and BUN). Renal dialysis may be needed when the patient
neal dialysis may lose as much as 6 to 8 g protein/day, and, as a cannot manage his or her own fluid balance, or when the detox-
result, may have hypoalbuminemia. Anorexia and a history of ification or excretory function of the kidney is not performing
weight loss suggest a catabolic state and therefore aggressive properly. Examples of this would include volume overload with
nutritional support should be provided. Patients should not be overt congestive heart failure in an anuric patient, life-threaten-
protein restricted in the perioperative phase just because they ing hyperkalemia, and intractable acidosis.
have renal failure as malnutrition significantly increases the
risk of septic complications in the perioperative period.
The normochromic, normocytic anemia that is often seen in The Patient with Hepatic Dysfunction
patients with CKD is usually well tolerated. The added stress Hepatic dysfunction was traditionally seen among patients with
and oxygen requirements that follow a surgical procedure, alcoholic hepatitis or chronic viral hepatitis. While the inci-
however, may have adverse consequences. Chronic dialysis is dence of these conditions has not changed, the overall number
estimated to remove as much as 3 L blood/year, and the reduced of patients with hepatic dysfunction has significantly increased
production of erythropoietin hampers red blood cell replace- with the obesity epidemic. Nonalcoholic fatty liver disease has
ment. The lifespan of red blood cells is also reduced in the become the most common cause of chronic liver disease in the

Lawrence_Chap01.indd 15 7/21/2012 5:57:02 PM


United States. Since liver disease is common and patients with

TABLE 1-11 Contraindication to Elective Surgery
liver dysfunction are frequently asymptomatic, the preoperative in Patients with Liver Disease
assessment of all patients undergoing surgery should include
a thorough history and physical examination to uncover risk
factors for and evidence of liver dysfunction. The evaluation Acute liver failure
should include a careful history to identify risk factors for liver Acute kidney injury
disease, including prior blood transfusions, illicit intravenous Acute viral hepatitis
drug abuse, sexual promiscuity, a family history of jaundice Alcoholic hepatitis
or liver disease, a personal history of jaundice, excessive alco-
hol intake, and the use of potentially hepatotoxic medications
including over-the-counter and herbal preparations. On physi- Hypoxemia
cal examination symptoms of pruritis or fatigue or findings Severe coagulopathy (despite treatment)
of palmer erythema, spider telangiectasias, abnormal hepatic
contour or hepatomegaly, splenomegaly, hepatic encepha-
lopathy, ascites, testicular atrophy or gynecomastia should be
looked for. Routine testing with liver biochemical tests preop-
eratively for screening purposes in asymptomatic patients with- preoperative evaluation and their liver dysfunction should be
out risk factors or physical findings indicating liver disease is optimized prior to elective surgery. Patients with advanced
not recommended. When liver disease is suspected based on liver disease because of their increased perioperative risk for
physical examination findings or liver biochemical abnormali- mortality should be managed by nonoperative measures.
ties, additional investigations should be undertaken, and should In patients with cirrhosis, the Child-Pugh classification and
include biochemical and serological testing for viral hepatitis, Model for End-stage Liver Disease (MELD) score should be
autoimmune liver disease, and metabolic disorders and radio- calculated to assist in preoperative risk assessment. The Child-
logic evaluation with abdominal ultrasonography, magnetic Pugh class is based on the serum bilirubin and albumin levels,
resonance imaging, or computed tomography scans. Although prothrombin time, and severity of encephalopathy and ascites
serologic and radiologic testing is often adequate for diagno- (Table 1-12). In addition to predicting mortality, the Child-
sis and perioperative risk assessment, liver biopsy remains the Pugh classification correlates with the frequency of postop-
gold standard for the diagnosis and staging of liver disease. erative complications, which include liver failure, worsening
Risk factors for surgery in patients with hepatic dysfunc- of encephalopathy, bleeding, infection, renal failure, hypoxia,
tion or cirrhosis are shown in Table 1-10. The mortality of and ascites. In general, elective surgery is well tolerated in
patients with liver disease depends on the degree of hepatic patients with Child class A cirrhosis, is permissible with pre-
dysfunction, the nature of the surgical procedure, and the operative preparation in patients with Child class B cirrhosis
presence of comorbid conditions. There are several contrain- (except those undergoing extensive liver resections or cardiac
dications to elective surgery in patients with liver disease, surgery), and is contraindicated in patients with Child class C
as shown in Table 1-11. When these contraindications are cirrhosis. The MELD score is based on serum bilirubin, serum
absent, patients with liver disease should undergo a thorough creatinine, and the international normalized ratio (INR) and is
calculated by the formula:
MELD score = (0.957 ln(serum Cr) + 0.378
ln(serum bilirubin) + 1.120 ln(INR) + 0.643) 10
TABLE 1-10 Risk Factors for Surgery in Patients (if hemodialysis, value for creatinine is automatically
With Hepatic Dysfunction/Cirrhosis set to 4.0)
Patient Characteristics Scores range from 6 to 40, with 6 reflecting early disease
Anemia and 40 severe disease. In patients undergoing laparoscopic
Ascites cholecystectomy with a MELD score of <8, the mortality
Child-Pugh classification
is 0%, while if the MELD score is >8, then the mortality is
around 6%. Among patients undergoing abdominal surgery
(other than laparoscopic cholecystectomy), orthopedic and
Hypoalbuminemia cardiovascular surgery, patients with a MELD score of 7 or
Hypoxemia less have a mortality rate of 5%, patients with a MELD score
Infection of 8 to 11 have a mortality of 10% and patients with a MELD
score of 12 to 15 have a mortality of 25%.
Multiple metabolic aberrations exist in the patient with
MELD score hepatic dysfunction or overt cirrhosis, even before the devel-
Portal hypertension opment of ascites. The most significant change is a profound
Prolonged prothrombin time (>2.5 s) that does not correct with vitamin K reduction in sodium excretion, frequently <5 mEq/24 hour,
Type of Surgery due to tubular reabsorption. The exact mechanism for this is
unknown but is thought to be due to multiple hormonal fac-
Cardiac surgery
tors. Challenging these patients with an oral sodium load fur-
Emergency surgery ther increases sodium and water retention. Many patients with
Hepatic resection hepatic dysfunction demonstrate, somewhat contrarily, intra-
Open abdominal surgery vascular volume depletion. The clinical implications of this
derangement in sodium metabolism should be obvious, and

Lawrence_Chap01.indd 16 7/21/2012 5:57:02 PM


TABLE 1-12 Child-Pugh Classification of Cirrhosis

Class Albumin Bilirubin Ascites Encephalopathy Nutritional State Mortality Rate (%)

A >3.5 <2.0 Absent Absent Good <10

B 3.03.5 2.03.0 Minimal Minimal Fair 40
C <3.0 >3.0 Severe Severe Poor >80

extreme diligence must be paid to fluid and electrolyte issues carries a postoperative mortality rate of as high as 50%. This
in the perioperative period. rate is reduced to 10% with proper treatment. The use of
Ascites increases the risk of wound dehiscence and abdom- intravenous ethanol, given in doses to keep serum ethanol
inal wall hernias after abdominal surgery. Also, large-volume concentrations below detectable limits, is being explored in
ascites can impair ventilation and cause respiratory compro- some centers.
mise. Ascites can be drained at the time of surgery; however, Patients with liver disease are at risk for increased bleeding.
it typically reaccumulates within days. Preoperative control of This impaired hemostasis can be due to decreased production
ascites with diuretics or transjugular intrahepatic portal caval of clotting factors because of hepatic synthetic dysfunction or
shunt (TIPS) is recommended. Medical therapy for ascites depletion of vitamin K stores due to malnutrition or decreased
includes salt restriction to 2 g/day with the combination of intestinal absorption. Platelet abnormalities, both in number
spironolactone and furosemide. and function that can lead to bleeding tendencies, are found
The underlying etiology of liver dysfunction in a signifi- in patients with advanced liver disease due to portal hyperten-
cant majority of patients is alcohol; therefore, in the perioper- sion-induced splenic sequestration and alcohol-induced bone
ative period, these patients are at risk for alcohol withdrawal. marrow suppression.
The alcoholic patient is protected from withdrawal symp- Patients with liver disease are at significant risk for protein-
toms by the administration of proper sedatives. The onset of energy malnutrition and patients with cholestatic liver disease
mild withdrawal symptoms can occur anywhere from 1 to 5 are at risk for fat-soluble vitamin malabsorption. Patients with
days after alcohol is discontinued. Major symptoms gener- alcohol-induced liver disease are often deficient in thiamine
ally peak at approximately 3 days, but have occurred as long and folate and have depleted levels of total body potassium and
as 10 days after withdrawal. These include delusions, trem- magnesium. These elements should be aggressively replaced
ors, agitation, and tachycardia. Benzodiazepines may prevent to prevent abnormalities of glucose metabolism and cardiac
major withdrawal symptoms if they are instituted prophylac- arrhythmia. Wernicke-Korsakoff syndrome (i.e., ataxia,
tically. Table 1-13 below illustrates typical approaches to ophthalmoplegia, and confusion) may follow if thiamine is
prevention of delirium tremens. Untreated delirium tremens not administered prior to the administration of glucose.

TABLE 1-13 Examples of Medication Regimens

Several different benzodiazepines and dosing regimens have been used and recommended. The following are examples of medications and dosing regimens.
Diazepam, 5 mg intravenously (2.5 mg/min). If the initial dose is not effective, repeat the dose in 5 to 10 min. If the second dose of 5 mg is not satisfactory, use 10 mg
for the third and fourth doses every 5 to 10 min. If not effective, use 20 mg for the fifth and subsequent doses until sedation is achieved. Use 5 to 20 mg every hour as
needed to maintain light somnolence.
Lorazepam, 1 to 4 mg intravenously every 5 to 15 min, or lorazepam, 1 to 40 mg intramuscularly every 30 to 60 min, until calm, then every hour as needed to maintain light
Haloperidol, 0.5 to 5 mg intravenously/intramuscularly every 30 to 60 min as needed for severe agitation. (Only to be used as adjunctive therapy with sedativehypnotic agents.)
Ethanol Infusionb
I. Initiate 5% alcohol drip at 0.8 mL/kg/hr (using ideal body weight). The alcohol drip should be a continuous infusion and not discontinued or placed on hold for any diagnos-
tic or operative procedures. The alcohol protocol is appropriate for patients admitted to a floor status level of care.
II. Measure blood alcohol content (BAC) at 6, 24, and 72 hr. If the blood alcohol level is >0.08%, hold for 2 hr and decrease rate by 50%.
III. If no symptoms of alcohol withdrawal:
after 24 hr from start, decrease rate by 50%.
after 48 hr from start, decrease rate further by 50%.
at 72 hr from start, stop and discontinue drip.
IV. If patient develops symptoms, increase rate by 50%. If symptoms continue for 6 hr, contact the resident on call.
From Mayo-Smith, et al. Management of alcohol withdrawal deliriuman evidence-based practice guideline. Arch Intern Med 2004;164:14051412.
From Dissanaike, et al. Ethanol prevents alcohol withdrawal syndrome. J Am Coll Surg 2006;203:186191.

Lawrence_Chap01.indd 17 7/21/2012 5:57:24 PM


For a more complete discussion of surgical diseases of the extremities, retards wound healing. Because most peripheral
liver, see Chapter 18, Liver. vascular disease in the patient with diabetes is small vessel in
nature, palpable pulses are common, even in the face of tis-
The Diabetic Patient sue ischemia. Often, the extent of small vessel disease extends
Glycemic control is maintained by a balance between insulin deep into the tissue, sparing the skin, much like a cone whose
and counterregulatory hormones such as glucagon, epineph- base is directed peripherally and whose apex extends in the
rine, cortisol, and growth hormone. Surgical stress induces a central portion of the extremity proximally. For a patient with
neuroendocrine response with release of these counterregu- diabetes, ingrown toenails or minor injuries to the feet are
latory hormones, which results in peripheral insulin resist- potentially serious problems that can lead to amputation or
ance, increased hepatic glucose production, and impaired mortality. Therefore, even minor procedures on the extremi-
insulin production with the potential of hyperglycemia and ties of diabetic patients are approached with utmost caution.
even ketoacidosis in some cases. The extent of this response Patients who require insulin to control their diabetes must
depends on the complexity of the surgery and the nature of have their dose adjusted to compensate for periods when food
postoperative complications. The task of the surgeon in man- is not allowed or when the hyperglycemic response to the
aging the diabetic patient is to achieve euglycemia. It is well stress of illness, surgery, or trauma is clinically significant.
understood that if blood glucose levels are too low, death can Patients who have diabetes that was previously controlled
quickly ensue due to starvation of glucose-dependent tissues by diet or oral agents may require insulin in the periopera-
(particularly, the brain) of their obligatory substrates. Tradi- tive period. Infectious etiologies of surgical disease or post-
tionally, surgeons have erred on the side of hyperglycemia, operative infections may promote hyperglycemia and even
reasoning that modest hyperglycemia is better tolerated than ketoacidosis. On the other hand, overzealous administration
hypoglycemia. Recent data would suggest that it is possible, of insulin may lead to hypoglycemia.
at least in the critical care environment, to achieve eugly- The perioperative management of patients with diabetes is
cemia safely and with better outcomes using a continuous approached as follows:
infusion of insulin. However, the safe application of this 1. Insulin is available in several types and is typically classi-
practice to the noncritical care environment has yet to be fied by its length of action. Rapid-acting and short-acting
demonstrated. insulin preparations are usually withheld when the patient
The preoperative evaluation of a diabetic patient includes stops oral intake usually at midnight the day before surgery.
assessment of metabolic control and any diabetes-associated Intermediate-acting and long-acting insulin preparations
complications including cardiovascular disease, autonomic are administered two-thirds the normal evening dose the
neuropathy, and nephropathy, which could impact surgical night before surgery and half the normal morning dose the
outcomes. The surgical patient who has diabetes should be morning of surgery. Long-acting oral agents are stopped 48
carefully questioned about the duration of the disease, insu- to 72 hours before surgery, while short-acting agents can
lin requirements, diet, degree of glucose control, last insulin be withheld the night before or the day of surgery.
administration, and peripheral symptoms (i.e., numbness, 2. The ideal method of providing insulin in the perioperative
extremity pain). During the physical examination, special period is debatable. Any regimen should however (1) main-
attention is given to the feet, looking for minor injuries, evi- tain adequate glycemic control to avoid hyperglycemia or
dence of poor hygiene, inadequate vascular supply, ulcers, hypoglycemia; (2) prevent metabolic disturbances; (3)
or decreased vibratory sensation. Patients who have positive be easy to understand and administer. The patient should
findings should give meticulous care to their feet (i.e., daily receive a continuous infusion of 5% dextrose to provide
washing, careful drying, application of softening lotion, pro- 10 g glucose/hour. Fingerstick glucose levels are monitored
tection from minor trauma, avoidance of pressure sores). intraoperatively and followed postoperatively at least every
The cardiac effects of patients with diabetes were dis- 6 hours. The goal is to maintain a glucose level of between
cussed previously. The incidence of cardiovascular abnormal- 120 and 180 mg/dL. It is generally considered preferable to
ities found on physical examination increases with the age of have the patient at the higher end of this range because of
the patient and the duration of the diabetes. Men with diabetes the adverse consequences of hypoglycemia. Sliding scale
may have twice the risk of cardiovascular mortality as their use of subcutaneous insulin has been the standard method
nondiabetic counterparts. Women have approximately four of glucose control in surgical patients. Alternatively, intra-
times the risk. Cardiac autonomic neuropathy may predispose venous insulin can be used with a continuous infusion of
patients to perioperative hypotension, so it is important to 1 to 3 units/hour of intravenous insulin being given. This
evaluate these patients for the presence of resting tachycar- approach is particularly helpful in the brittle diabetic. In
dia, orthostatic hypotension, peripheral neuropathy and loss the postoperative period, close attention should be paid not
of normal respiratory heart rate variability. only to the patients blood sugar, but also to the patients
Gastroparesis, which is also believed to be caused by auto- carbohydrate intake.
nomic neuropathy, may delay gastric emptying and increase 3. Diabetic ketoacidosis (DKA) can develop in patients with
the likelihood of aspiration. Gastroparesis is suggested if the either type I or type II diabetes. DKA is deceptively easy to
patient gives a history of prolonged fullness after eating, or of overlook because it can mimic postoperative ileus. It may
constipation. A splash of fluid heard with the stethoscope over present as nausea, vomiting, and abdominal distension, or
the stomach at a time when the stomach should be empty may in association with polyuria (which is commonly mistaken
suggest the presence of gastroparesis. for mobilization of intraoperative fluids). For this reason,
The risk of infection is substantially greater for the patient patients with type I diabetes (and many with type II dia-
with diabetes. Hyperglycemia has an adverse effect on betes) should have their urinary ketone level monitored by
immune function, especially phagocytic activity. The reduced dipstick. This method is faster and much less costly than
blood flow in patients with vascular disease, especially to the following serum ketone levels, and it gives a fairly accurate

Lawrence_Chap01.indd 18 7/21/2012 5:57:24 PM


picture of developing ketoacidosis. A glucose level that is 7 to 10 days (decrease by half for parenteral use), is frequently
<250 mg/dL does not mean that the patient is not at risk for employed to ameliorate some of the adverse effects of gluco-
DKA; DKA develops because of the metabolism of fuel in corticoids on wound healing. Care should be taken in renally
the absence of glucose. Hence, the development of DKA or hepatically impaired patients and supplemental Vitamin A
does not depend on a certain level of glucose, but on the should be of short-term use only, during the first few postop-
absence of insulin. erative days, as large doses may cause Vitamin A toxicity.

The Adrenally Insufficient Patient The Pregnant Patient

Historically, any patient who had received even small doses of Multiple anatomic and physiologic changes accompany a nor-
glucocorticoid within the 12-month period before surgery was mal pregnancy, altering the presentation of many surgical dis-
given preoperative glucocorticoid coverage, often in amounts eases and mimicking others. The pregnant womans response
well exceeding amounts produced by the hypothalamic to these conditions can also be altered. The enlarging uterus
pituitaryadrenal (HPA) axis even in times of stress. To keep displaces abdominal viscera and can alter the location of pain
the issue of glucocorticoid replacement in some sort of per- in some common intra-abdominal conditions such as appen-
spective, it is useful to remember that patients with Cushings dicitis. A gravid uterus can compress the inferior vena cava
syndrome produce the equivalent of 36-mg hydrocortisone/day. and reduce venous return when the woman assumes the supine
Additionally, appreciation of the adverse effects of glu- position. Pelvic venous compression produces or exacerbates
cocorticoids has prompted a reconsideration of preoperative hemorrhoids in over one-third of pregnant women. Lower
glucocorticoid coverage. Documented complications of glu- extremity venous insufficiency and the hypercoagulable state
cocorticoid therapy include increased susceptibility to infec- of pregnancy itself increase the risk of venous thromboembolic
tion, impaired tissue healing, and abnormalities of glucose events, especially if the pregnant patient is placed at bed rest.
metabolism. Although high-dose glucocorticoid use was pre- The surgeon caring for a pregnant woman is caring, in
viously thought to be linked to upper gastrointestinal hem- effect, for two patients, and the mothers physiology is often
orrhage, more recent data have called this association into preserved at the expense of reduced uterine perfusion. Some
question. of the most significant physiologic changes during pregnancy
So then, who should be considered for glucocorticoid sup- occur to the circulatory system. Heart rate, stroke volume,
plementation, and how much should be given? A prednisone- and plasma volume are increased. Erythrocyte volume is also
equivalent dose of 20 mg/day for at least 3 weeks can be increased but not to the same degree as plasma volume, result-
presumed to be associated with HPA axis suppression. Physi- ing in a reduction of the hematocrit. This increase in blood
cal findings of a Cushingoid appearance should also raise the volume can mask blood loss or delay the classic presentation
index of suspicion. of hypovolemia, especially after injury. The appearance of
Present recommendations are based on the degree of surgi- normal vital signs can be deceptive and obscure fetal distress.
cal stress anticipated (i.e., minor, moderate, or major) and are The leukocytosis associated with a normal pregnancy reduces
detailed in Table 1-14. In all cases, patients should receive the utility of this laboratory test.
their morning steroid dose with a sip of water. Respiratory rate and tidal volume are increased. This
The role of steroids in the management of critically ill increase in minute ventilation lowers the arterial partial pres-
patients remains unresolved, despite recent multicenter, sure of carbon dioxide. This occurs despite a reduction in
randomized, placebo-controlled studies. It remains difficult to FRC and residual volume imposed by the restriction of dia-
conclusively demonstrate a beneficial effect of steroids in the phragmatic motion secondary to the enlarging uterus. Post-
critically ill, and the adverse effects of these agents are well operatively, the potential for atelectasis and other pulmonary
described. complications is increased.
High-dose glucocorticoids are well known to impair Most pregnant women experience reflux symptoms to
wound healing. Vitamin A, 10,000 to 25,000 IU enterally for some degree. Gastric acid production is increased slightly,
but the primary problem is the delay in gastric emptying, the
result of the action of progesterone in reducing gastric smooth
muscle contractility. Nausea and vomiting are common in
TABLE 1-14 Stress Steroid Coverage the first trimester, and these symptoms can be confused with
gastrointestinal conditions that are surgical in nature.
Steroid Replacement: Take Usual It is best when possible to avoid a surgical procedure
Magnitude of Procedure AM Steroid Dose, and: during pregnancy, but surgical emergencies must be handled
when they present. If surgery is necessary, it is best performed
Minor procedures or surgery No extra supplementation is necessary during the second trimester, when the risk of precipitating
under local anesthesia spontaneous abortion or early labor is lowestapproximately
(e.g., inguinal hernia repair) 5% in women undergoing general anesthesia and abdominal
Moderate surgical stress 50 mg hydrocortisone IV just before the surgery. Precipitating labor, and perhaps fetal demise, appears
(e.g., lower extremity procedure and 25 mg of hydrocor- to be related more to the underlying pathology than the anes-
revascularization, total joint tisone every 8 hr for 24 hr. Resume thesia. Laparoscopy can be performed safely as well during
replacement) usual dose thereafter. the second trimester, albeit with changes in trocar positioning
Major surgical stress 100 mg of hydrocortisone IV just prior to and reducing abdominal insufflation pressure.
(e.g., esophagogastrectomy, induction of anesthesia, and 50 mg Appendicitis and biliary tract disease are the most common
total proctocolectomy every 8 hr for 24 hr. Taper dose by reasons for gastrointestinal surgery in the pregnant woman. Pan-
half per day to maintenance level. creatitis occurring during pregnancy is usually related to biliary
tract disease. Bulk laxatives, stool softeners, and suppositories

Lawrence_Chap01.indd 19 7/21/2012 5:57:24 PM


are usually sufficient for hemorrhoids. Acute hemorrhoidal Rh-immunoglobulin therapy, unless the injury is relatively
thrombosis can be drained with the use of local anesthesia. Rec- minor and remote from the uterus.
tal bleeding is also associated with colonic malignancy, and com-
plaints of bleeding should not be blindly ascribed to hemorrhoids The Geriatric Patient
but investigated by endoscopy irrespective of gestational age.
Historically, women who were diagnosed with malignant The aging of the American population will continue for many
conditions were advised to terminate the pregnancy. Fortu- decades to present some special challenges to surgeons. The
nately, this is no longer the case. Women today share in the elderly have less reserve than their younger counterparts. They
decision making regarding the pregnancy as well as therapeu- are often on medications that can distort physiologic responses,
tic choices. Diagnostic delays, however, are still common in for example, -blockers. They are also often on medications
pregnant women with breast cancer. This is in part due to the that can impact the response to surgery, for example, warfa-
normal changes that take place in the breasts of a pregnant rin or platelet aggregationinhibiting agents. Their ability to
woman. Breast masses detected in pregnant women should be negotiate everyday activities may be impaired at baseline, per-
investigated, and imaging is commonly employed as a first haps due to sensory impairment, difficulty in ambulation, or
step. Mammography can be performed safely with shielding dementia. One of the conundrums that arises in the context
of the uterus. False-negative mammograms are unfortunately of providing surgical care for an elderly patient is whether to
common owing to the density of the active breast tissue. Ultra- proceed with an aggressive plan of intervention. It is always
sonography avoids any potential risk of ionizing radiation, but important that the patient and physician talk openly about the
it also has an increased rate of false-negative results during level of aggressiveness to be exerted on behalf of the patient.
pregnancy. Regardless of imaging results, biopsy should be In the elderly, this issue assumes critical proportions. Repeated
performed on clinically suspicious masses. Core, incisional, discussions with patients and their families should be held,
or excisional biopsies are all appropriate choices, and can beginning preoperatively and continuing in the postoperative
be performed under local anesthesia. Fine-needle aspiration phase. Generally, patients wish to feel that aggressive medical
cytology has also been shown to be accurate in the pregnant care will be rendered as long as there is a reasonable chance for
patient, but requires interpretation by a skilled pathologist. meaningful survival. While these discussions are uncomfort-
Breast cancer in pregnant women has the same progno- able, they are as important to the patients care as any compo-
sis when matched for age of the patient and stage of disease, nent of the historical database. It is also important to remember
despite being predominantly estrogen receptor negative. that surgical care is rendered among individuals who take a
Breast conservation surgery can be performed when appro- personal interest in the overall well-being of the patient. Some-
priate and chemotherapy administered after the first trimester. times, this means that medical care focuses more on alleviating
Radiation therapy is held until after delivery. Continuation of pain than on prolonging life. These discussions are best held
the pregnancy does not appear to adversely affect outcome in in a quiet, comfortable place, away from distractions. It is also
women with breast cancer. important to note that discussions about end-of-life issues do
Rectal cancer is the most common colonic malignancy, and not constitute some sort of legal activity. There are no forms to
when discovered during the first half of the pregnancy should be be signed. These discussions are just like any other conversa-
resected. When discovered during the last half of the pregnancy, tion a doctor and patient might have about the patients care,
resection is generally postponed until after delivery. As in in which the strengths and weaknesses of different approaches
patients with breast cancer, chemotherapy is relatively safe after are compared, until the physician and patient arrive at a plan
the first trimester, but radiation is withheld until after delivery. of action. The special difference, of course, is that end-of-life
One in every 14 pregnancies is complicated by injury. discussions are the patients best chance to determine his or her
Every injured woman of childbearing age should be screened destiny. These discussions should be treated with the reverence
for pregnancy. As noted above, the changes in a womans that such subject matter would naturally evoke.
physiology may mask severe fetal distress. Resuscitation of
the fetus requires dutiful attention to preserving the mothers
blood volume and oxygenation. The classic manifestations OPERATIVE MANAGEMENT
of hemorrhagic shock signify that the fetus has been in dis-
tress for some time. Early fetal monitoring is essential in the
initial assessment and resuscitation of the pregnant trauma Documentation
patient. Diagnostic studies should be obtained when needed The Medical Record
and not withheld for fear of teratogenesis. Indications for The medical record is a concise, explicit document that
surgical exploration following maternal trauma include intra- chronologically outlines the patients course of treatment.
peritoneal hemorrhage, hollow visceral injury, penetrating There are three primary purposes of the medical record. The
abdominal injury, and uterine or fetal injury. first purpose is to record in one common and accessible loca-
Fetal loss occurs in 15% of all women severely injured tion the data and thought processes that form the basis for
during pregnancy. Placental abruption can occur even after the treatment teams understanding of the patients status and
minor injury and is not consistently accompanied by vaginal the rationale for the treatment plans proposed for the patient.
bleeding. The presence of a hard uterus, larger than expected This section of the chart contains progress notes from vari-
for gestational age, is suspicious for abruption. Disseminated ous disciplines (Physicians; nurses; respiratory therapists;
intravascular coagulopathy is an ominous complication that occupational, speech, and physical therapists; clinical phar-
can occur with hours of placenta abruption or amniotic fluid macists; clergy; nutrition support services; and so forth). It
embolization. Because sensitization of Rh-negative women also contains data from laboratory and other diagnostic stud-
occurs with miniscule amounts of fetal Rh-positive blood, ies. The second purpose of the chart is to transmit instructions
all injured Rh-negative women should be considered for about the patients care. This is the orders section. The final

Lawrence_Chap01.indd 20 7/21/2012 5:57:24 PM


purpose of the chart is to provide a record of the events that documentation leads to distortion of the facts in the record
occurred during the patients care. Careful thought should be and misconceptions on the part of others who are peripher-
given to the information placed in the record; this informa- ally involved with the patients care. Inaccuracy is a pow-
tion must be relevant to the course of treatment or diagnos- erful deterrent to the quality of patient care at all levels.
tic workup. Before notes are written, consideration should be Suspicions and theories can take on the appearance of fact
given to the following six points: if they are perpetuated over time in the medical record.
1. Does the information pertain to patient care? Only infor- Once such fallacies become embedded in the record, it can
mation that pertains to the actual care of the patient should take a great deal of research within the chart to uncover the
be entered into the medical record. The medical record truth. Therefore, diagnostic labels should be factual rather
should not be used to relay messages among consulting than speculative.
services. Extraneous information is inappropriate and may 6. Does the note serve the best interest of the patient, the phy-
generate medicolegal liability. Examples include editorial sician, and the health care team? The medical record is kept
comments about the appropriateness or inappropriateness on behalf of the patient to document the events, timing,
of recommendations made by other Physicians. If there is and thinking relating to the care given during the period of
genuine disagreement about the appropriate plan of man- hospitalization. The record is a confidential document and
agement, then the reasons supporting the plan of manage- cannot be revealed to anyone who is not directly involved
ment chosen should be documented in the chart, without in the care of the patient, nor can it be revealed without
editorial comment about the competency of the Physicians the patients or a responsible agents written consent. An
who have written dissenting opinions. individual who discloses such information without this
2. Is the information of value in documenting the treatment consent breaches the ethical contract between patient and
course? Little value is obtained in repeating factual material physician.
that has been previously documented. In teaching institu- Increasingly, health care providers are making the transition
tions, it is common to see history and physical examinations from a paper medical record to an electronic medical record
or progress notes recorded by students, house staff, and (EMR). In 1991, the Institute of Medicine (IOM) released an
attending Physicians. The delivery of care in an educa- influential report, The Computer-Based Patient Record: An
tional environment is by necessity repetitive. Students gain Essential Technology for Health Care. The IOMs vision for
important experience in writing progress notes that reflect the EMR is of a document that (1) has a standardized for-
careful and thoughtful evaluation of the patient. Students mat and nomenclature, (2) is easily searchable, (3) is quickly
often obtain important medical information, and their notes accessible to those who need to participate in the care of
should be carefully written. The best progress notes are the patient, and (4) can be linked with databases that could
those in which the assessment and plan are carefully laid improve health care in an evidence-based manner and mini-
out, with a clear rationale demonstrating why certain diag- mize errors in the delivery of health care. In 1996, a federal
nostic hypotheses are being entertained, what the therapeutic law known as the Health Insurance Portability and Account-
options are, and why certain options are favored over others. ability Act (HIPAA) was passed. Compliance is required of
3. What details will be important for the future care of the virtually all health care providers, and failure to comply can
patient? Operative notes are perhaps the best illustration result in civil (monetary) or criminal (imprisonment) penal-
of the importance of identifying potential needs for future ties. This law specifies the ways in which medical records
care. For example, recording surgical findings is more may be accessed, and by whom. While it was not the intent of
important than noting the type of suture used to perform an this law to hinder medical care, it is clear that there are many
anastomosis. A careful description of the abdominal organs reasons why great care must be taken in being certain that the
as they are inspected and palpated may be of value if future medical record accurately reflects the patients care in a man-
review becomes necessary. Information about blood loss, ner that respects each individuals privacy. In addition to the
blood and fluid replacement, and operative time is more advantages surrounding data management, a computer order
relevant than many of the technical nuances of the opera- entry system is considered among the most important compo-
tive procedure. The thought process used in diagnosing an nents of a hospitals overall program to promote and ensure
illness or selecting a therapy is often more important than patient safety. The rate of EMR use has remained low, but
the technical details. is gradually increasing, with 25% of office-based Physicians
4. Is the information accurate? Extreme care should be taken using some EMR system as of 2005. However, only 10% of
to ensure the accuracy of information that is entered into the Physicians have a fully integrated EMR, with computerized
medical record. Confusion may occur when verbal reports order entry, computerized prescription writing, full test result
of diagnostic studies written into the progress notes do not reporting, and electronic progress notes. In 2009, approxi-
agree with formal reports, once they are typed, signed, and mately $19 billion was provided by the federal government
filed. Erroneous information can lead to disastrous results as directed by the American Recovery and Reinvestment Act
and may be more damaging than no information. Every to help defray some of the large economic burden incurred by
effort should be made to maintain accuracy and consistency Physicians as they convert to an EMR.
in the information that is recorded. In some circumstances, The medical record can be the physicians and the patients
clinical decisions are made based on a verbal report. When best ally or worst enemy. Documentation of all findings,
this situation occurs, it is appropriate to note it (e.g., Ver- results, rationales for diagnostic and management strategies,
bal report of positive blood culture received from the lab; and explanations to the patient, particularly in terms of risks,
plan removal of central line). benefits, anticipated results, and therapeutic alternatives, can
5. Are suspicions and theories clearly defined as such? An protect both the patient and the physician. The art in mastering
inexperienced physician may not precisely differentiate the medical record is achieving a balance between brevity and
suspicions, theories, and possibilities from reality. Incorrect completeness.

Lawrence_Chap01.indd 21 7/21/2012 5:57:24 PM


Physicians Orders however, specifically write their own routine in sufficient detail to
The physicians order section of the medical record should ensure that their plans are carefully followed.
be treated with care. Orders must be entered precisely, with Some nursing care functions must also be identified.
the intent of being followed, not interpreted. Unfortunately, These include special positioning, turning, pulmonary exer-
the latter is often the case because of the hasty scribblings cises, and care of wounds or drainage tubes. Foley catheters
of Physicians that may be unclear, illegible, or inaccurate, are placed to gravity drainage, nasogastric tubes to some
although computerized physician order entry (CPOE) is part type of suction apparatus, and wound drains to either suc-
of a robust safety program to minimize such opportunities tion or dependent drainage. The staff is informed specifi-
for error. Orders should be written with sufficient detail to cally about the management of these drains or tubes. Daily
eliminate possible misunderstanding. There is no excuse for care of the incision site is clearly noted. Retrograde infec-
illegible handwriting or imprecise orders. Every aspect of the tion from incision sites, especially with urinary catheters and
patients life, including diet, level of activity, and access to the wound drains, is a major contributor to morbidity. Patient
bathroomeven what the patient is to breatheis the respon- positioning is extremely important in preventing pulmonary
sibility of the physician once the patient enters the hospital. problems and preventing aspiration of the gastric contents in
Orders include the elements listed in Table 1-15. Content patients who are receiving enteral tube feedings. Other nurs-
and format may vary among institutions, but the principles ing instructions include the recording of fluid intake or out-
are the same. Usually, the first orders written concern gen- put from urinary catheters and drains; specific instructions
eral nursing care. Identification of the physician or team that for tube care, stripping, or irrigation; and notification of the
is responsible for the patient is important so that the staff physician in the event of a specific occurrence (e.g., urine
knows whom to contact if problems or questions arise. List- output <30 mL/hour, chest tube drainage >100 mL/hour).
ing the working diagnosis or reason for admission gives the The type and rate of intravenous fluid administration are
staff a general idea of the problem and sets the tone for the also specified. When multiple intravenous sites are used, it is
delivery of services. The frequency of vital signs is next. Any helpful to specify which fluids are to be infused at which sites.
special nursing evaluations (e.g., neurologic function) are also To prevent potentially fatal medication errors, meticu-
indicated. If the physician wishes to be notified of any of these lous attention to detail is mandatory when writing medica-
assessments (e.g., temperature >38.5C), the staff is informed. tion orders. The notation sequence is type of drug, dosage,
Diet specifications or NPO (nothing by mouth) orders are also route of administration, and frequency. These orders should
indicated. Special diets are required by some patients (e.g., those be absolutely clear and legible. If a physician is uncertain of
with diabetes, those undergoing special diagnostic procedures). the spelling of a drug name, he or she should consult a refer-
Too frequently, hospitalization is prolonged or expensive proce- ence. It is important to use only standard abbreviations, and
dures must be repeated because of lack of attention to the details the reader is strongly encouraged to become familiar with
of prescribing the appropriate diet. The level of patient activity is the Official Do Not Use List published by the Joint Com-
specified as well. Such orders are generally considered routine, and mission on the Accreditation of Healthcare Organizations
some hospitals may have standard protocols. Prudent Physicians, (Table 1-16). Writing medications on a separate section of

TABLE 1-16 Official Do Not Use List of the Joint

TABLE 1-15 General Considerations for Writing Commission on the Accreditation of
Orders Healthcare Organizations

Abbreviation Potential Problem Preferred Term

Physician/team responsible
U (for unit) Mistaken as zero, Write unit
four or cc
Immediate plans
IU (for international unit) Mistaken as IV (intrave- Write international unit
Vital signs/special checks/notification parameters nous) or 10 (ten)
Diet Q.D., Q.O.D. (Latin Mistaken for each other. Write daily and every
Level of activity abbreviation for once The period after the Q other day
Special nursing care instructions daily and every other can be mistaken for
day) an I and the O can
be mistaken for I
Wound care
Trailing zero (X.0 mg), Decimal point is missed Never write a zero by
Tubes/drains: management and care
Lack of leading zero itself after a decimal
Intake/output: frequency (.X mg) point (X mg), and
Intravenous fluids always use a zero
Medications: drug, dose, route, frequency before a decimal
point (0.X mg)
MS MSO4 MgSO4 Confused for one Write morphine sulfate
another. Can mean or magnesium
Laboratory orders morphine sulfate or sulfate
Special procedures/x-ray magnesium sulfate
Miscellaneous Source: http://www.jointcommission.org/patientsafety/donotuselist/.

Lawrence_Chap01.indd 22 7/21/2012 5:57:24 PM


the order sheet so that they are not mixed in with nonmedica-
TABLE 1-17 Sample Preoperative Note
tion orders may be advantageous; in this way, confusion and
oversights are avoided. Orders for routine medications (e.g.,
analgesics, laxatives, sleeping pills) are written first, followed Diagnosis: Cholelithiasis
by medications for the patients specific needs. Reviewing the Proposed surgery: Cholecystectomy with operative cholangiogram
medication lists daily is an excellent habit. Changes in drugs, History and physical: Completed (dictated)
dosage, or frequency are confusing for both the pharmacy and
Grade II/VI systolic murmur at apex
the nursing staff. If drugs are changed, writing an order to
stop the original drug, then ordering the new one is the best Hypertension (controlled)
approach. In most institutions, parenteral nutritional products Laboratory values: CBC: 14.5/41.5% 7,500
are prepared in the pharmacy; therefore, total parenteral nutri- Electrolytes: 140 | 4.2/26 | 101 Bun 10
tion orders are placed with the medication orders. Glu 105
Laboratory studies and special diagnostic procedures
should be specified as well. Special procedures, such as radi-
ographs, require additional thought. Request slips for these ECG: NSR-normal
studies should specifically state the presumptive diagnosis Present meds: HCTZ 50 mg qd
and the reason for the test. Personal consultation with the Blood: type and hold (specimen in blood bank)
radiologist or technician avoids confusion and prevents delays
Operative permit: Signed and on chart; risks, rationale, benefits,
or unnecessary repetition of procedures. If those who perform
and alternatives have been explained in detail;
the tests are aware of the reason for the testing, the results
patient understands and agrees to proceed
are nearly always more productive. Some procedures require
with the surgical plans
special preparation of the patient; therefore, these instructions
must be included in the orders. Routine or daily labora- Miscellaneous information:
tory or radiology orders are wasteful, rarely contribute to care, Signature _______________
and should be avoided. In the occasional situation in which CBC, complete blood count; BUN, blood urea nitrogen; GLU, glucose; CXR, chest x-ray; NAD, no
serial studies are needed to follow some aspect of the patients appreciable disease; ECG, electrocardiogram; NSRs, normal sinus rhythm; HCTZ, hydrochlo-
course, a stop time should be specified (e.g., Please draw rothiazide.
hematocrit q6h 24 hour). Laboratory and diagnostic stud-
ies should be used to confirm clinical suspicions and not as a
shotgun approach to reveal a diagnosis.
The miscellaneous category in Table 1-15 is intended for important components are listed in Table 1-18. The important
other orders that may be necessary, including requests for con- elements of the discharge note are listed in Table 1-19.
sultation, procurement of procedural permits or old records, or Event notes should be recorded whenever there is an unex-
admission of a patient to a special study or protocol. pected event in the patients course. These should briefly sum-
The orders are only as complete as you make them. Clar- marize what the problem was and the reasons for the steps
ity and legibility allow for efficient and appropriate delivery taken to address the problem. Discharge notes should be
of services. As previously noted, computerized order entry concise and list the patients reason for hospitalization (also
systems are increasingly common and are widely regarded as referred to as the principal diagnosis), a brief summary of
an essential component of any program to minimize medical the patients hospital course, what medications the patient is
error. to be discharged on, what medications the patient will take
after discharge, where the patient is to go after discharge, what
the patients level of activity is, and what the plan for follow-
Progress Notes up is. It is not necessary that the discharge summary recapitu-
A brief preoperative note to summarize the workup and the late each detail of the patients hospitalization.
pertinent physical and diagnostic studies is usually written In summary, the medical record is a legal document that con-
the day before surgery. These notes serve as a checklist to tains important information about the patients hospital course and
ensure that the important aspects of preoperative preparation
are completed. An example is shown in Table 1-17. A night
of surgery note should be recorded to document the condition
of the patient after the operation. Important information to be TABLE 1-18 Operative Note
included in this note would be the patients comfort level and
vital signs, fluid balance, pertinent examination findings, and Procedure:
any critical laboratory values caregivers would need to know Findings:
within the next few hours.
Surgeons: Attending surgeon:
Daily progress notes record the patients clinical course
throughout his or her hospital stay. Noting the hospital day Estimated blood loss:
number, the postoperative day, or the days after injury is help- Crystalloid replaced: Blood products:
ful. The format for progress notes varies among hospitals and Anesthesia:
even among services within the hospital. All notes should be
dated, timed, signed, and legible. A brief, handwritten opera-
tive note should list the important elements of the operation, Tubes/drains:
with consideration given to recording information that might Disposition:
be important in the immediate perioperative period, before the Signature:
official typed report is appended to the medical record. These

Lawrence_Chap01.indd 23 7/21/2012 5:57:25 PM


Nasobiliary tubes are usually placed endoscopically,

TABLE 1-19 Discharge Note
either to facilitate drainage of the biliary tree when there is
an obstructing process (stone, tumor, stricture) or to facilitate
Admission diagnosis: Date: drainage of bile via the biliary tract in cases of biliary fistula.
Discharge diagnosis: Date: T-tubes are placed within the common bile duct for the
Operative procedure: purpose of drainage. They are kept to closed gravity drainage.
Gastrostomy tubes may be placed surgically. When placed
Hospitalization course:
endoscopically, they are referred to as percutaneous endo-
Disposition: scopic gastrostomy (PEG) tubes. They may be used for drain-
Home care instructions: age or for feeding.
Activity Jejunostomy tubes can be placed surgically or endoscopi-
Diet cally (via the stomach). When placed endoscopically, they
may be placed in combination with a PEG tube. These are
typically placed for long-term nutritional access.
Wound care
Other Respiratory Tract Tubes
Discharge medications: Chest tubes are placed into the pleural cavity to evacuate air
(pneumothorax), blood (hemothorax), or fluid (effusion).
Follow-up instructions:
They are connected to a special suction system that (1) per-
Miscellaneous: mits a constant level of suction (usually 20 cm H2O), (2)
allows drainage of air and liquid from the pleural cavity, and
(3) prevents air from entering the pleural space from the out-
side. This latter function is known as a water seal. These
his or her response to diagnostic and therapeutic interventions. three functions can be achieved with the use of a three bot-
It is also a place where information given to the patient by the tle system, or a proprietary manufactured chest drainage and
health care providers can be documented. Despite the inconven- collection system.
ience involved, the time and effort devoted to thoughtful record Endotracheal tubes for adults are cuffed to maintain a seal
keeping returns many dividends when future review is necessary. between the tracheal wall and the tube. These tubes are used
when patients need short-term mechanical ventilation or when
Tubes and Drains they cannot maintain a patent airway.
Tracheotomy tubes are placed directly into the trachea
Before discussing individual types of tubes and their use, it
via the neck. They are used for patients who require long-
is useful to note that the size of many of these tubes is given
term mechanical ventilation or who cannot maintain a patent
as French size. French size refers to the outer diameter of
airway over the long term.
a catheter. Multiplying the French size by 0.33 will give the
outer diameter of the catheter in millimeters. Urinary Tract Tubes
Bladder catheters, commonly referred to as Foley catheters,
Gastrointestinal Tract Tubes
are placed to straight drain.
Nasogastric tubes are usually used to evacuate the gastric
Nephrostomy tubes are usually placed in the renal pelvis
contents. They are most commonly used in patients who have
to drain urine above an area of obstruction or above a delicate
ileus or obstruction. The modern nasogastric tube is a sump-
ureteral anastomosis.
type tube. The sump function is achieved by bonding a smaller-
Tubes placed percutaneously to drain abscesses are often
diameter tube onto the larger-bore (usually 18 Fr) tube. When
known as pigtail catheters. They are usually placed by inter-
the main tube is placed to continuous suction, there is a small
ventional radiologists with the help of imaging technology.
amount of air that will be drawn in by the sump tube, pre-
venting the development of a suction lock between the main Surgical Drains
tube and the gastric wall. Therefore, sump tubes should be Closed suction drains (Jackson-Pratt and Hemovac are two
placed to continuous suction. You may occasionally see a common types) are placed intraoperatively to evacuate actual
nonsump tube; these should be placed to intermittent suction or potential fluid collections. They are usually connected to
to break the seal that forms between the tube and the gastric a collapsible bulb or compressible box collection receptacle.
wall. Nasogastric tubes may also be used to feed the patient Sump suction drains, sometimes known as Davol drains, are
in some cases. If feeding is the intended purpose of the tube, very large. Although they are made of silicone, they tend to be
a soft, fine-bore tube is preferable to a stiff, large-bore tube. stiff. They are placed to continuous suction and are used for sit-
Nasoenteric tubes are usually intended for feeding. These uations when the drainage is expected to be thick or particulate.
should be soft and fine bore. A word about safety is in order. Passive tubes (Penrose drains) simply maintain a pathway
Nothing should be instilled into a feeding tube of any kind for fluid to follow, without suction to enhance flow. These are
(nasogastric or nasoenteric) unless the position of the tube is soft, cylindrical latex drains. Because suction is not applied to
known. Auscultation of injected air over the epigastrium can be them, they are very much a two-way path for bacteria.
misleading; a tube can be intrabronchial and still transmit the
sound of injected air to the epigastrium. The position of a feed-
ing tube can only be definitively confirmed with a radiograph or Wound Care
by direct palpation at the time of operation. Instilling tube feeds, In general, surgical wounds heal either by primary intention
medications, or radiographic contrast material into an intrapul- or by secondary intention (see Chapter 7, Wounds and Wound
monary (or intrapleural) tube can have lethal consequences. Healing). To heal by primary intention means that the wound

Lawrence_Chap01.indd 24 7/21/2012 5:57:25 PM


edges have been apposed, whether by sutures, wound clips, least every other day. If heparin is chosen, it should be given
tapes, or dermal adhesives. To heal by secondary intention preoperatively to obtain the greatest protection. Intermittent
means that the wound edges have been left unapposed. Usu- pneumatic compression (IPC) devices produce reductions in
ally, there is a dressing of some sort used to collect wound DVT rates similar to those of unfractionated heparin and may
fluids and help keep the wound from closing prematurely. be viewed as adjunctive. Their main liability is poor patient
A common situation in which healing by secondary inten- tolerance. The data regarding the prevention of venous throm-
tion would be encouraged would be in the management of an boembolism by IPCs are not strong. Presently, the mainstay
abscess. A saline-moistened cotton gauze dressing is used to of venous thromboembolism prophylaxis in surgical patients
gently fill the cavity. (The wound cavity should not be packed is some form of subcutaneous heparin. The routine general
tightly because this leads to tissue ischemia.) This helps to surgical patient is well protected by the unfractionated hepa-
collect drainage and to prevent the abscess cavity from sealing rin. Low-molecular-weight heparin is recommended for the
over. A variety of substances are used to moisten the gauze for trauma patient. Close communication with the anesthesiolo-
wounds managed in this way. Some examples include 0.25% gists is important if epidural analgesia is being considered in
acetic acid solution, Dakins solution (sodium hypochlorite), a patient who might receive low-molecular-weight heparin
and povidoneiodine solutions. Each of these can be shown because of the risk of spinal epidural hematoma formation.
to inhibit fibroblast proliferation in tissue culture, and neither
has any special advantage over plain, sterile saline solution.
Pain Management
It is appropriate to consider the subject of pain management Malignant Hyperthermia
in surgical patients. Physicians are often justifiably criticized This is a potentially fatal, hypermetabolic, autosomal domi-
for neglecting to attend to the pain of their patients as closely nant condition of skeletal muscle that is reported to occur
as they might monitor, for example, their laboratory values. in one in 14,000 children and one in 50,000 adults. Several
Asking the patient how their pain level is should be a routine genetic mutations are associated with malignant hyperthermia,
part of the review of systems taken on daily rounds, in the but all result in a disruption of intracellular calcium metabo-
clinic, or in the office. For patients who cannot report pain lism. Problems with the ryanodine receptor (calcium-release
(e.g., those in the intensive care unit, who may be mechani- channel) are found in over 50% of patients with this disorder,
cally ventilated and unable to speak), attention to their facial while problems with the dihydropyridine receptor are found
expressions and vital signs will give clues as to their level of in others. The result is a massive buildup of intracellular cal-
discomfort. The nature of the patients disease process and his cium released from the sarcoplasmic reticulum. This produces
or her comorbidities will determine the type of pain manage- violent and sustained muscle contraction and rigidity, heat
ment strategy he or she requires. For example, many patients production, and acidosis. Muscle necrosis and rhabdomyoly-
with thoracic or abdominal incisions are well served with sis may occur. The clinical findings in heat stroke and neuro-
epidural analgesia administered by the Anesthesia Pain Ser- leptic malignant syndrome are similar, and individuals prone
vice. Where possible, intravenous patient-controlled analgesia to malignant hyperthermia are thought to be more suscepti-
should be used for the intense pain that accompanies the early ble to these other conditions. Inhalational halogenated anes-
postoperative state. Once the patient is able to take medica- thetic agents and succinylcholine are known triggers of the
tions orally, the transition to oral pain medication is simple. syndrome as are extreme stress (heat) and vigorous exercise.
In the intensive care unit, where patients may not be able to A family history of relatives who have had problems with
manage the patient-controlled analgesia apparatus, continu- anesthetic agents may be the only preoperative clue. Suscep-
ous intravenous infusions of narcotics are appropriate and tible individuals may be confirmed with a muscle biopsy and
should be titrated by the nurse to keep the patient comfortable stimulated contraction studies.
without being overly sedated. An abrupt rise in end-tidal carbon dioxide is the first
sign. Masseter muscle rigidity is seen early in the syndrome
Deep Vein Thrombosis Prophylaxis in children, but not consistently in adults. Body temperature
Venous thromboembolism will afflict 25% of postoperative may climb by 1 to 2 every 5 minutes and reach extraordi-
patients if they are afforded no prophylaxis. Surgical patients nary levels. Temperature elevation, on the other hand, may not
are at particular risk for venous thromboembolism because present for up to 36 hours after exposure to the triggering agent.
they have each of Virchows three risk factors for venous Tachycardia, cyanosis, and muscle rigidity are prominent fea-
thrombosis: stasis, hypercoagulability, and endothelial injury. tures. Compartment syndromes may develop. Rhabdomyoly-
A variety of means have been examined in the effort to reduce sis may produce myoglobinuria. Cardiac rhythm disturbances
the incidence of postoperative deep vein thrombosis (DVT). appear to be associated with the hyperkalemia and hypercal-
Excellent evidence-based data show that surgical patients cemia that accompany muscle necrosis. Mixed respiratory and
should routinely receive such prophylaxis. Low-dose unfrac- metabolic acidosis is common, and a bleeding diathesis similar
tionated heparin is as effective in this population as low- to disseminated intravascular coagulopathy has been reported.
molecular-weight heparin and is usually less expensive. Use Early recognition is the key to successful treatment. Thirty
of any heparin compound carries a small but real risk of hep- years ago, mortality rates ranged as high as 70% but today have
arin-induced thrombocytopenia (HIT). The low-molecular- been reduced to <5%. The first step in management is to dis-
weight heparins have a lower risk of associated HIT. While continue the triggering agent. Dantrolene, a muscle relaxant
this thrombocytopenia is usually transient, there is a form, that blocks calcium release from the sarcoplasmic reticulum
known as white-clot syndrome, which can result in stroke, and disrupts excitationcontraction coupling, is the only agent
loss of limbs, or death. Thus, patients on routine heparin available for treatment. It is given by rapid intravenous push in
prophylaxis should have their platelet counts monitored at doses of 1 mg/kg (both adults and children) and continued until

Lawrence_Chap01.indd 25 7/21/2012 5:57:25 PM


symptoms subside or a maximum dose of 10 mg/kg has been of inspiratory exercises. Chest physiotherapy may also begin,
reached. Dantrolene is also available in oral form, and although particularly for patients with productive cough or chronic
the absorption is slow, it is consistent. Prophylactic oral dosing bronchitis. Re-expansion techniques (incentive spirom-
is 4 to 8 mg/kg in three to four divided doses 1 to 2 days prior etry) are appropriate for all patients. Some may even bene-
to elective surgery and continued for 1 to 3 days following the fit from chest physiotherapy. The most important strategies
procedure. Patients taking oral dantrolene may notice somno- involve adequate postoperative pain management, frequently
lence and muscular weakness. Hyperthermia is treated by cool- obtained with epidural analgesia, and early mobilization.
ing blankets, but not to the point where the patient is shivering. One of the advantages of minimally invasive surgery is the
Renal support in the form of mannitol, bicarbonate (contro- significant reduction in atelectasis as well as other more seri-
versial), and volume infusion is provided in the case of myo- ous pulmonary problems. Pharmacologic interventions and
globinuria from rhabdomyolysis. A careful search for occult diaphragmatic pacing have not enjoyed much clinical success
compartment syndrome is made and, if found, fasciotomy is or enthusiasm, although these interventions are still practiced
performed. Respiratory support with mechanical ventilation in some centers.
is frequently required to correct the respiratory component of
the acidosis. Dantrolene is usually effective in managing the Surgical Wound Failure
metabolic component of the acidosis, and bicarbonate infusion
is not generally recommended. Hyperkalemia is managed in Wound healing is a complex, but predictable and highly orches-
the standard fashion with exchange resins and insulin therapy trated, series of cellular, hormonal, and molecular actions that
if necessary. Seizure activity is treated with benzodiazepines. are initiated at the time of injury. The details of wound healing
are discussed in detail in Chapter 7, Wounds and Wound Heal-
Atelectasis ing. Acute wound healing failure involves an alteration in this
process as the result of mechanical forces, infections, or aberra-
Despite the frequent occurrence of atelectasisin up to 90% tions of the normal biologic response of injured tissue.
of patients having a general anestheticthere is no consensus Dehiscence, or acute surgical wound failure resulting in
regarding its etiology, its treatment, or even its clinical sig- disruption of the fascial closure, is acute mechanical failure
nificance. The definition of atelectasis varies from that of a of the surgical closure. The force exerted across the wound
simple collapse of the adult alveolus to one that requires clini- is greater than the strength of suture material or of the fascia
cal features of collapse or consolidation, unexplained fever itself. This latter failure is generally due to ischemia of the
(temperature >38C), a positive chest radiograph, or evidence tissue from suture material placed too tightly or becoming too
of infection on sputum microbiology. Alveolar unit collapse tight as edema develops at the site of wounding. Poor suturing
occurs with essentially all general anesthetics, regardless of technique can also be to blame. Local infection can also lead
the agents used. to destruction of the fascia.
General anesthesia results in a reduction of FRC by 400 to The spontaneous discharge of serous fluid from a wound is
500 mL in the adult. This reduction may fall below CV in many a sign heralding acute fascial dehiscence. These patients should
patients. The supine positioning loads the diaphragm, espe- be returned expeditiously to the operating room for examina-
cially if mechanical ventilation and paralytic agents are used, tion and repair of the closure. Perhaps nothing is more dramatic,
compressing lung tissue in the basal segments by as much as for both patient and doctor, than witnessing dehiscence of the
5%. Extrapolated to the entire lung, this represents up to 20% abdominal closure and evisceration of the abdominal organs.
of all functioning alveolar units. It is easy to see that obesity In such a case, the exposed organs should be covered with ster-
multiplies this effect. Under anesthesia, patients do not sigh or ile towels soaked in saline solution and the patient taken to the
cough, and mucociliary cleaning of the tracheobronchial tree operating room immediately. Occasionally, a deep space infec-
is impaired. Mucous plugging of small airways may result. tiona subphrenic, pelvic, or interloop abscessis associated
Absorption atelectasis, the uptake of gas from the alveoli in with this problem. (See Chapter 9, Surgical Infections, for fur-
the face of proximal obstruction, further contributes to lung ther discussion of intra-abdominal infections.)
unit collapse. This is especially true if high concentrations of
oxygen are used for induction or during the surgery. A loss or
a change in the physical properties of surfactant may further Surgical-Site Infection
contribute to the process. The effect is an increase in shunt It is estimated that over 500,000 cases of surgical-site infec-
fraction, that is, low ventilation to perfusion ratio, resulting in tions occur in the more than 27 million operative procedures
hypoxia. The postoperative period is characterized by incisional performed yearly, representing one-quarter of all nosocomial
pain, somnolence from analgesic use, suppressed cough, lack of infections. The frequency varies from hospital to hospital,
mobility, and nasopharyngeal instrumentation. These factors all surgeon to surgeon, operation to operation, and patient to
contribute to perpetuation of a situation in which tidal ventila- patient, and is presently followed as one of a number of qual-
tion is reduced and periodic re-expansion of collapsed alveolar ity measures reported to the federal government, tracked by
units by maximum inspiratory efforts is suppressed. third-party payers and employer consortiums and available in
Debate continues over whether atelectasis is associated with the public domain. Surgical-site infections are the second most
fever or whether the condition predisposes (or is the prodrome) common nosocomial infection and will occur in 2% to 5%
to more serious respiratory problems such as pneumonia or the of all surgical patients. Emerging antibiotic-resistant organ-
adult respiratory distress syndrome. There is experimental evi- isms are a growing problem. Surgical-site infections increase
dence that atelectasis alters host defenses, but the clinical sig- the length of hospital stay and hospital costs. Furthermore,
nificance of these findings has yet to be elucidated. acute wound failure can have devastating consequences in the
Management of postoperative atelectasis should begin form of fascial dehiscence, pseudoaneurysm formation, anas-
preoperatively, under ideal conditions, by encouraging cessa- tomotic leak, fistula formation, incisional hernia, deep space
tion of smoking for 8 weeks preoperatively and the institution infection, and mortality.

Lawrence_Chap01.indd 26 7/21/2012 5:57:25 PM


Factors contributing to surgical-site infections are discussed Fever

in Chapter 8, Surgical Infections. Signs of surgical-site infections An elevation in a patients core temperature postoperatively is
are those associated with inflammation: redness (rubor), swell- so common that many mistakenly consider it a normal post-
ing (tumor), localized heat and erythema (calor), and increased operative state. Next to requests for laxatives, analgesics, and
pain at the incision site (dolor). Tachycardia may be the first sleep aids, calls from the nursing staff regarding temperature
sign and fever may develop only later. Spontaneous drainage elevation are perhaps the most common. If asked to define
from the surgical wound indicates that there has been a delay in fever, most will offer a simple thermal definition without
recognition of this postoperative problem. Delay in recognition the important corollaries as to time of day, anatomic site
leads to destruction of the fascia and contributes to dehiscence of temperature determination, or the apparatus used to take
or incisional hernias. Prompt drainage minimizes these sequelae the measurement. The benchmark of 37C as normal body-
and antibiotics play a secondary role, unless there are extenuat- temperature was established circa 1868 and has only recently
ing circumstances. Failure of the patients tachycardia, fever, or been critically reviewed. To describe fever in purely thermal
ileus to resolve should suggest a deeper site of infection, and terms is a misleading oversimplification. The febrile response
additional diagnostic studies may be necessary. Occasionally, is a complex physiologic reaction to a stimulus that involves
the diagnosis is made by surgical exploration. not only a cytokine-mediated rise in core temperature, but also
Guidelines have been developed by the Centers for Disease the generation of acute-phase proteins and activation of the
Control to minimize the incidence of surgical-site infections endocrine and immune systems (Table 1-21). The pure ther-
and are shown in Table 1-20. mal definition of fever is further flawed because it implies a
single entity when in fact it represents a pasticcio of many
TABLE 1-20 Center for Disease Control
different temperatures, each representing a different body
Surgical-Site Infections Prevention region and state of activity. Additionally, fever should not be
Guidelines, 1999 confused with hyperthermia, which is a rise in body tempera-
ture not associated with a pyrogen.
Strength of The causes of fever are multiple and include noninfectious
Recommendation Recommendation (Table 1-22) as well as infectious etiologies (Table 1-23).
Some conditions have been classified as both infectious and
Do not remove hair unless it interferes with the operation 1A noninfectious, for example, acalculous cholecystitis, phle-
If removed, remove immediately before operation with 1A bitis. The classification, obviously, depends on whether the
electric clippers condition is associated with bacterial infection.
Shower or bathe with antiseptic agent night before surgery 1B The Society of Critical Care Medicine has adopted the
Surgeon performs surgical scrub for 25 min with 1B guideline that a temperature elevation to 38.3C is the trig-
appropriate antiseptic ger to initiate an investigation. The evaluation process begins
with a review of the circumstances surrounding the patient:
After scrubbing, keep hands up and away from body; dry 1B
patient location (intensive care unit vs. ward), length of
hands with sterile towel; don sterile gown and gloves
hospitalization, presence of mechanical ventilation and its
Identify and treat all remote infections before surgery 1A
Keep hospital stay as short as possible II
Administer antimicrobial agent only when indicated and 1A
select based on published recommendations for a TABLE 1-21 Characteristics of the Febrile State
specific operation and efficacy against most common
Endocrine and Metabolic
Increased production of glucocorticoids
Administer antimicrobial agents by IV timed to ensure bac- 1A
tericidal serum and tissue levels when incision made Increased secretion of growth hormone
Maintain therapeutic levels during operation and, at most, 1A Increased secretion of aldosterone
a few hours after closure Decreased secretion of vasopressin
Before colorectal elective operations, in addition to IV 1A Decreased levels of divalent cations (necessary for bacterial replication)
antibiotics, mechanically prep the colon with cathartic Secretion of acute-phase proteins
agents and enemas; administer nonabsorbable oral
antimicrobial agents in individual doses the day before
surgery Shift in blood flow from cutaneous to deep

For cesarean sections in patients at high risk, administer IV 1A Increased pulse and blood pressure
antimicrobial agents immediately after cord is clamped Decreased sweating
Do not use vancomycin routinely for prophylaxis 1B Behavioral
Shivering (rigors)
1A, Strongly recommended for implementation and supported by well-designed experimental,
clinical, or epidemiologic studies; Search for warmth (chills)
1B, Strongly recommended for implementation and supported by some experimental, clinical,
or epidemiologic studies and strong theoretical rationale; Anorexia
II, Suggested for implementation and supported by suggestive clinical or epidemiologic studies
or theoretical rationale.
Modified from Mangram AJ, Horan TC, Pearson MI, et al. The Hospital Infection Control
Practices Advisory Committee. Guideline for prevention of surgical site infection 1999. Infect Adapted from Saper CB, Breder CD. The neurologic basis of fever. N Engl J Med
Control Hosp Epidemiol 1999;20:247280, with permission. 1994;330(26):18801886, with permission.

Lawrence_Chap01.indd 27 7/21/2012 5:57:25 PM


tract infection (a colony count >105 CFU/mL) does not apply

TABLE 1-22 Noninfectious Causes of Fever
to catheterized intensive care patients. Further, bacteriuria and
urinary tract infection are not synonymous. Most patients with
Alcohol/drug withdrawal urinary catheters for more than 24 hours will have bacteria or
Atelectasis white cells in the urine, and this should not trigger antimicro-
Posttransfusion fever bial therapy.
Once the diagnosis is established, appropriate therapeutic
Drug fever
steps can be taken. As mentioned previously, in a few select
Cerebral infarction/hemorrhage clinical circumstances, it is appropriate to use broad-spectrum
Brain injury antibiotics. Generally speaking, these situations involve criti-
Adrenal insufficiency cally ill patients in whom withholding antibiotic therapy for
Myocardial infarction 24 to 48 hours until definitive cultures or diagnostic studies
are completed could lead to disastrous consequences. Most
intensivists select broad-spectrum drugs, chosen on the basis
Acalculous cholecystitis of sensitivity profiles of their own units, and then switch to
Ischemic bowel more focused therapy when the cultures return.
Aspiration pneumonitis The question arises as to whether the fever itself should
be treated with antipyretics. Much divergent opinion on this
issue exists, and there is little prospective scientific evidence
Subarachnoid hemorrhage to support either position. Fever is an adaptive response that
Fat emboli conferred a survival advantage on warm-blooded animals.
Transplant rejection Temperature elevation enhances immune function by increas-
DVT/phlebitis ing antibody production; increasing cytokine expression;
enhancing neutrophil, lymphocyte, and macrophage func-
Pulmonary emboli
tion; and reducing bacterial replication. Temperature eleva-
Gout/pseudogout tion also confers a resistance to bacterial invasion. Still, some
IV contrast reaction health care providers feel that fever is harmful and noxious
GI bleeding and should be suppressed. The conclusions that can be drawn
Cirrhosis (without primary peritonitis)
from the literature are summarized as follows:
Short courses of antipyretics in approved doses carry a low
risk of toxic side effects.
Decubitus ulcer
The benefits of antipyretic use to the patient are uncer-
Adapted from Marik PE. Fever in the ICU. Chest 2000;117(3):855869, with permission. tain, other than perhaps the analgesic effect. The loss of
the immunoprotective effects of fever is concerning and
potentially harmful. There are no good comparative data
on this issue. The increase in metabolic demand (10% for
each degree Celsius increase) associated with fever may
duration, instrumentation (e.g., catheters, vascular lines, tubes be poorly tolerated in the elderly or debilitated, especially
in the nose or chest), duration of the instrumentation, medi- those with cardiac or pulmonary conditions.
cations, surgical sites and the reason for the surgical proce- Children should not be given aspirin.
dure (e.g., elective, emergent, trauma, gastrointestinal tract), Antipyretics do not prevent febrile seizures or raise the
current treatments, and diagnosis. This first step, if performed seizure threshold.
carefully and thoughtfully, will indicate the direction the doc- Cooling blankets should not be used to treat fever (although
tor should take to investigate the cause of the fever. Secondly, they are used to treat hyperthermia). The patient should not
a directed physical examination is performed to look for clues be cooled to the point of inducing shivering.
and/or confirmation of a suspected source. Table 1-23 can If antipyretics are used, they should be used on a scheduled
be used as a checklist to guide the evaluation process. Only basis and not as the occasion arises.
after these two steps have been taken should consideration Indomethacin and nonsteroidal anti-inflammatory drugs
be given to ordering diagnostic studies. Undirected blanket should not be used in patients with coronary artery disease.
ordering of laboratory tests, random cultures, and radio- Anything that increases the cerebral metabolic rate in
graphs are appropriate only in very specific circumstances patients with traumatic brain injuries (e.g., fever, seizures)
(e.g., patients on prolonged mechanical ventilation, those who increases cerebral oxygen demand and cerebral blood flow.
are immunosuppressed, or those with indwelling catheters or This can increase intracranial pressure.
monitoring devices). For the majority of postoperative surgi-
cal patients, a selective approach to confirmatory testing is
cost-efficient, effective, and high-quality medical practice.
The most common nosocomial infectious causes of fever in
the intensive care units are ventilator-associated pneumonia, In 2000, the IOM issued a report, To Err is Human, which
sinusitis, catheter-related sepsis (primarily gram-negative), looked at population-based studies of medical error. The
Clostridium difficile colitis, abdominal sepsis, and complicated report concluded that between 44,000 and 98,000 Americans
wound infections. Notably absent from this list are urinary tract die yearly in hospitals from medical mistakes. This report
infections. Unless it is pyelonephritis, a urinary tract infection brought the issue of medical safety to the forefront of our
is rarely a cause of fever. The standard definition of a urinary national consciousness. A cross section of stakeholders

Lawrence_Chap01.indd 28 7/21/2012 5:57:26 PM


TABLE 1-23 Physical Examination Checklist for Investigating Cause of a Fever

Anatomic Site Condition Clue

Head and Neck
Sinusitis/otitis Nasal/oral instrumentation/facial fracture
Meningitis Skull fracture/instrumentation/craniotomy/CSF leak
Parotitis/periodontal abscess; Elderly/periodontal disease/dehydration/oral instrumentation
Peritonsillar/pharyngeal abscess Immunosuppression/facial fracture
Deep neck infection Surgery/penetrating injury (especially digestive tract)/periodontal disease
Pneumonitis/lung abscess Intubation/mechanical ventilation/contusion/penetrating injury/aspiration
Mediastinitis Esophageal injury/sternotomy/neck exploration/penetrating thoracic
Empyema Hemothorax/tube thoracostomy/duration of thoracic instrumentation
Endocarditis Central vascular access/TPN/valvular disease (e.g., mitral valve
prolapse)/periodontal disease
Pericarditits Immunosuppression/broad-spectrum antibiotics
Abdomen and Retroperitoneum
Intra-abdominal abscess Previous celiotomy/splenectomy/visceral organ repair/anastomosis/
enteric contamination/bullet tract/possible missed injury
Acalculous cholecystitis Age/hypotension/broad-spectrum antibiotics/diabetes
Ischemic viscera Mesenteric injury/hypotension/pressors
Colitis Broad-spectrum antibiotic use/diarrhea
Pancreatitis (necrotizing) Hypotension/biliary stones/splenectomy/direct injury
Urinary tract Bladder instrumentation/comorbid urinary tract disease/urinary tract
Prostatitis Instrumentation/duration/age
Primary peritonitis Hepatic failure/cirrhosis/ascites
Pylephlebitis Intra-abdominal process/abscess
Occult perirectal abscess Hematogenous malignancy/diabetes/
Diverticular disease/appendicitis Preexisting disease/direct injury
Occult compartment syndrome Unconscious/extremity fracture/casts/hypotensive episodes/
immobilization (gluteal compartments)/ crush injury
Phlebitis/arteritis Duration of hospitalization/instrumentation/injury
Wounds (Surgical or Traumatic)
Superficial or deep abscess Presence/contamination/time to definitive management/GI injury/diabe-
tes/vascular disease
Necrotizing soft tissue infection GI injury/diabetes/immunosuppression
Necrotizing myositis/ischemia Occult compartment syndrome/unconsciousness
Decubitus ulceration/abscess Immobilization

within the health care system, from government policy devel- relied heavily on Crew Resource Management strategies in
opers (e.g., the Center for Medicare and Medicaid Services) designing systems to minimize error, and, if error should
to business (e.g., the Leapfrog Group), to regulators (e.g., occur, generate useful (rather than accusatory or recrimina-
Joint Commission on the Accreditation of Healthcare Organ- tive) discussion. Principles such as standardization of care,
izations), as well as individual practitioners and their profes- structured handoffs, simplification, use of forcing functions
sional bodies (e.g., the American College of Surgeons), took (e.g., computer order entry), avoiding reliance on memory,
note and began to approach the problem of patient safety from timeouts, and use of checklists prior to procedures have helped
a more scientific and systems-based perspective. In 2006, the reduce the volume of medical error. The U.S. Department
National Quality Forum published a list of never events, of Veterans Affairs originally developed the National Surgi-
which are listed in Table 1-24. The medical community has cal Quality Improvement Program (NSQIP), which has been

Lawrence_Chap01.indd 29 7/21/2012 5:57:26 PM


TABLE 1-24 Events that Must Never Occur

Surgical Events
Surgery performed on the wrong body part
Surgery performed on the wrong patient
Wrong surgical procedure on a patient
Retention of a foreign object in a patient after surgery or other procedure
Intraoperative or immediately postoperative death in a normal healthy patient
Product or Device Events
Patient death or serious disability associated with the use of contaminated drugs, devices, or biologics provided by the health care facility
Patient death or serious disability associated with the use or function of a device in patient care in which the device is used or functions other than as intended
Patient death or serious disability associated with intravascular air embolism that occurs while being cared for in a health care facility
Patient Protection Events
Infant discharged to the wrong person
Patient death or serious disability associated with patient disappearance for more than 4 hr
Patient suicide, or attempted suicide resulting in serious disability, while being cared for in a health care facility
Care Management Events
Patient death or serious disability associated with a medication error
Patient death or serious disability associated with a hemolytic reaction due to the administration of ABO-incompatible blood or blood products (transfusion of the wrong
blood type)
Maternal death or serious disability associated with labor or delivery on a low-risk pregnancy while being cared for in a health care facility
Patient death or serious disability associated with hypoglycemia, the onset of which occurs while the patient is being cared for in a health care facility
Death or serious disability (kernicterus) associated with failure to identify and treat jaundice in newborns
Stage 3 or 4 pressure ulcers acquired after admission to a health care facility
Patient death or serious disability due to spinal manipulative therapy
Environmental Events
Patient death or serious disability associated with an electric shock while being cared for in a health care facility
Any incident in which a line designated for oxygen or other gas to be delivered to a patient contains the wrong gas or is contaminated by toxic substances
Patient death or serious disability associated with a burn incurred from any source while being cared for in a health care facility
Patient death associated with a fall while being cared for in a health care facility
Patient death or serious disability associated with the use of restraints or bedrails while being cared for in a health care facility
Criminal Events
Any instance of care ordered by or provided by someone impersonating a physician, nurse, pharmacist, or other licensed health care provider
Abduction of a patient of any age
Sexual assault on a patient within or on the grounds of a health care facility
Death or significant injury of a patient or staff member resulting from a physical assault (i.e., battery) that occurs within or on the grounds of a health care facility

adopted by the American College of Surgeons. NSQIP pro- Prevent Surgical-Site Infectionsby reliably delivering
vides to each surgeon risk-adjusted outcome data. This has in the correct perioperative antibiotics at the proper time
turn led to reductions in complication rates and in mortality. Prevent Ventilator-Associated Pneumoniaby implement-
An Institute for Healthcare Improvement 100,000 Lives ing a series of interdependent, scientifically grounded steps
campaign enlisted 3,100 hospitals to implement six new Implementation of these practices has been estimated to have
proven safe practices: resulted in approximately 122,000 lives saved. Finally, current
Deploy Rapid Response Teamsat the first sign of patient approaches to team-based care emphasize clear communica-
decline tion with a tone of mutual respect in an atmosphere in which it
Deliver Reliable, Evidence-Based Care for Acute Myo- is safe to call attention to error. A cornerstone of this approach
cardial Infarctionto prevent deaths from heart attack is the recognition that no one individual can possibly single-
Prevent Adverse Drug Events (ADEs)by implement- handedly possess the expertise to coordinate every aspect of
ing medication reconciliation a patients care. The highly hierarchical model of health care
Prevent Central Line Infectionsby implementing a delivery with the physician at its center is transitioning to a
series of interdependent, scientifically grounded steps truly multi- and interdisciplinary model.

Go to http://thePoint.lww.com/activate and use your scratch-off code on the inside cover of this book to access
bonus chapters, question bank, videos, and more.

Lawrence_Chap01.indd 30 7/21/2012 5:57:26 PM


Questions therapy, an estimate of liver dysfunction given by the model for
Choose the best answer for each question. end stage liver disease (MELD) score is needed. Which one of the
following laboratory studies is needed to calculate a MELD score
1. A 52-year-old man is in the clinic to discuss treatment of a newly for this patient?
diagnosed pancreatic cancer. He has no significant past medical A. Alkaline phosphatase
history. He takes no medications. There is no evidence of meta-
B. Serum creatinine
static disease, and the tumor is small and appears to be resectable
C. Serum ammonia
by pancreaticoduodenectomy (Whipple procedure). Optimal treat-
D. Serum albumin
ment would also include adjuvant radiation therapy and chemo-
E. Serum gamma glutamyl transpeptidase ( GT)
therapy. Informed consent for this patient is best defined as
A. a form that can be used as a legal defense should a complica-
4. Which of the following patients is at the lowest risk for postopera-
tion occur during the treatment of the patients problem.
tive deep vein thrombosis?
B. a process in which the physician and patient discuss the risks
and benefits of different approaches to the patients problem. A. An 18-year-old male with femur and lumbar fractures
C. a process in which every possible complication of treatment is B. A 55-year-old morbidly obese female undergoing total knee
enumerated. replacement
D. a theoretical construct with little practical utility. C. A 62-year-old man undergoing prostatectomy for cancer
E. a philosophical principle that applies to surgical procedures but D. A 45-year-old woman undergoing hysterectomy and bilateral
not medication administration. salpingo-oophorectomy and debulking for ovarian carcinoma
E. A 38-year-old woman undergoing carpal tunnel release
2. A 60-year-old woman is being evaluated for surgery to repair an
abdominal aortic aneurysm under general anesthesia. She smoked 5. A 28-year-old man is undergoing an operation for right inguinal
a pack of cigarettes daily for 35 years, but quit 5 years ago when she hernia. The anesthesiologist notices that his end-tidal CO2 value
had a myocardial infarction (MI) complicated by congestive heart fail- rises abruptly, and the patients jaw is stiff. The patients tempera-
ure. She still has occasional orthopnea. She also has hypercholester- ture is 41C, his heart rate is 130 beats/minute, and his blood
olemia and hypertension. Which one of the following factors suggests pressure (BP) is 130/75 mm Hg. Which of the following abnormali-
the greatest risk for a cardiac complication following her surgery? ties would be expected if a sample of his blood were tested at this
A. History of cigarette smoking point in the operation?
B. Congestive heart failure with orthopnea A. Hyperkalemia
C. General anesthesia B. Hypocalcemia
D. Hypertension C. Alkalosis
E. Hypercholesterolemia D. Anemia
E. Hypoalbuminemia
3. A 45-year-old man with a 25-year history of hepatitis C and
cirrhosis is found to have a small hepatocellular carcinoma of
the right lobe of the liver. In order to assess his risk for surgical

Lawrence_Chap01.indd 31 7/21/2012 5:57:27 PM


Answers and Explanations value for creatinine is automatically set to 4). Albumin is a component
1. Answer: B of the Childs-Pugh classification, but not the MELD score. Alkaline
phosphatase is useful in determining biliary tract obstruction. Gamma
Informed consent is a process in which the physician and patient dis-
GT is very sensitive for hepatobiliary disease and is best used to deter-
cuss the risks and benefits of different approaches to the patients
mine if an isolated elevation of alkaline phosphatase is due to liver
problem. This includes discussion of the most likely outcomes of treat-
rather than bone disease.
ment (including the decision to observe rather than operate). Informed
consent permeates most of the discussions physicians have with 4. Answer: E
their patients, although the discussions may not be labeled as such. It Patients who are immobile, who have congestive heart failure or
applies to medication choices as much as to surgical decision making, malignancy, who undergo pelvic or joint replacement operations, or
although a separate consent form is generally not obtained each time who have vertebral, pelvic, or long bone fractures are at highest risk.
a new medication is prescribed. Carpal tunnel release does not confer increased risk of deep vein
2. Answer: B thrombosis.

General anesthesia does not itself increase risk of cardiac complica- 5. Answer: A
tions. The factors that do increase such risk include ischemic heart This is a classic description of malignant hyperthermia. The typical
disease, congestive heart failure, chronic kidney disease, cerebrovas- electrolyte picture is that of rhabdomyolysis, with hyperkalemia, hyper-
cular disease, or high-risk operations such as major vascular surgery. calcemia, and acidosis. Malignant hyperthermia is not known to affect
3. Answer: B red cell mass or albumin levels. The patient should be given 100%
oxygen, the operation should be stopped and the wound closed, and
The MELD score formula is (0.957 ln(Serum Creatinine) + 0.378
dantrolene should be administered.
ln(Serum Bilirubin) + 1.120 ln(INR) + 0.643 ) 10 (if hemodialysis,

Lawrence_Chap01.indd 32 7/21/2012 5:57:27 PM

Fluids, Electrolytes, and
Acid-Base Balance

1. Know normal electrolyte composition of body fluids. 4. Understand methods of determining normal and periopera-
2. Understand the fluid compartments in the body and how tive fluid requirements for patients.
they vary with age and obesity. 5. Understand normal acidbase status of surgical patients
3. Understand and treat common electrolyte abnormalities in and how to treat abnormal acidbase situations in surgical
surgical patients. patients.

For most physicians, the topics of fluids and electrolytes are for <1% of the population. Unfortunately, the information
boring, mundane, and generally glossed over or ignored. regarding this young male is usually applied to the other 99%
Unfortunately, this indifference or lack of understanding of the population, which results in so many of the complica-
regarding fluid and electrolyte management results in a host of tions seen in surgical patients. One must extrapolate, not apply
complications. Some of these complications include increased directly, this information to the care of patients.
length of stay, increased cost, wound infection, delayed wound In both males and females, TBW is directly proportional
healing, anastomotic failure, and tachyarrhythmia. There are to muscle mass, which is about 70% water, and inversely
some estimates that one in five patients develops one or more related to fat, which is about 10% water. Consequently, TBW
complications as a result of fluid and electrolyte management equivalent to 60% of weight only applies to the small fraction
errors. Many of these complications are preventable if the of todays population who are male, young, and physically
physician pays as much attention to the nuances of fluids and fit. TBW may be as little as 35% of weight in the morbidly
electrolytes as to the more exciting aspects of surgery, such obese; the very elderly, who lose muscle as they age; or those
as the operating room. who lose muscle rapidly because of disease or injury. TBW
Understanding and managing fluids, electrolytes, and acid is estimated to be about 55% in young healthy physically fit
base status are critical aspects of the treatment of surgical females.
patients. This chapter provides a brief overview of fluid, elec- TBW is partitioned into two main compartments. In the
trolyte, and acidbase balance before discussing clinical prob- ideal young healthy male, the intracellular fluid represents
lems specific to surgery and surgical patients. It is intended about two-thirds of TBW (40% of body weight, or about 28 L
to be an introduction to this subject. For more complete and in a 70-kg man), and the extracellular fluid (ECF) one-third
comprehensive information, see the many available texts and (20% of body weight, or about 14 L in the same individual).
articles in the literature, some of which are listed at the end of However, as noted previously, in those with significant reduc-
this chapter. A table of normal serum laboratory values for tions in lean body mass or the morbidly obese, these ratios
common electrolytes is provided in the online glossary. change such that extracellular space fluid in these individuals
may equal or even exceed intracellular fluid as a percentage of
total body water.
NORMAL PHYSIOLOGY There is little difference in the electrolyte composition of
the two ECF subdivisions, plasma and interstitial space. In
Total Body Water and Compartments plasma (Table 2-1), sodium is the chief extracellular cation
Total body water (TBW) in the adult varies according to age, with smaller amounts of potassium, calcium, and magnesium
sex and lean body mass. Historically, and in most textbooks, present. The corresponding anions are chloride, bicarbonate,
this refers to the healthy, young 70-kg male who now accounts and smaller amounts of proteins, sulfates, and organic acids.


Lawrence_Chap02.indd 33 7/21/2012 5:58:21 PM


has no effect on osmolarity, does not include such movements

TABLE 2-1 Normal Plasma Values of Common
of water between the cells and the interstitial fluid.

Electrolytes Concentration Units Sodium

Cations Total body sodium is estimated at 63 mEq/kg, but one-third
is fixed in bone. The other two-thirds or 40 mEq/kg, most of
Sodium 135145 mEq/L
which is extracellular, is the exchangeable fraction. Sodium
Potassium 3.55.0 mEq/L and its related anions represent 97% of the osmotically active
Calcium 8.010.5 mg/dL particles that are normally present in the ECF compartments.
Magnesium 1.52.5 mEq/L Extracellular osmolarity is estimated by the formula:
Anions [Na+] [glucose (mg/dL) 18] +
Chloride 95105 mEq/L [blood urea nnitrogen (BUN) 2.8],
Bicarbonate 2430 mEq/L
Phosphate 2.54.5 mEq/L where [Na+] is serum sodium concentration. If the value
approximates 290 10 mOsmol/L, it can be reasonably
Sulfate 1.0 mEq/L
assumed that extracellular osmolarity is within normal limits.
Organic acids 2.0 mEq/L The normal adult sodium requirement is 1 to 2 mEq/kg/
Albumin 3.05.0 g/dL day, although the usual oral intake far exceeds this amount.
Total protein 6.08.4 g/dL Normal kidneys excrete sodium when intake is high and con-
serve it when intake is low maintaining fairly constant body
sodium. Renal sodium resorption can be so efficient that
nearly none is lost in the urine during maximum conservation.
In the interstitial space, the ionic composition differs from Assuming normal renal perfusion and membrane function,
plasma only with respect to its lower concentration of protein both sodium and water are filtered at the glomerulus. In the
and the related minor changes in chloride and bicarbonate lev- proximal tubules, large amounts of each are recovered. Ulti-
els. In contrast to the extracellular compartment, the intracel- mately, however, the determination of renal conservation or
lular dominant cations are potassium and magnesium and the excretion of sodium or water depends on selective processes
dominant anions are phosphates, sulfates, and proteins. The that occur at more distal tubular sites.
striking differences in intracellular and extracellular electro- Sodium resorption in exchange for potassium and hydrogen
lyte composition are maintained by selective permeability of ion secretion in the distal tubules is a direct effect of the adre-
cellular membranes. Free diffusion of proteins, chloride, and nal cortical hormone aldosterone. This action helps to main-
multivalent ions is limited. Various transporter systems in the tain both extracellular volume and osmolarity. Extracellular
cell wall promote the movements of electrolytes across the cell volume reduction, particularly in the intravascular space, is
membrane such that sodium remains mainly outside the cell a potent stimulus for aldosterone release. This response is
and potassium primarily in the cell. Water is rapidly and freely triggered by a decrease in renal perfusion, which causes the
diffusible among all compartments including intracellular fluid. juxtaglomerular apparatus to secrete renin. Renin, in turn,
Movement of water from one compartment to another is cleaves angiotensinogen to produce angiotensin I, which is
passive and determined by the action of physical forces exerted then converted by angiotensin-converting enzyme (ACE) to
across the intervening membranes. The capillary membrane angiotensin II, a potent stimulator of aldosterone secretion.
that separates the interstitial and intravascular spaces, under When activated by a decrease in volume, stretch receptors in
most circumstances, is freely permeable to water, electrolytes, the atria can also increase aldosterone secretion. The potas-
and solutes, but not to proteins. Consequently, the net flow of sium level, which is usually inversely related to serum sodium
water between these two spaces is a function of the balance concentrations, is the most sensitive stimulator of aldosterone,
between fluid pressures generated on either side of the mem- acting via depolarization of cells in the zona glomerulosa.
brane and the effective colloid osmotic pressures. Colloid Adrenocorticotropic hormone (ACTH) can also stimulate
oncotic pressure is generated by the higher concentrations of aldosterone production, but this is a minor role. The secretion
nondiffusible protein in the plasma and the endothelial gly- of aldosterone is suppressed by extracellular volume expan-
cocalyx. On the other hand, the exchange of water between sion, increased sodium concentration, and decreased potas-
the intracellular and interstitial compartments is totally deter- sium concentration.
mined by osmotic gradients across the cell membranes. Nor- Antidiuretic hormone (ADH, Vasopressin) is released
mally, there is no gradient and no significant net water flow in from the posterior pituitary gland in a diurnal fashion, peaking
either direction because the osmolarity, or number of osmoti- between 2 and 4 oclock in the morning, and to a lesser extent
cally active particles per liter of solution on either side of the in the early afternoon. The early morning peak is usually not
membrane, is the same. When ECF becomes hypo-osmolar considered in patients and as a result, unnecessary fluid infu-
relative to normal values, water flows into the cells in which sions in response to a drop in urine output and a perceived
the osmolarity is higher. A new equilibrium is reached, and hypovolemia are common. For example, if a patient is in the
the osmolarity of both compartments is less than the normal postoperative phase, has normal blood pressure and pulse
285 mOsm/L. Similarly, hyperosmolarity develops in both pressure, and has warm extremities and full veins, increased
compartments if extracellular osmolarity is increased. In this fluid infusions in response to an early morning drop in urine
case, osmotic equilibrium is reached by an egress of water output are not indicated.
from the cell into the extracellular space. In contrast, isotonic There is increased ADH secretion in response to decreased
fluid expansion or contraction of the extracellular space, which blood volume; increased plasma osmolarity; and, to a lesser

Lawrence_Chap02.indd 34 7/21/2012 5:58:22 PM


extent, angiotensin II and other secondary stimuli. It increases The bicarbonatecarbonic acid buffer system in ECF is one of
the reabsorption of water from cells in distal convoluted the most important components. Its relation to pH is described
tubules and collecting tubules through aquaporins in the api- by the Henderson-Hasselbalch equation and its modifications:
cal membrane of these cells. This effect and its modulation
are important in the regulation of fluid volume and osmolar-
ity in the body. Intracranial osmoreceptors adjacent to the pH = 6.1 + log [HCO3]/0.03 Paco
P 2
anterior wall of the third ventricle and in the hypothalamic, 7.4 = 6.1 + log 24 mEq/L/1.20 mEq/L.
supraoptic, and paraventricular nuclei initiate ADH secretion
when plasma osmolarity rises. They also inhibit ADH secre-
tion when plasma osmolarity decreases. The production and A more useful variation of these equations is:
release of ADH also depend on the activity of volume recep- [H +]] 24 Paco2/[HCO3].
tors in the right and left atria. Decreased extracellular volume
sensed in the right atrium and the carotid arteries leads to ADH CO2 is transported in the plasma in three forms: dissolved CO2,
secretion. Increased volume sensed in the left atrium leads to CO2 bound to proteins, and free bicarbonate. If the laboratory
inhibition of ADH release. Volume-dependent responses usu- reports CO2 content in the serum electrolyte panel, [HCO3]
ally override the effects of the osmoreceptor controlling sys- concentration can be roughly calculated from the serum elec-
tem when the two are in conflict. trolytes by subtracting 1 for the dissolved CO2, and 1 to 2 for
the bound fraction. If [Paco2] and [HCO3] are normal, then the
Potassium [H+] is 40 nmol. The value for [H2CO3] can be determined as
In the normal young adult, total body stores of potassium are the arithmetic product of a proportionality constant (0.03) and
approximately 50 to 55 mEq/kg, 98% of which is intracellular the Paco2. In clinical practice, direct measurements of arterial
at a concentration of 150 mEq/L cell water. The ECF com- pH and Paco2 are readily available, and [HCO3] can be cal-
partment (including plasma) of the ideal70-kg young male culated or derived from a nomogram, assuming all measure-
contains a total of 70 mEq of K+ (present at a concentration ments are reliable. The pH is determined by the ratio [HCO3]/
of 3.5 to 5.0 mEq/L in 14 L of ECF). The normal adult daily [H2CO3], which normally is approximately 20:1. A change in
potassium requirement is 0.5 to 0.8 mEq/kg/day and is directly either the numerator or the denominator can alter the ratio
proportional to lean body mass. The usual potassium intake and the resulting pH value. In addition, a change of either
averages 100 mEq/day, but 95% is excreted in the urine and [H2CO3] or Paco2 can be compensated by a corresponding
5% is lost in feces and sweat. In the kidney, most of the filtered change in the same direction of the other, restoring the ratio to
potassium is resorbed in the proximal tubular system. Never- 20:1 and the pH to 7.40. Thus, pulmonary regulation of Paco2
theless, selective secretion or absorption in the distal tubule and renal tubular regulation of plasma HCO3 are important
determines net renal excretion or conservation. Unlike its abil- determinants of extracellular pH.
ity to conserve sodium, the kidney can only decrease potassium As effective as the [HCO3]/[H2CO3] buffer system is, and
excretion to approximately 10 mEq/L. Potassium excretion is as available as its substrates are from metabolic sources, even
directly related to circulating levels of aldosterone, cellular and in combination with all other extracellular buffers it cannot
extracellular potassium content, and tubular urine flow rates. maintain arterial pH at normal levels in the face of all chal-
Acidbase disturbances also exert a significant influence. lenges. Intracellular buffer systems play a major role. As much
as 50% of fixed acid loads and 95% of hydrogen ion changes
AcidBase Balance that result from excessive retention or excretion of CO2 are
buffered in the cells. The movement of hydrogen into and out
Discussions in this chapter reflect the more common histori- of the cell involves cationic exchanges that cause reciprocal
cal interpretation of acidbase balance and acidbase distur- shifts of potassium. Thus, acidosis, in which hydrogen ions
bances. However, a more recent interpretation of acidbase move from an area of high concentration (extracellular) to an
using the concept of strong ion difference is gaining support. area of low concentration (intracellular), causes potassium to
If the student is interested multiple references to this approach move out of the cell. Alternatively, if intracellular hydrogen
to acidbase, search for the term strong ion difference. ions increase, potassium moves to the extracellular compart-
Acidbase balance is in effect the bodys management of ment. As a result, the potassium concentration in interstitial
large amounts of endogenously produced hydrogen ion. There fluid (and serum) increases. On average, for every 0.1 change
is a 40 to 60 mmol load of fixed nonvolatile organic acids in pH, the K+ changes inversely by about 0.3 mEq/L. Alkalosis,
(i.e., sulfuric, phosphoric, and lactic acids), some of which in which hydrogen ions move from an area of high concentra-
are ingested and some of which are produced by metabolic tion (intracellular) to one of low concentration (extracellular),
activity. In addition, 13,000 to 20,000 mmol of carbon diox- causes the opposite movement of potassium into the cell. As
ide (CO2) constitutes the volatile acid load. Normally, the a result, the extracellular potassium concentration decreases.
free hydrogen ion concentration of ECFs is maintained at Thus, acidosis is associated with hyperkalemia, and alkalo-
40 nmol/L or at a pH of 7.40 0.05. Maintenance at this level sis is associated with hypokalemia. The usual assumption of
is accomplished by the combined action of three mechanisms: a direct relation between serum levels and total body stores
1. Buffering systems that are present in all body fluids and of potassium is not valid. Changes in serum potassium con-
that immediately offset changes in hydrogen concentration centration that are induced by acidbase alterations can have
2. Pulmonary ventilation changes that can promptly adjust significant clinical implications, particularly with regard to
the excretion of CO2 myocardial irritability and function. For example, if the serum
3. Renal tubular function, which, over time, can contribute by potassium is measured as 3.4 mEq/L and the pH is 7.20, the
modulating the urinary excretion or conservation of acid or true serum potassium may be as low as 2.8 mEq/L when the
base pH is corrected to normal.

Lawrence_Chap02.indd 35 7/21/2012 5:58:23 PM


FLUIDS AND ELECTROLYTES IN THE TABLE 2-3 Daily Electrolyte Requirements

Example: 70 kg, 175 cm
The three essential components that must be addressed when Electrolyte mEq/kg male
considering fluid and electrolyte therapy for surgical patients
are: Sodium 1.02.0 70140 mEq
Maintenance Potassium 0.50.8 3556 mEq
Resuscitation Chloride 1.02.0 70140 mEq
Replacement a
Potassium requirements are directly proportional to lean body mass.
Maintenance involves meeting the requirements for fluid and
electrolyte intake that and deficits that are present. Replace-
ment refers to the provision for ongoing and additional losses both salt and water increase when ambient temperatures rise
that occur during the course of therapy. Each component to more than 32C (85F). This increase is caused by hypo-
must be addressed in the three phases of surgical care: that tonic salt losses from sweating. Additional intravenous fluid
is, preoperative, intraoperative, and postoperative. With each replacement with 0.45% saline may be appropriate in this
component of therapy, comorbidities such as the presence of case. However, since the sodium loss in sweat is directly pro-
cardiac or renal disease and the pathophysiology of the clini- portional to the rate of secretion and may exceed 100 mEq/L,
cal problem being treated must also be considered. additional sodium infusions may be required in cases where
With no unusual stresses or losses and normal renal func- sweat rate and volume are unusually high.
tion, the fluid and electrolyte balance is maintained by the As with all aspects of good surgical care, the management
intake of adequate amounts of water, sodium, potassium, and of fluid and electrolyte balance starts with assessment. The
chloride to balance daily obligatory losses. Intake is calcu- surgeon uses the information obtained from a thorough his-
lated to balance outputs of 12 to 15 mL/kg/day urine, 3 mL/ tory and physical examination to identify current or poten-
kg/day stool water, 0 to 1.5 mL/kg/day sweat, 10 mL/kg/day tial problems and determine what laboratory data are needed
combined insensible losses from the lungs and skin and an to confirm the diagnosis. Preoperative risk assessment and
endogenous input of approximately 3 mL/kg water from the management is essential. In the context of elective surgery,
oxidation of carbohydrate and fat. These estimates apply to the standard precaution of loading the patient with fluids
adults. More universal guidelines for calculating fluid and before surgery to prevent intraoperative hypotension is incor-
electrolyte requirements have also been devised. Probably the rect since it has been recently shown that the vast majority
most accurate calculations are based on surface area, but they of patients admitted for elective surgery do not have hypov-
are cumbersome, requiring measurement of height as well as olemia, as was previously thought.
weight and a nomogram for transposing the measurements into The initial workup could reveal underlying comorbid
a value for surface area. For this reason, the common practice conditions that would have a significant impact on the
is to determine water and electrolyte needs as a function of age patients ability to tolerate an operation. These findings may
and weight. Guidelines for fluid and electrolyte requirements significantly influence the fluid therapy during and after the
using age and body weight are shown in Tables 2-2 and 2-3. operation. If stressful surgery is contemplated (e.g., abdomi-
If the entire intake is to be delivered intravenously, 5% dex- nal aortic aneurysm repair, pulmonary or pancreatic resec-
trose in water is used to meet most of the water requirements tion), central venous or pulmonary arterial monitoring in the
because the kidney reabsorbs nearly all of the sodium and perioperative period may be required. However, systolic and
chloride that the body needs. The fluid used to replace ongo- mean blood pressure and heart rate have been shown in the
ing losses or existing deficits should reflect the composition of noncritically ill patient to be as predictive, if not more pre-
the deficits or losses as much as possible. Usually, 0.45% or dictive, of fluid needs compared with central monitoring. A
0.9% saline can be given to provide the necessary sodium and history of diuretic and digitalis therapy may call attention to
chloride. Potassium is added in divided amounts to the various the possibility of hypokalemia or hyponatremia. Low pre-
solutions. In this way, its delivery is spread out over time. operative serum potassium levels can fall even lower during
Overall estimates of daily needs must be adjusted for fever surgery, particularly in patients who are under general anes-
and high ambient temperatures. Insensible skin and pulmonary thesia, are hyperventilated, and/or have hypocapnic respira-
losses increase with elevations of body temperature (10% to tory alkalosis. If hyponatremia is present on admission, the
15% per C, 8% per F). These losses may require an additional margin of safety between asymptomatic and symptomatic
500 mL or more of salt-free water per day in febrile patients. low serum sodium concentrations is reduced, making, even
Similar needs for more water because of increased pulmonary relatively small, additional decreases potentially hazardous.
insensible losses occur in patients with tracheostomies who Depending on the severity of the planned surgery, a patient
are breathing unhumidified air or gas mixtures, especially with with chronic pulmonary obstructive disease may need an
hyperventilation. In a slightly different way, requirements for arterial blood gas evaluation as part of the preoperative

TABLE 2-2 Daily Fluid Requirements

Adult, mL per Kilogram Child > 5 kg, mL per Kilogram

Per m2 Age 2555 Age 5565 Age > 65 First 10 kg Second 10 kg >20 kg
1,200 mL 35 30 25 100 50 20

Lawrence_Chap02.indd 36 7/21/2012 5:58:25 PM


workup. Similarly, BUN, serum creatinine, and electro- In the immediate postoperative period the fluid, electro-
lyte studies are indicated in a patient who has a history of lyte, and acidbase needs of the patient, for the most part, are
chronic renal disease. With any of these disorders, any defi- related to monitoring and maintaining hemodynamic stability,
cits and ongoing needs must be identified and addressed in and the adequacy of ventilation. Careful attention should be
the preoperative period. paid to the volume and electrolyte content of all fluids given to
Fluid, electrolyte, and acidbase imbalances must be iden- the patient. This needs to be accurately recorded in the medi-
tified and treated promptly in patients who are acutely ill. This cal record that is reviewed in the daily care of the patient. In
requirement is even more important in patients who need an many patients who have had relatively uncomplicated and
urgent operation. The admitting history and physical exami- stress-free elective surgery (i.e., inguinal herniorrhaphy, chol-
nation should clarify the extent of the deficit, and appropriate ecystectomy) and in whom oral intake will be resumed within
directed laboratory data should be obtained immediately. In 48 hours, this process is accomplished simply by physical
patients who are vomiting or who have had prolonged gastric examination and serial observations of pulse rate, arterial
drainage, the presence of hypokalemic, hypochloremic meta- blood pressure, respiratory frequency, and urine output, and
bolic alkalosis should be anticipated, rapidly confirmed and by the administration of intravenous fluids as described for
treated with replacement of volume, potassium, and chloride maintenance in Table 2-2. Another guideline frequently cited
losses. In these circumstances, profound potassium depletion in the literature for estimating normal daily fluid requirements
is present if the urine pH is acidic (this paradoxical aciduria is the 4:2:1 rule, which states that for normal maintenance flu-
is explained in more detail later). If emergency surgery is indi- ids per hour, 4 mL are given for the first 10 kg, 2 mL for the
cated, potassium replacement may be needed in 10 to 20 mEq/ second 10 kg, and 1 mL for the remainder of the weight. This
hour doses. If more than 10 mEq/hour is infused, the patient rule or the 100:50:20 rule recommended for children (as seen
should be placed on a cardiac monitor. in Table 2-2) should not be used to estimate fluid requirements
Isotonic vascular volume depletion caused by fluid seques- in the elderly since substantially more fluid would be infused
tered into interstitial space, either systemically as seen in than is actually required. The differences in fluid requirements
sepsis or inflammatory response syndrome or locally such as using these different methods of calculating fluids may seem
with peritonitis (bacterial or chemical), intestinal obstruction, trivial at times, but the significance can be more clearly seen if
extensive soft tissue inflammation or trauma, is common. The as an example we apply each method to the young 70-kg male
term third space loss should be abandoned since the fluid and the elderly 70-kg slightly obese male whose lean body
sequestered in the interstitial space in areas of injury is still mass is substantially reduced. The 4:2:1 rule would result in
part of the functional ECF. Like hemorrhage, these fluid shifts 110 mL/hour or 2,640 mL infused in 24 hours. The 100:50:20
to the ECF effectively reduce intravascular volumes, and must rule used mostly in pediatrics would result in 2,500 mL in
be replaced promptly. Balanced salt solutions (lactated Ring- 24 hours, not much different and probably not clinically
ers solution or normal saline) are normally used to replace significant. However, since the elderly patient has less lean
the isotonic losses. The indications of how much to give are body mass, we should apply the 25 mL/kg rule (Table 2-2),
not always apparent. In this case, clinical observation of hemo- which would result in only 1,750 mL required for 24 hours.
dynamic changes (i.e., tachycardia, narrowed pulse pressure, In many patients, this would not seem important but if given
hypotension), decreasing urine output (<0.5 mL/kg/hour), and over 3 days, the elderly patient would receive over 2 L of
laboratory evidence of isotonic volume contraction (i.e., ris- excess fluid and if given for 5 days he would receive almost
ing hematocrit and serum BUN: creatinine ratio >20:1, urine 4 L of excess fluid. Since the elderly have decreased renal
sodium concentrations <20 mEq/L) makes it clear that the and cardiac function, this excess fluid could result in pleural
losses are significant. With continuous monitoring as intrave- effusions, pulmonary and peripheral edema (particularly if the
nous fluid is given, improvements in hemodynamic parameters patient is also hypoproteinemic), and even congestive heart
and hourly urine output, to near-normal values, indicate that failure. This excess fluid is not innocuous. It is imperative that
vascular volume has been restored to normal levels. The goal changes in lean body mass and weight with age be considered
is to optimize the hemodynamics, not to maximize them. The when calculating fluid requirements.
latter has been shown to increase morbidity and mortality. To In patients who have had more surgically stressful proce-
avoid clinically significant dilutional hyponatremia, care must dures that involve extensive dissection or resection, the flu-
be taken to limit the intravenous administration of hypotonic ids needed may be greater because of the fluid sequestered
solutions (i.e., D5W, 0.45 NS, etc.) to patients who need large in the area of dissection (i.e., soft tissue injury) but must also
volumes of fluid to replace deficits in circulating blood volume. be adjusted appropriately in patients with clinical conditions
During surgery, attention is focused on maintaining circu- that might affect fluid balance such as known compromise of
lating volumes and adequate tissue perfusion as monitored by cardiac, renal, or pulmonary function. In these patients, addi-
urine flow rates and central venous or pulmonary arterial pres- tional monitoring with central venous or pulmonary arterial
sures. Crystalloid solutions are used initially to replace whole pressure, hourly urine output collected with an indwelling
blood losses, but packed red blood cells and colloid solutions catheter in the bladder, and serial arterial blood gas with pH
may also be used. For patients who undergo major abdominal measurement may be necessary. Inadequate respiratory gas
or thoracic surgery, Ringers Lactate or normal saline solu- exchange may require the use of endotracheal intubation and
tion should be used to replace the isotonic fluid sequestered in mechanical ventilation. Infusions are needed to replace flu-
injured tissue. The use of hypotonic intravenous fluid should ids that move into interstitial space in local areas of injury
be limited to the replacement of evaporative water losses or systemically such as in sepsis syndrome or inflammatory
since these hypotonic fluids lead to dilutional hyponatremia. response syndrome. This fluid shift can continue for 48 to
In patients who have compromised pulmonary function, arte- 72 hours, or even longer in the elderly. In addition to daily
rial blood gas and pH studies are performed intraoperatively maintenance needs, gastric, intestinal, biliary, and pancreatic
to monitor gas exchange and acidbase balance. drainage should be replaced. If these losses are >1,000 mL

Lawrence_Chap02.indd 37 7/21/2012 5:58:25 PM


changes causing a leakage of fluid from the vascular system

TABLE 2-4 Composition of Normal Body Fluidsa
into the interstitium. Fluid accumulation in the lungs may
predispose patients to pneumonia, respiratory failure, pleu-
Fluid Na+ K+ Cl HCO3
ral effusions, and pulmonary edema. The excretory demands
Plasma 135150 3.55.0 98106 2230 of the kidney are increased, and the resulting diuresis may
Stomach 10150 412 120160 0 lead to urinary retention mediated by the inhibitory effects of
anesthetics and analgesics on bladder function. Gastrointesti-
Bile 120170 312 80120 3040
nal motility may be inhibited, prolonging postoperative ileus.
Pancreas 135150 3.55.0 60100 35110 Excess interstitial fluid may decrease tissue oxygenation with
Small intestine 80150 28 70130 2040 implications for wound (anastomotic) healing.
Colon 50100 1030 80120 2530 Close attention to a patients fluid needs, particularly in
Perspiration 3050 5 3050 0
the elderly or those with compromised renal or cardiac func-
tion, must continue until the patients renal and gastrointesti-
The composition of most gastrointestinal fluids and of perspiration varies according to the rate nal functions return to normal and all fluid, electrolyte, and
of secretion
nutritional requirements are being met by oral intake. At this
point, with the exception of chronically ill patients, who may
have ongoing needs, requirements should stabilize.
in 24 hours, consideration should be given to replacing these
deficits milliliter for milliliter with an appropriate intravenous
infusion. The electrolyte content of these infusions generally FLUID AND ELECTROLYTE DISORDERS
can be determined by knowing the electrolyte composition of IN A SURGICAL PATIENT
the fluid lost, as described in Table 2-4.
To determine more accurately what must be replaced, Disorders of Volume
fluid samples may be analyzed for their electrolyte composi-
tion. Daily weights are used to assess fluid volume depletion Loss of intravascular volume is the most common cause of
or retention, recognizing that gains or losses >250 g (0.5 lb) hypotension and low urine output in the surgical patient.
represent changes in body fluid content. As valuable as it is to The loss may be secondary to hemorrhage internally such as
monitor ECF status, weight gains and losses related to inter- from traumatic injury, from gastrointestinal bleeding, or from
stitial sequestration of fluid and their management must be external losses such as lacerations. Vascular volume may also
considered. During replacement of these losses, weight gains decrease due to loss of plasma into the interstitial compart-
do not represent hypervolemia. Rather they are caused by the ment due to burns, sepsis, and local or systemic inflamma-
replacement of needed extracellular volume to compensate for tory response to injury. Fluid losses from the gastrointestinal
the volume that was lost or sequestered. Similarly, diuresis and tract (e.g., vomiting, diarrhea, nasogastric suction) as well as
associated weight loss is expected 3 or more days postopera- increased evaporation of water as a result of fever or open
tively when the sequestered fluid accumulations are mobilized abdominal surgery are also common.
(i.e., moved into the intravascular compartment). This excreted Hypervolemia and increases in total body water above
fluid should not be replaced. When this fluid is mobilized, intra- requirements (fluid overload) are usually secondary to excess
vascular volumes are likely to be high, making additional intra- replacement of fluids or to renal failure. The majority of sur-
venous fluid infusion undesirable. On the other hand, in patients gical patients do not demonstrate early congestive heart fail-
who are receiving parenteral nutrition with hyperosmolar glu- ure even during resuscitation.
cose solutions, increased urine output should not be interpreted
simply as appropriate excretion of excess fluids. In fact, the high Volume Depletion
urine output in these patients may be caused by osmotic diuresis Volume depletion may be due to acute blood loss, ECF loss, or
that is independent of the patients volume status. This condi- total body water reductions. An accurate history and physical
tion requires prompt recognition and correction with intrave- examination is essential to ascertain if one or all of the deficits
nous fluids to avoid severe hyperosmolar volume contraction. are present. For the most part, losses from the gastrointesti-
Several issues in perioperative management may account nal tract are from vomiting, diarrhea, nasogastric suction, and
for the administration of excessive amounts of fluid. These from enteric fistulas, resulting in ECF volume depletion. As
include errors in the assessment of preoperative fluid deficits; shown in Table 2-4, most fluids from the gastrointestinal tract
dehydration, primarily derived from prolonged preoperative are isotonic and therefore can be replaced with most common
fasting and bowel preparation; the status of the circulation replacement fluids such as normal saline or Ringers lactate.
and cardiac function after general and regional anesthesia; The intracellular compartment is affected only if osmolar
the extent of blood loss; the desire to avoid blood transfusion; concentrations change. Because of acid secretion from the
alternate reasons for a decrease in urine output; and misin- stomach, gastric losses usually result in a large fluid and chlo-
terpretation of central venous pressure (CVP) or pulmonary ride loss and significantly less sodium loss. Since the chloride
pressures (if measured) from fluid infusion. loss is also associated with hydrogen loss, patients usually
Administration of fluid in excess to the patient needs may become alkalotic, and their kidneys compensate for this by
cause several problems after surgery and needs to be avoided. holding onto sodium and excreting potassium. The resulting
Hypervolemia increases demands on cardiac function, due to hypochloremic, hypokalemic metabolic alkalosis needs to be
an excessive shift to the right on the Frank-Starling myocardial treated with a higher chloride solution such as normal saline.
performance curve, and may potentially increase postopera- Isotonic depletion of functional extracellular volume
tive cardiac morbidity. Hypervolemia also stimulates the pro- also occurs with third space losses, which are similar to
duction of atrial natruretic factor, which results in endothelial serum (plasma minus some protein). These are particularly

Lawrence_Chap02.indd 38 7/21/2012 5:58:25 PM


significant in burns, crush injuries, long bone fractures, peri- of reduced tissue perfusion as seen with whole blood loss.
tonitis, severe pancreatitis, intestinal obstruction, pleural effu- Tables 2-5 and 2-6 demonstrate what the signs of ECF loss
sions, and large areas of soft tissue infection. Excess urinary are in normal adults. These may be exacerbated or hidden
loss of water and electrolytes can lead to volume depletion as in the older population as seen in Table 2-6. Neurologic and
is seen with diuretic therapy, high output renal failure, or with cardiovascular signs are more prominent with acute losses
osmotic diuresis associated with nonelectrolyte hyperosmolar whereas tissue signs may not be evident for up to 24 hours.
solute loading (e.g., glucose, mannitol, angiographic contrast In acute circumstances, a clinician is more dependent on
media). Finally, there are volume depletions involving losses of hemodynamic parameters such as change in heart rate, pulse
water and excess of solute. These losses include excessive free pressure and oliguria, elevated hematocrit and urinary con-
water excretion associated with primary deficiencies of ADH, centration in the case of interstitial fluid sequestration, or
including diabetes insipidus. This is most commonly seen in decreased hematocrit and oliguria, and urinary concentration
head injury patients, but nephrogenic causes of diabetes insipi- in the case of blood loss. As renal perfusion becomes more
dus and increased evaporative losses from burn injuries or restricted, BUN and soon creatinine rise. It is imperative that
increased sweating with evaporative losses from the skin and the clinician understands the difference between acute renal
respiratory tract in a febrile patient can also cause this prob- failure as a cause for oliguria and a rise in BUN and creati-
lem. These hypotonic losses create a hypernatremic hyperos- nine, and oliguria associated with fluid depletion showing a
molar state in the extracellular compartment that draws water rise in BUN and creatinine. Obviously, these are opposites
from the cell. This repletion of the extracellular space typically in treatment for one would exacerbate the problems of the
is seen with very high urine output, and hypotension is a late other. Several methods are used to distinguish prerenal failure
effect. Volume loss due to hemorrhage and the resulting hypo- from renal failure. The more accurate test would be to obtain
tension are more fully explained in the chapter on shock. serum and urine electrolytes. A urine sodium concentration
of <20 mEq/L, a BUN/creatinine ratio of 20:1, and urine
osmolality >400 mOsm/L (in the absence of glycosuria or the
Presentation and Diagnosis
excretion of other osmotically active particles) are all helpful.
Volume loss from the extracellular space (which holds 40% A more exact test is the fractional excretion of sodium (FeNa)
of the total body water or 20% of total body weight in the
young healthy man) is usually more rapid than loss from the Fe Na = [(U NNa PCR )/(P
PNa U CCr ) 100].
intracellular space. More recent studies suggest the average
blood volume of an adult is a little over 6% of body weight, A FeNa of <1% is characteristic of prerenal azotemia while
not the 7% commonly quoted in many publications but is >2% is most common with renal injury. In acute renal failure,
increased with living at higher altitudes to about 6.5% and urine sodium usually increases to >40 mEq/L as renal tubular
to 7.5% to 8.5% in children and neonates. In order to dem- absorption of sodium is impaired. The BUN/creatinine ratio
onstrate clinically significant physiologic changes, usually falls to 10 or less because creatinine starts to rise faster than
one needs to lose more than 10% to 15% of the intravascu- BUN, and urine osmolality approaches plasma osmolality of
lar volume. Signs of plasma volume deficits include signs 270 to 280 mOsm/L.

TABLE 2-5 Signs of ECF Depletion

10% Depletion 20% Depletion 30% Depletion

Clinical 2% weight loss 4% weight loss 6% weight loss

Thirst Apathy Stupor or coma
Mildly reduced urine output Drowsiness Skin cool, pale, cyanotic, with poor turgor
Decreased skin turgor Eyes sunken
Dry mucous membranes Tachycardia
Longitudinal tongue furrowing Pulse weak and thready
Tachycardia Hypotension
Orthostatic hypotension Urine output <15 mL/hr
Urine output < 30 mL/hr
Laboratory Slightly elevated hematocrita Elevated hematocrita Greatly elevated hematocrita
Elevated WBC
Slightly elevated urine specific gravity Modest elevation in BUN and creatinine Elevated BUN/creatinine ratio (>10:1 up to 25:1)
Elevated BUN/creatinine ratio (>10:1 up to 25:1) Urineb specific gravity <1.020, urine osmolarity
Urine specific gravity 1.020, urine osmolarity <500 mOsm/L, urine sodium >20 mEq/L
>500 mOsm/L, urine sodium 1015 mEq/L
Comments Findings can be overlooked on evaluation Findings are always evident Findings are very obvious
In the absence of bleeding, hematocrit increases about 1% for every 500 mL ECF deficit.
These urine findings reflect acute tubular necrosis.

Lawrence_Chap02.indd 39 7/21/2012 5:58:25 PM


TABLE 2-6 Responses to ECF Depletion in the Elderly

System Signs or Symptoms in Younger Persons Signs or Symptoms in Persons >65 Years Old

Intravascular Orthostatic hypotension Common in healthy elderly

Hypotension May be masked by preexisting hypertension
Tachycardia Maximal heart rate decreases with age
Reduced pulse volume Masked by rigid vessels
Reduced CVP or PaOP May not reflect heart function or volume status
Oliguria May be less marked if preexisting renal impairment is present
No signs of fluid overload or heart failure Preexisting hypoproteinemia and ankle edema may be present
Interstitial Dry skin and mucous membranes Common in the elderly
Dry tongue Unreliable at any age
Reduced tongue volume May be useful
Sunken eyes A late sign at any age
Reduced skin turgor Unreliable in the elderly
Miscellaneous Reduced deep tendon reflexes May be an age-related change
Distal anesthesia May be an age-related change
Drowsiness May be caused by infection, medication, hypothyroidism, or depression
Apathy May be caused by infection, medication, hypothyroidism, or depression
Anorexia May be caused by infection, medication, hypothyroidism, or depression
Stupor or coma A late, nonspecific sign
Ileus A late, nonspecific sign
CVP, central venous pressure; PaOP, pulmonary artery opening pressure.

Treatment resuscitation or for most replacements. The addition of 50 g

The most efficacious test that a physician can do is a good of glucose to a solution that is given rapidly may result in
history and physical examination. A measurement of pos- hyperglycemia and an osmotic diuresis. Glucose solutions
tural blood pressure and pulse can be very helpful (orthostatic also frequently have somewhat lower pH than solutions not
measurement). An increase of >10 heartbeats per minute or containing glucose. How fast one corrects the volume is com-
a decrease >15 mm Hg systolic blood pressure on a sitting mensurate with the need and the ability of the patient to accept
patient should raise suspicion of intravascular depletion. This the fluid load that is delivered. The longer a deficit has taken
is more valuable in younger patients since the elderly may to occur, the more cautious a clinician should be in replacing
not be able to compensate and sudden drops in blood pres- it. These electrolyte abnormalities will be discussed in more
sure may occur. Correction of the volume depletion requires detail in the next section. When deficits are moderate, com-
a diagnosis that depletion is the problem, an estimate of the plete replacement should be carried out, at least over 24-hour
extent of the depletion, and an estimation of what fluid losses periods. If deficits are large and consequences severe with
need to be replaced. Table 2-5 helps to describe the difference physiologic abnormalities such as hypotension and tachycar-
between a 10%, 20%, and 30% depletion of ECF, although dia, and needs are more urgent; the therapeutic priority should
these are fairly inexact findings. Hypotension usually does be to correct the hemodynamic and perfusion inadequacies as
not occur in a young healthy adult, until there is a loss of at rapidly and safely as possible. The rapidity of resuscitation
least 25% intravascular volume. Isotonic extracellular deficits is dependent not only on the patients physiology and on the
caused by intestinal, biliary, pancreatic, or third space losses acuity of the physiologic changes, but also on the ability to
are best treated with lactated Ringers solution or normal deliver the fluid. Smaller intravenous lines, such as 20- and
saline if hyperchloremia is not a problem (Table 2-7). Large 22-gauge, significantly restrict the amount of fluid that can be
volumes of Lactate-containing solution should be used with given rapidly. Poiseuilles law states that the amount of resist-
care in patients who have gastric outlet obstruction as a cause ance to flow through a system is dependent on the radius to the
of vomiting or nasogastric secretions because these patients fourth power (R = L/r4). This means that using a 16-gauge
become hypochloremic and metabolically alkalotic. The pH intravenous compared to a 20-gauge can more than double
of Ringers Lactate is approximately 6.5 while the pH of nor- the amount of fluid given over for a period of time. A bolus
mal saline is approximately 5.0. Inadequate replacement of is an amount of fluid given as fast as possible (not 999 on
chloride and inadequate correction of the alkalosis can exac- an infusion pump). A rapid infusion of a liter of crystalloid
erbate both of these problems. For replacement of nasogas- solution, or in case of bleeding, blood, may be necessary to
tric output, a solution of one-half normal saline (77 mEq/L achieve hemodynamic stability. In cases of ongoing mas-
of sodium, 77 mEq/L of chloride) with 20 to 40 mEq/L of sive fluid losses, the infusion of fluid must obviously exceed
potassium most likely will match the electrolyte losses from the egress of fluid; therefore, it is not unusual for patients to
the vomiting. Glucose solutions should not be utilized for receive several liters over a rapid period of time in order to

Lawrence_Chap02.indd 40 7/21/2012 5:58:26 PM


TABLE 2-7 Composition of Commonly Used Intravenous Solutions

Glucose (g/L) Na+ (mEq/L) K+ (mEq/L) Cl (mEq/L) Lactatea (mEq/L) Ca++ (mEq/L)

0.9% Sodium chloride (normal 154 154

Lactated Ringers solution 130 4.0 109 28 3.0
5% dextrose water 50
5% dextrose in 0.45% sodium 50 77 77
3% sodium chloride 513 513
Converted to bicarbonate.

stabilize the hemodynamics. Once again, one should not use rule does not apply, especially in the unstable patient. A patient
a glucose-containing solution during these rapid corrections who is losing blood and is hemodynamically unstable usually
because of the iatrogenic hyperglycemic-induced osmotic requires blood in addition to significant amounts of crystalloid.
diuresis, which may actually increase fluid losses. Volume
losses are corrected with isotonic solutions. Ringers Lactate Prognosis
is the fluid of choice for blood loss and should be given with a The prognosis for patients with volume depletion depends
3:1 ratio because there is little oncotic gradient, and the egress first on the underlying physiology including the duration of
of the isotonic fluid from the intravascular to the extracellu- the loss; secondly, the amount of depletion that takes place
lar space is rapid. The infusions of colloid solutions, which without repletion, and the ability to stop the ongoing losses.
contain albumin, are not usually indicated in the rapid resusci- As patients arrive in severe shock for prolonged period of
tation of traumatic injury for multiple reasons. The use of nor- time, resuscitative efforts must be extremely aggressive and
mal saline is acceptable as a replacement fluid with the caveat may not succeed. Most patients who arrive shortly after their
that if one is using large amounts of normal saline, one risks fluid loss or are in the hospital while they are losing fluid
hyperchloremia and worsening acidosis. Lactated Ringers is should be able to survive. Part of the surgeons responsibility
usually the preferred solution for large-volume resuscitation. is to control any blood loss and to replace all losses from the
While replacing fluid, one must be also aware that potas- gastrointestinal tract or other sites.
sium abnormalities must be corrected rapidly along with
abnormalities of glucose and osmolality changes. If changes Volume Excess
are chronic and severe, too rapid correction of sodium and Volume excess, for any or all fluid compartments, can occur
osmolality may result in dire neurologic consequences and from abnormal fluid retention, excessive or inappropriate
swelling of the neurons (pontine demyelination). fluid intake, or a combination of both. However the terms
Determinations of end points for resuscitation are still fluid overload and volume excess are frequently used
mainly clinical in nature. Weight changes are extremely dif- indiscriminately and inappropriately. For example in many
ficult to document accurately in the acute stages. Measure- situations involving inflammatory response syndromes or
ment of fluid input and output gives some valuable data for sepsis, the patient may develop peripheral edema or pleural
large fluid shifts, but is not very valuable in making immediate effusions but still have an intravascular volume deficiency.
clinical decisions. During resuscitation, repeat examination of Patients who have signs of congestive heart failure may pre-
the patient is imperative with the examination of vital signs sent with a gastrointestinal bleed, and they are hypovolemic
such as pulse, blood pressure, urine output, and if possible or even though their total body water is increased. Too often
necessary, additional monitoring with central venous or pul- physicians equate edematous states with vascular hyperv-
monary artery catheters. Electrolytes and serum lactate and olemia, which leads to inappropriate care. The physician
blood pH, as well as base excess calculations, should be selec- caring for the patient should determine as closely as pos-
tively used to help determine end points of fluid resuscitation. sible, based on history and physical examination, the status
If there is no acute renal failure or significant chronically com- of each fluid compartment and then detail this in the docu-
promised renal failure, then a urine output of >0.5 mL/kg/hour mentation (medical record). For example in the patient with
in adults or 1.0 mL/kg/hour in children should be achieved. This sepsis syndrome, the physician might document (or at least
volume of urine output indicates adequate repletion of vascular think) the patient has an increase in interstitial fluid caus-
volume. If the patient is showing signs of prerenal azotemia, ing peripheral edema but based on their heart rate and blood
these should resolve rapidly with repletion of the fluid. pressure the patient also has a vascular volume deficit. In
It is often said that the dumbest kidney is smarter than the the case of the patient with congestive heart failure and a GI
smartest doctor. Similarly, in the absence of continuing blood bleed, the statement (or thought) should be similar, that is,
loss, hemoglobin may not reflect immediate losses, and replace- the patient has a vascular volume deficit even though she has
ment of blood and electrolytes is necessary to once again sta- peripheral edema. There are certainly circumstances where
bilize the vital signs mentioned above. Transfusing blood in all compartments are increased in which case the statement
stable patients should not be undertaken unless there is either (thought) could be the patient has an increase in all fluid
symptomatology or the hemoglobin is <7 g/dL. However, in the compartments and is particularly hypervolemic. By being
acute situation, replacing blood is much more empiric, and this more descriptive, there is less chance of misinterpretation by

Lawrence_Chap02.indd 41 7/21/2012 5:58:26 PM


other physicians reading the notes and therefore less chance electrolyte imbalances. Electrolyte imbalances are rarely iso-
of error in treating the patient. lated because the body must maintain electrical neutrality; com-
Intravenous fluid therapy with balanced salt solutions is a plex homeostatic and metabolic mechanisms exist to maintain
common iatrogenic cause of ECF expansion. Overexpansion the neutral state. Attempts to correct a low serum level by sim-
of the extracellular compartment may occur immediately ple oral or parenteral replacement of an ion may not improve
during or after surgery, during trauma resuscitation, or later the patients condition because associated abnormalities are not
when maximal hormonal responses to stress (i.e., increases treated. Although electrolyte abnormalities are often corrected
in ADH and aldosterone) are operating to diminish sodium easily, if untreated they may be fatal. Artifactual abnormali-
and water excretion by the kidney. Frequently, even though ties of serum electrolytes may result from numerous factors
the interstitial fluid may increase, the vascular volume including improper collection or handling of blood specimens.
may be decreased, increased, or even normal. The risk for Table 2-1 shows normal values for most electrolytes, but they
increased ECF is greater in any patient that has comorbidi- may vary slightly from one laboratory to another.
ties that may contribute to ECF expansion but particularly
the elderly. Sodium
Hypotonic fluid excess is usually due to inappropriate The sodium ion is the principal solute that determines ECF
administration of salt-poor solution resulting in hyponatremia. osmolarity and fluid volume balance in the body. An increase
Hypernatremic extracellular volume expansion is due to the in extracellular sodium concentration creates an osmotic gra-
administration of sodium loads that are not balanced by appro- dient that draws water out of cells. A decrease in extracellu-
priate water intake. In this case, water moving out of cells in lar sodium concentration does the reverse. These changes in
response to increased extracellular osmolarity may result in cell volume produce the symptoms associated with abnormal
intracellular depletion of water but increased interstitial and serum sodium concentrations. Disorders of sodium balance
vascular volumes. Hypertonic extracellular volume expan- are usually associated with disorders of fluid balance.
sion can also be induced by the rapid infusion of nonelec-
trolyte osmotically active solutes (e.g., glucose, mannitol). In Hyponatremia
this case, hyponatremia rather than hypernatremia is present. Hyponatremia results from the presence of excess body water
Plasma sodium concentration decreases as a result of dilution relative to total body sodium and the failure of the kidneys
by the solution being infused, and the sodium-free water is to excrete the excess water. The serum sodium concentra-
drawn from the cells into the extracellular space in response tion does not always reflect true total body sodium content,
to the osmolar gradient created by the infused nonelectrolyte or even osmolarity. For example, total body sodium may be
solute load. If the patient has hyperglycemia, the measured increased in patients with chronic cardiac, hepatic, or renal
serum sodium will decrease 3 mEq/L for every 100 mg/dL disease, but hyponatremia persists because of a proportionally
increase in serum glucose above 100 mg/dL. greater increase in water. Alternatively, total body water may
be normal or decreased, but there is a proportionally greater
Presentation and Diagnosis decrease in total sodium.
The clinical presentation of extracellular volume excess may Etiology Hyponatremia may be associated with decreased,
range from simple weight gain, small decreases in hemoglobin increased, or normal ECF volume and each requires a different
and hematocrit (signifying hemodilution), modest elevation of approach to correct the abnormality. The more common causes
peripheral and CVP, and dependent sacral or lower extremity of hyponatremia are shown in Table 2-8. In surgical patients,
edema; to extreme changes with congestive heart failure, pleu-
ral effusions, pulmonary edema, anasarca, and hepatomegaly.

Treatment TABLE 2-8 Causes of Hyponatremia

Treatment is adjusted according to the severity and rate of
development of fluid compartment changes and related clinical Excess Water Ingestion or infusion of excess free water (e.g.,
findings. If it is determined that the patient has an increase in psychogenic polydipsia, or replacement of isotonic
all fluid compartments, treatment might be as simple as fluid gastrointestinal and third space fluid losses with
or sodium restriction. If symptoms are severe, the patient may hypotonic fluid)
need diuresis along with replacement of potassium losses. If the Physiologic response to surgical stress, starvation, or
patient in thought to have a vascular volume deficit, then careful hypovolemia (causing enhanced metabolic produc-
replacement with crystalloid or blood products may be needed, tion of free water)
even though the patient has peripheral edema suggesting an SIADH (syndrome of inappropriate ADH secretion)
increase in total body water. Treatment should also be specific
Enhanced ADH activity
to the organ system or systems affected and should be instituted
according to appropriate guidelines for treating those diseases. Advanced cardiac, renal, or hepatic disease
Excess Sodium Loss Thiazide diuretics
Metabolic alkalosis
If properly diagnosed and treated, most patients do well. How-
ever, major morbidity and even death can occur if patients are Ketoacidosis
misdiagnosed or treated inappropriately. Adrenal insufficiency
Artifactual Hyperlipidemia
Disorders of Electrolyte Concentrations Hyperproteinemia
As noted previously, a thorough history and physical are ADH, antidiuretic hormone.
essential in determining the etiology and proper treatment of

Lawrence_Chap02.indd 42 7/21/2012 5:58:26 PM


dilutional hyponatremia occurs most commonly when Disorders that involve total body sodium excess, in addition
hypotonic fluids are used to replace significant isotonic gas- to disproportionate volume excess, are treated by restriction
trointestinal or third space losses. The concern in this situation of both sodium and water.
is that intravascular volume may be restricted even though the Hyponatremia associated with volume contraction is
patient may have decreased volumes of one or more of the treated with combined sodium and volume repletion, usually
body compartments, leading to more problems with fluid bal- with normal saline or lactated Ringers solution. The rate of
ance. Catabolic breakdown of body tissues, which occurs with repletion is dictated by the degree of volume deficit. In most
surgical stress and caloric deprivation, metabolically gener- cases, rapid restoration of volume and sodium is not only
ates approximately 1 mL sodium-free water for each gram of unnecessary but also hazardous, because it can cause rapid
fat or muscle that is catabolized. Excretion of excess water shifts of intracellular water and undesirable neurologic con-
in response to decreased serum osmolarity is impaired after sequences.
surgery or other trauma due to the reabsorption of sodium and Hypertonic saline solutions (2% or higher concentra-
water as a result of the secretion of aldosterone and of ADH. tions) are indicated only when hyponatremia causes life-
With proper replacement of vascular volume, aldosterone threatening neurologic disturbances. To estimate the amount
secretion is blunted but ADH secretion may persist because of of sodium needed to correct the serum deficit, multiply the
secondary factors such as stress that stimulate ADH secretion. decrease in serum sodium (in milliequivalents) by total body
Dilutional hyponatremia also occurs in patients who have water (in liters) as a percentage of total body weight remem-
advanced cardiac, renal, or hepatic disease and increased total bering the relationship of total body water to age, sex, and
body sodium, because these patients accumulate proportion- body habitus:
ally more water than sodium.
Artifactually very low serum sodium values are seen in the mEq Na+ needed = (140 measured serum Na+) TBW,
presence of severe hyperglycemia and hypertriglyceridemia, where TBW, estimated % of body water body weight (kg).
or after intravenous infusion of lipids. In the cases associ- Failure to correct total body water for age changes and
ated with increased lipid content, the water in the intravascu- body habitus could result in significant infusion of excess flu-
lar space is partially replaced so the concentration of sodium ids. For example, if a patient is 75 years old but has a body
in the total sample is low, even though the concentration of mass index (BMI) of 40, they might have a total body water
sodium in plasma water may be normal, or even high. of as little as 40%. If the traditional formula is used with total
Presentation and Diagnosis The primary clinical manifestations body water of 60% body weight, the patient would receive far
of hyponatremia are the signs and symptoms of central nerv- more sodium and water that s/he actually needs.
ous system dysfunction. Osmotic forces draw water into the TBW is used because both intracellular and extracellular
cells, and cerebrospinal fluid pressures increase because of imbalances must be corrected. The goal is to increase the
cerebral and spinal cord swelling. Neurologic disturbances serum sodium level sufficiently to eliminate the symptoms. No
occur as a result. The severity of any neurological disturbance more than one-half of the total calculated amount of sodium
is directly related to both the degree of hyponatremia and is given in the first 12 to 18 hours and at a maximum rate of
the rapidity with which it develops. Serum sodium between 12 mEq/L of concentration per 24 hours since rapid correction
130 and 120 mEq/L may cause irritability, weakness, fatigue, of chronic hyponatremia >12mEq/L/day can cause osmotic
increased deep-tendon reflexes, and muscle twitches if the central pontine myelinolysis. In this entity, the myelin sheaths
hyponatremia developed rapidly (10 to 15 mEq/L in <48 hours, of nerve cells in the pons are destroyed. The resulting neuro-
or faster), but the patient may be completely asymptomatic if logic damage is usually permanent and may be debilitating.
it develops over time. If left untreated, severe hyponatremia Over the next 24 to 48 hours, the remainder of the deficit
may lead to seizures, coma, areflexia, and death. can be corrected with normal saline. Any underlying condi-
In diagnosing hyponatremia, serum and urine sodium, serum tions must also be treated. Responsible drugs should be dis-
and urine osmolality, and pH may be assessed. Blood tests can continued, if possible. The patient usually improves for a day
exclude associated electrolyte abnormalities (e.g., hyperglyce- or so but then deteriorates, with a spectrum of neurologic
mia, liver diseases, acidbase disorders). Volume status must findings that can include fluctuating levels of consciousness,
be assessed by accurate history and physical examination. seizures, pseudobulbar palsy, and paralysis. Some patients
Treatment Treatment of hyponatremia depends on the cause, improve after several weeks, but others have significant per-
severity, and nature of any associated volume abnormality. manent disability.
Psychogenic polydipsia is treated with water restriction. Most Prognosis Once properly treated, the prognosis of hypona-
dilutional hyponatremia that is iatrogenically induced in the tremia usually depends on the prognosis of the underlying
perioperative period, seen as an asymptomatic decrease in condition. Severe neurologic symptoms may have irreversible
serum sodium along with modest extracellular volume expan- sequelae.
sion, is readily treated by simple fluid restriction. Thiazide
diuretics cause hyponatremia by blocking the resorption of Hypernatremia
sodium and chloride in the cortical-diluting segment. How- Hypernatremia results from excess body sodium content rela-
ever, because the resorption of salt in the ascending limb of the tive to body water. Clinically significant hypernatremia, serum
loop of Henle is not blocked, excretion of very concentrated sodium >150 mEq/L, is less common than hyponatremia, but
urine is still possible. This concentration permits the retention it can be just as lethal if it is allowed to progress unchecked.
of water while sodium, potassium, and chloride are depleted. Etiology Hypernatremia may result from the loss of water alone
The best treatment for this condition is discontinuation of the (e.g., hypothalamic abnormalities, nonreplaced insensible
diuretic. In patients who have chronic hyponatremia, even losses); from the loss of water and salt together (e.g., gastroin-
when serum sodium concentration is very low, correction of testinal losses, osmotic diuresis, excessive diuretic use, central
serum sodium must be done slowly, 12 mEq/L/ day or less. or nephrogenic diabetes insipidus, burns, excessive sweating);

Lawrence_Chap02.indd 43 7/21/2012 5:58:27 PM


as a side effect of many drugs (e.g., alcohol, amphotericin B, the volume is replaced initially with normal saline since the
colchicine, lithium, phenytoin); or from increased total body patient usually has a vascular volume deficit in addition to a
sodium without any water loss (e.g., Cushings syndrome, total body water deficit. The nature of the fluid required may
hyperaldosteronism, ectopic production of ACTH, iatrogenic change as different needs become apparent. The process of
sodium administration, ingestion of seawater). reversing hypernatremia requires close monitoring. If water
When body fluids become hypertonic, compensatory thirst is replaced too rapidly, osmotic shifts can produce cellular
is stimulated. Therefore, severe hypernatremia occurs only in edema. Brain cells accumulate intracellular solute slowly in
situations in which a person cannot obtain water (e.g., infancy, response to slowly developing extracellular hypertonicity;
disability, altered mental states). a sudden decrease in extracellular osmolarity leads to rapid
Presentation and Diagnosis The pathophysiologic consequences swelling of brain cells, causing serious neurologic dysfunc-
of hypernatremia reflect both extracellular volume losses and tion. As with other electrolyte disturbances, underlying prob-
cellular dehydration that result from water shifts in response lems must also be treated. Correcting vascular volume deficit
to osmotic pressure. The severity of the clinical manifestation is the first priority.
is directly related to both the degree of hypernatremia and the Prognosis The prognosis depends on the severity of the symp-
rapidity with which it develops. Serum sodium concentrations toms, the correct treatment, and the prognosis of the underly-
>160 mEq/L may be associated with signs and symptoms of ing disorder. Neurologic symptoms, once they develop, may
dehydration, including decreased salivation and lacrimation; be irreversible.
dry mucous membranes; dry, flushed skin; decreased tissue tur-
gor; oliguria (except when dehydrating renal water loss is the Potassium
cause); fever; and tachycardia. Signs and symptoms also include As the principal intracellular cation, potassium is a major
those of neuromuscular and neurologic disorders, from twitch- determinant of intracellular volume. It is a significant cofac-
ing, restlessness, and weakness, to delirium, coma, seizures, and tor in cellular metabolism. Extracellular potassium plays an
death. Intracranial hemorrhage is a common postmortem finding important role in neuromuscular function.
in patients who die of hypernatremia; the hemorrhage is thought
to result from cell shrinkage, with associated decreases in brain Hypokalemia
volume and decreased intracranial pressure, which disrupts the Hypokalemia is defined as a serum potassium <3.5 mEq/L.
intracranial blood vessels. Unfortunately, many of these signs When total body potassium is deficient, there may also be
and symptoms are not very reliable in the elderly. deficiencies of magnesium and phosphorus. The exact relation
In addition to the history and physical, which would be the between magnesium and potassium is unclear; however, many
basis for diagnosing the underlying cause, measurement of factors that cause renal potassium wasting also cause renal mag-
serum sodium, urine sodium and urine and plasma osmolality nesium wasting (e.g., loop and thiazide diuretic use). The oppo-
may also help. Hematocrit may be high because of dehydration. site is also true (e.g., potassium and magnesium sparing with
amiloride). Hypophosphatemia and hypocalcemia often accom-
Treatment pany hypokalemia. Potassium deprivation may impair calcium
The treatment of hypernatremia consists of correcting the resorption by the kidney, resulting in a negative calcium bal-
relative or absolute water deficit, which can be estimated in ance. This change, in turn, alters phosphorous metabolism.
several ways. The simplest accurate general rule is that for Etiology Hypokalemia may reflect potassium deficiency that
every liter of water deficit, serum sodium increases 3 mEq results from inadequate intake, gastrointestinal tract losses,
above the normal value of 140 mEq/L. If deficits are modest, or renal losses. Hypokalemia may also reflect shifts from the
they can be replaced orally or with intravenous 5% dextrose in extracellular to the intracellular compartment (e.g., insulin
water. If deficits are more severe, the TBW deficit is calculated administration or alkalosis).
according to the formula to estimate total body sodium. The Gastrointestinal losses (e.g., diarrhea, vomiting, biliary or
relative water deficit (in liters) is equal to the milliequivalent pancreatic fistulae, malabsorption and rarely villous adenoma)
change in serum Na+/140. The water must be replaced slowly, can be major factors in hypokalemia. The highest gastroin-
with no more than one-half given over the first 12 to 24 hours. testinal concentrations of potassium are found in the colon
For pure water loss, 5% dextrose is infused intravenously. and the rectum. Prolonged vomiting or nasogastric aspira-
Therefore, if a standard young 70-kg patient had a serum tion causes hypokalemia through a combination of factors. In
sodium value of 150, the water deficit is calculated as follows: addition to the loss of potassium in the gastric fluid, the loss of
hydrogen and chloride ions produces hypochloremic hypoka-
mEq change in serum Na + = (measured serum Na 140) lemia metabolic alkalosis. The increase in extracellular pH
TBW wt in kgk causes movement of potassium into the cells, which makes
the hypokalemia worse. As noted before, a change in pH of
or 0.1 units causes a reciprocal change in serum potassium of
mEq change in serum Na + = (150140) 0.6 70 0.3 to 0.5 mEq. As the hypokalemia worsens, in the alkalotic
= 10 42 state, the kidneys conserve hydrogen ions by excreting potas-
= 420 sium. Also, the high bicarbonate and low chloride concentra-
Water deffiicit in liters = 420/140 = 3 L. tions in the renal tubules cause greater resorption of sodium
in the distal tubule, causing additional urinary potassium loss.
In patients with associated sodium deficits, if symptoms of Finally, extracellular volume deficits stimulate aldosterone
dehydration predominate, the vascular volume deficit is ini- activity, which also increases renal potassium excretion. The
tially replaced with normal saline. If neurologic symptoms interaction of these mechanisms, if uncorrected, produces
are more prominent, half-normal saline (0.45%) is used. If noticeable intracellular and extracellular potassium depletion,
the sodium loss is large (e.g., diabetic hyperosmolar coma), which is not reflected in the serum level. At this point, because

Lawrence_Chap02.indd 44 7/21/2012 5:58:27 PM


of the need to conserve potassium, renal tubular hydrogen ion and the potassium should be infused through a central line if
excretion increases, urinary potassium loss decreases, and a rate higher than 10 mEq/hour is ordered. Too rapid intrave-
paradoxical aciduria appears (i.e., acidic urine in the presence nous administration can cause hyperkalemia and fatal cardiac
of severe alkalosis). arrhythmias. Generally, dextrose-containing solutions are not
Hyperglycemia, primary or secondary aldosteronism, renal used, as intravenous dextrose increases endogenous insulin,
tubular acidosis, elevated ACTH, licorice ingestion, acute leu- which induces the movement of potassium into cells and
kemia, or corticoid excess also causes renal potassium losses. causes the serum level to decrease further, making repletion
Hypokalemia is often iatrogenic, the result of treatment with more difficult. A serum potassium level lower than 2.9 mEq/L
thiazides, loop diuretics, or carbonic anhydrase inhibitors and may reflect depletions of several hundred milliequivalents or
inadequate replacement of potassium losses. By an unknown more of the intracellular pool and thus require much more
mechanism, magnesium deficiency decreases distal renal supplementation and close monitoring.
tubular potassium resorption. If the magnesium deficiency If hypokalemia is caused by hypomagnesemia, magnesium
is not corrected, renal losses continue, and it is difficult to repletion will help correct it. When hypokalemia and hypocalce-
correct the hypokalemia. mia occur together they must both be treated; treatment of only
one may cause the patient to become symptomatic to the other.
Presentation and Diagnosis Prognosis Most hypokalemia is moderate and relatively easy to
Hypokalemia usually does not become clinically significant correct. The prognosis depends on the severity of symptoms,
until serum potassium decreases to <3.0 mEq/L. In general, correct treatment, and the prognosis of the underlying disorder.
the severity of symptoms is proportion to the degree of defi-
cit and the rapidity with which it develops. Additionally, the Hyperkalemia
consequences of hypokalemia are exacerbated by alkalosis, Hyperkalemia is a serum potassium level >5.0 mEq/L.
hypocalcemia, and digoxin therapy. Hypokalemia may cause Etiology As in hypokalemia, the etiology of hyperkalemia is
neuromuscular symptoms that range from skeletal muscle usually multifactorial. It can be caused by exogenous load-
weakness and fatigue to paresthesias, paralysis, and rhabdo- ing (e.g., from excessive dietary intake in a patient with renal
myolysis. Deep-tendon reflexes may be diminished or absent. failure or from parenteral sources, such as high-dose penicil-
Hypokalemia causes increased production of ammonia in the lin therapy), transfusions of many units of stored blood bank,
renal tubules, which may worsen hepatic encephalopathy. Other or too vigorous correction of hypokalemia. Endogenous load-
symptoms include anorexia, polyuria, and nausea and vomiting ing occurs whenever large amounts of intracellular potassium
associated with paralytic ileus. Total body potassium depletion are released into the extracellular space (e.g., crush injuries,
produces cellular atrophy and negative nitrogen balance. Renal hemolysis, lysis and absorption of large hematomas, catabo-
tubular function is impaired, which may result in polyuria and lism of fat and muscle tissue because of stress or starvation, or
polydipsia because of decreased concentrating ability. rapid rewarming after severe hypothermia). Hyperkalemia can
Cardiac abnormalities are the most important and wor- also be caused by decreased renal excretion, which may result
risome consequences of hypokalemia and may appear in from adrenal insufficiency and impaired aldosterone activity,
the presence of digoxin, even with relatively mild deficits. but most often it is caused by intrinsic renal disease. Shifts of
Progressive electrocardiogram (ECG) abnormalities include potassium from the intracellular to the extracellular compart-
low-voltage, flattened, or inverted T waves, with prominent ment also cause hyperkalemia (e.g., acute metabolic or res-
U waves, depressed S-T segments, prolonged P-R intervals, piratory acidosis, insulin deficiency, therapy with digitalis and
and (at levels of 2.0 mEq/L) widened QRS complexes. A related cardiotonic agents). In diabetic ketoacidosis, hyper-
rapid decrease in serum potassium may lead to cardiac arrest. kalemia may be seen, even with total body potassium deficit.
If the deficiency is mild and the cause is clear from the his- Numerous drugs may cause hyperkalemia. Impaired renal
tory, serum potassium may be the only test required, with the excretion can be caused by diuretics (e.g., spironolactone, tri-
digoxin level measured if the patient is being treated with this amterene, amiloride) and by nonsteroidal anti-inflammatory
medication. If hypokalemia is more severe or refractory to treat- drugs (NSAIDs), -adrenergic antagonists, and ACE inhibi-
ment, other serum electrolytes, including calcium and magne- tors. Digitalis preparations, arginine, -adrenergic antagonists,
sium, should be measured. An arterial blood gas determination and some poisons, for example, can cause shifts of potassium
can exclude acidbase disturbances, and urinary electrolytes out of the intracellular compartment, raising the serum level.
can be used to exclude renal hyperexcretion. If the hypoka- Artifactually high serum potassium results from hemolysis
lemia patient has normal blood pressure, serum bicarbonate of the blood specimen, from obtaining a blood specimen from
and urine potassium should help distinguish among metabolic a vein into which potassium is being infused, and occasionally
causes, gastrointestinal losses, dietary deficiency, and osmotic from high platelet or leukocyte counts.
or drug-induced diuresis. If the patient is hypertensive, plasma Presentation and Diagnosis Although hyperkalemia causes
renin and aldosterone levels may help identify the cause. peripheral muscle weakness that ultimately progresses to res-
Treatment Treatment of hypokalemia involves replacing potas- piratory paralysis, the most important signs and symptoms are
sium and correcting the underlying cause. Whenever possible, cardiac. The first ECG abnormality is peaked T waves, best seen
potassium is repleted orally, with pills or liquid. Most peo- in the precordial leads, at serum concentrations between 6.0 and
ple find the taste of potassium solutions unpleasant. Enteric- 7.0 mEq/L. Further elevations produce multiple ECG abnor-
coated tablets should not be used, because they can cause malities, including flattened P waves, increased P-R intervals,
small bowel ulceration. In patients with normal kidneys, the decreased Q-T intervals widened QRS complexes, depressed
oral dose should not exceed 40 mEq/4 hour. If the intravenous S-T segments, and complete heart block with atrial asystole. At
route is required, the rate should not exceed 10 mEq/hour, elevations >8.0 mEq/L, more widened QRS complexes merge
with the dose repeated as often as necessary to increase the with T waves to produce a sine wave appearance. This change is
serum level to 3.5mEq/L. The patient should be on a monitor followed by ventricular fibrillation and cardiac arrest.

Lawrence_Chap02.indd 45 7/21/2012 5:58:28 PM


Diagnosis is made by measuring the serum potassium level. Chloride

It is usually relatively simple to determine the cause, but since Chloride is the major extracellular anion (Table 2-1). It is ubiq-
significant hyperkalemia is uncommon if the kidneys are nor- uitous in the diet, absorbed in the small and large intestines,
mal, serum BUN, creatinine, and urine output should also be and excreted by the kidneys. Chloride balance usually paral-
measured. Anuric patients accumulate potassium, but a source lels sodium balance, except when hypochloremia results from
must be sought in hyperkalemia in nonoliguric patients. Even the loss of acidic gastric contents. Although no signs or symp-
in the presence of renal insufficiency, medication or exces- toms are specific to abnormalities of chloride balance, changes
sive dietary intake is often responsible. A 12-lead ECG must in extracellular chloride content can significantly affect fluid,
be performed. If the patient is being treated with digoxin, a electrolyte, and acidbase balance and their management.
digoxin level should be obtained. If the patient had a crush
injury, serum and urinary myoglobin should also be measured. Hypochloremia
If spurious hyperkalemia is suspected (e.g., from a Hypochloremia is a serum chloride concentration <95 mEq/L.
hemolyzed specimen, from blood drawn above an intravenous In severe respiratory acidosis, metabolic compensation invol-
site), blood should be redrawn for a serum potassium level ves renal tubular resorption of bicarbonate to decrease the
measurement or a plasma potassium level ordered. However, extracellular acidosis that is caused by CO2 retention and chlo-
treatment of a very high serum potassium level should not be ride depletion. As respiratory acidosis resolves and CO2 reten-
delayed while waiting for results. tion decreases, renal excretion of excess bicarbonate allows the
Treatment The primary goal of the treatment of hyperkalemia pH to return to normal. Hypochloremia impairs renal bicar-
is to reduce serum potassium to levels that are not life threat- bonate excretion, however, and if serum bicarbonate remains
ening. In mild hyperkalemia (<6 mEq/L), the simplest meas- high in the presence of decreased CO2 tension, metabolic alka-
ures are to restrict potassium intake, eliminate causes such as losis results and persists until the chloride deficit is corrected.
potassium-sparing diuretics, and treat fluid volume or acid Etiology Hypochloremia classically results from the loss of acidic
base disorders. Potassium-wasting diuretics may be adminis- gastric contents, either by vomiting or by nasogastric suction.
tered, and hormone deficiencies may be replaced. It can result from renal losses caused by diuretics, nonoliguric
For potassium levels between 6.5 and 7.5 mEq/L, 10 units acute and chronic renal failure, or compensatory renal tubular
insulin is administered intravenously along with 25 g glucose resorption of bicarbonate in response to respiratory acidosis.
intravenously over 5 minutes. This therapy shifts potassium Presentation and Diagnosis The signs and symptoms are those
from the extracellular to the intracellular compartment and of the accompanying disorder. The diagnosis is made by
may reduce serum potassium by as much as 1 mEq/L. A simi- measuring serum chloride.
lar shift may be created by administering a bicarbonate infu- Treatment In general, hypochloremia is treated with solutions
sion or by injecting 45 mEq sodium bicarbonate intravenously that contain sodium chloride and potassium chloride in a ratio
over 5 minutes to induce a shift to a more metabolic state. reflecting the underlying problem and by serum electrolyte
These compartments shifts last only a few hours. Sodium concentrations. Ammonium chloride is rarely needed and
polystyrene sulfonate, a cation-exchange resin, administered should not be used in patients with advanced liver disease or
orally or rectally actually removes potassium form the body. hepatic failure because it may precipitate or increase encepha-
Each gram of the resin binds approximately 1 mEq potas- lopathy. It is important to correct hypochloremia along with
sium. The oral dose is 25 g resin suspended in 50 mL 20% other deficits in the treatment of hypochloremic hypokalemic
sorbitol solution every 4 to 6 hours. The rectal dose is 50 g in metabolic alkalosis. Hydrochloric acid may rarely be used in
100 to 200 mL 35% sorbitol given as a retention enema every severe refractory hypochloremic metabolic alkalosis. Extreme
4 hours. Patients with potassium levels >6.5 mEq/L are moni- care must be taken with its use since even 1 to 2 mL of extrava-
tored with continuous ECG. sation can produce substantial tissue necrosis.
Serum potassium levels >7.5 mEq/L in a patient with evi- Prognosis Hypochloremia has no specific prognostic signifi-
dence of cardiac toxicity should be treated with an intravenous cance. The prognosis depends on the underlying disorder.
infusion of 10 to 30 mL 10% calcium gluconate given slowly
over 5 minutes to reduce cardiac muscle electrical excitability Hyperchloremia
temporarily while other methods are used to rid the body of Hyperchloremia is a serum chloride level >115 mEq/L and is
potassium. Rapid infusion of calcium is dangerous and is jus- uncommon in surgical patients.
tified only when hyperkalemia is severe. Electrocardiographic Etiology Hyperchloremia may occur in association with
monitoring is advisable during treatment of hyperkalemia, hypernatremia, in renal tubular acidosis, or after the adminis-
and it is mandatory if calcium is being infused. tration of excess potassium chloride or ammonium chloride.
Hemodialysis and peritoneal dialysis also remove potas- It may be caused by surgical diversion of urine into segments
sium form the body and may be necessary in patients with of bowel (e.g., ileal urinary conduits, ureterosigmoidostomy).
renal failure. They may be used along with more rapid meth- In these cases, the bowel mucosa absorbs excess chloride in
ods to reduce serum potassium in moderate to severe hyper- exchange for bicarbonate, especially when evacuation of the
kalemia. In treating hyperkalemia with dehydration and urine is delayed.
acidosis in diabetic ketoacidosis, care must be taken not to Presentation and Diagnosis The signs and symptoms are those
allow serum potassium to decrease to hypokalemic levels. of the accompanying disorder. The diagnosis is made by
Prognosis Hyperkalemia itself does not affect recovery from measuring serum chloride.
illness or surgery, and it is usually correctable. However, car- Treatment There is no specific treatment of hyperchloremia.
diac events caused by hyperkalemia may be fatal if the hyper- Treatment is directed at the underlying disorder.
kalemia and its effects are not promptly treated. The prognosis Prognosis Hyperchloremia has no prognostic significance. The
of patients with hyperkalemia is often related to the underly- prognosis depends on the nature and treatment of the underly-
ing cause (e.g., renal failure). ing disorder.

Lawrence_Chap02.indd 46 7/21/2012 5:58:28 PM


Calcium TABLE 2-9 Causes of Hypocalcemia in Surgical

Calcium is a common divalent cation, almost all of which is Patients
found in hydroxyapatite crystals in bone. On the surface of
bone, bone calcium participates in exchange with ECF cal-
cium. Of the small amount of calcium in the ECF, approxi- Artifactual as a result of hypoalbuminemia
mately 40% is bound to plasma protein and 10% is complexed Acute pancreatitis
with bicarbonates, citrate, and phosphate. Only the hormo- Surgically induced hypoparathyroidism (transient or permanent)
nally regulated ionized portion, the remaining 50%, is physi- Necrotizing fasciitis
ologically active. This small proportion is of vital importance,
Inadequate intestinal absorption
however, primarily because of its role in neuromuscular activ-
ity. The normal range of total serum calcium is 8.0 to 10.5 mg/ Inflammatory bowel disease
dL, and that of ionized calcium is 4.75 to 5.30 mg/dL. Most Pancreatic exocrine dysfunction
bound calcium is bound to albumin, and total serum calcium Mucosal malabsorptive syndromes
is dependent on serum albumin. Total calcium values may Excessive fluid losses from pancreatic or intestinal fistulae
appear artifactually subnormal in hypoalbuminemic patients
unless a correction factor, such as the following, is used: Chronic diarrhea
Renal insufficiency with impaired calcium resorption
Corrected total Ca + + = [0.8 (4.0 patient s albumin)] Hypomagnesemia
+ total sserum Ca + + . Hyperphosphatemia
In this formula, 4.0 represent normal serum albumin. The pro-
portion of calcium bound to proteins is dependent on pH; it is
decreased by acidosis, with a concomitant increase in ionized
(e.g., hypomagnesemia, any type of true hypoparathyroidism),
calcium. The level of serum ionized calcium is a more accu-
(2) ineffective (e.g., vitamin D disorders, chronic renal failure,
rate indicator of physiologic activity than total calcium.
pseudohypoparathroidism), or (3) overwhelmed (e.g., hyper-
The usual adult dietary intake of calcium is 1 g or more/day.
phosphatemia). Artifactual hypocalcemia occurs when the
Two-thirds of this calcium passes through the intestine and is
serum albumin is low and total calcium rather than ionized
excreted in stool, and one-third is absorbed in the small intes-
calcium is measured.
tine, regulated by vitamin D. In normal kidneys, approximately
Presentation and Diagnosis The clinical manifestations of
10% of filtered calcium reaches the distal tubules, where resorp-
hypocalcemia reflect the role of calcium in neuromuscular
tion is increased by parathyroid hormone (PTH) and metabolic
activity. Early symptoms of hypocalcemia include circu-
alkalosis, or is decreased by hypophosphatemia and metabolic
moral tingling, numbness and tingling of the fingertips, and
acidosis. Overall calcium homeostasis, largely regulated by
muscle cramps. Hyperactive deep-tendon reflexes develop,
PTH, is the result of intestinal absorption, renal excretion, and
with a Chvostek sign (unilateral facial spasm when the
calcium exchange between bone and the ECF. Although severe
facial nerve on the side is lightly tapped), tetany, and Trous-
abnormalities of calcium metabolism are uncommon in surgi-
seaus sign (carpopedal spasm), eventually progressing to
cal patients, symptomatic abnormalities are seen.
seizures. The patient may be confused or depressed. Pro-
Hypocalcemia longed Q-T intervals are seen on ECG.
Hypocalcemia is defined as total serum calcium <8 mg/dL. It In acidosis, the ionized fraction of serum calcium increases
is seen in many conditions common to surgical patients, sev- at the expense of the bound fraction. Because only the ion-
eral of which are acute problems. ized fraction is active, symptoms may not appear, even with
Etiology Hypocalcemia is often seen in surgical patients low total serum calcium. With severe alkalosis, the reverse
(Table 2-9). In acute pancreatitis, the etiology of hypocalcemia occurs, and symptoms may appear even when the measured
is unclear. It probably results from a combination of calcium total serum calcium is normal.
binding in saponified tissue, PTH deficiency or dysfunction Hypocalcemia can occur after blood transfusion, as a result
in the kidney and bone, and decreased protein-bound cal- of citrate binding and dilution. However, evidence suggests that
cium as a result of hypoalbuminemia. Magnesium deficiency at moderate rates of blood transfusion, endogenous release of
decreases PTH release and activity. Phosphate increases bone calcium from bone is adequate to prevent hypocalcemia. Only
deposition of calcium, decreasing the available circulating with massive transfusion and volume replacement at rates of
pool. Inadequate intestinal absorption of calcium may result 100 mL/minute or higher is there any need to give supplemental
from inflammatory bowel disease, pancreatic exocrine dys- calcium.
function, or malabsorption syndromes. Excessive fluid losses Diagnosis is made by measuring serum calcium (the
from chronic diarrhea or pancreatic or intestinal fistulas may ionized portion if possible), along with serum potassium,
also seriously deplete extracellular calcium and cause other magnesium, phosphate, and alkaline phosphatase. Other
electrolyte abnormalities. Low serum calcium levels are seen electrolyte abnormalities and acidbase disorders must be
with severe soft tissue infections, such as necrotizing fasciitis. excluded. Serum albumin is measured, as well as BUN
Artifactual hypocalcemia is seen when serum albumin is low and creatinine. Measurement of urinary calcium can help
and total calcium, rather than ionized calcium, is measured. assess calcium intake. It may ultimately prove necessary to
Vitamin D deficiency may result from synthetic failure in renal measure vitamin D levels to help make the diagnosis of idi-
or hepatic disease, or from conversion to inactive metabolites opathic hypoparathyroidism. During physical examination,
caused by the anticonvulsants phenytoin and phenobarbital. a search should be made for a transverse surgical scar on the
Another way to classify hypocalcemia is according to anterior neck, which would suggest previous thyroidectomy
its relation to PTH, which may be (1) deficient or absent or parathyroidectomy.

Lawrence_Chap02.indd 47 7/21/2012 5:58:28 PM


Treatment Treatment of symptomatic hypocalcemia is directed anorexia, nausea, and vomiting. As serum calcium increases,
at correcting the calcium deficit, normalizing the relation severe headaches, diffuse musculoskeletal pain, polyuria, and
between ionized and protein-bound calcium by correcting polydipsia develop.
acidbase disorders, and treating the underlying causes. When The combination of decreased oral intake, vomiting, and
the need for correction is urgent (e.g., severe, highly sympto- polyuria leads to hypovolemia and dehydration, which may
matic hypocalcemia), calcium gluconate or calcium chloride become pronounced. The ECG shows shortened Q-T intervals
is infused. Hypocalcemia associated with chronic disorders is and widened T waves. With normal or elevated phosphate,
treated over the long term with oral calcium lactate. Vitamin calcification may develop in the kidneys as well as in unusual
D supplements may be needed; the high doses required in locations (e.g., heart, skin). Pancreatitis and renal failure may
hypoparathyroidism may be reduced if urinary calcium loss is develop as well. The renal failure has multiple causes, including
decreased with thiazide diuretics. volume depletion, nephrocalcinosis, and deposition of nephro-
Prognosis Disorders of calcium balance can be treated with toxic myeloma proteins or light chains. When serum calcium
complete resolution of symptoms. Underlying disorders must increases to 15 mg/dL, and above, confusion and depression
also be identified and treated. progress to somnolence, stupor, and coma. This degree of
hypercalcemia results in death unless it is corrected promptly.
Hypercalcemia Diagnosis is made primarily by a careful history, including
Hypercalcemia is defined as an excessive amount of calcium all medications, and blood tests. PTH levels are assessed, and
in the blood, that is, total serum calcium >10.5 mg/dL. imaging procedures are used to locate a tumor. Squamous cell
Etiology The more common causes of hypercalcemia are shown carcinoma of the bronchus and hypernephromas can produce
in Table 2-10. In surgical patients, primary and secondary PTH-related peptide. In a patient with a known malignancy,
hyperparathyroidism and metastatic breast cancer are among the presence of symptomatic bone metastasis may be the ini-
the common causes. In fact, more than 90% of hypercalcemic tial presentation of some malignancies, such as those originat-
patients who have no symptoms other than depression and ing in the prostate or breast.
fatigue have primary hyperparathyroidism. Malignancies cause Treatment Initially, calcium intake is restricted, hydration
hypercalcemia both by bony involvement and by the secretion status improved, and urinary calcium excretion increased.
of PTH-like substances that affect calcium metabolism. Malig- If the patient is symptomatic or calcium level is high, the
nancies that are sufficiently advanced to cause hypercalcemia patient should be hospitalized. Large volumes of intrave-
are usually symptomatic. Mobilization of calcium from bone in nous normal or half-normal saline are infused. Loop diu-
bedridden patients can cause mild, asymptomatic hypercalce- retics enhance calcium excretion; however, their use is
mia. The milk-alkali syndrome (e.g., hypercalcemia, alkalosis, controversial except in patients with congestive heart fail-
and renal failure) results from excessive intake of calcium and ure because they may increase resorption of calcium from
absorbable antacids. Rare causes of hypercalcemia included bone and worsen hypercalcemia. Great care must be taken
Williamss syndrome (a constellation of congenital defects and during the process of vigorous hydration and diuresis, with
abnormal sensitivity to vitamin D) and vitamin A intoxication, close monitoring of volume status to avoid fluid overload
possibly by increasing bone resorption. and particularly hypervolemia. Meticulous assessment and
Presentation and Diagnosis The initial clinical manifesta- replacement of electrolytes are necessary. Hypomagnesemia
tions of hypercalcemia are nonspecific: weakness, fatigue, can develop as a result of forced diuresis. Bisphosphonates
(e.g., pamidronate) are used in combination with calcitonin
(which has a very rapid onset and short duration of action)
to inhibit bone resorption. Gallium nitrate, which is nephro-
TABLE 2-10 Causes of Hypercalcemia toxic, is used in the treatment of cancer-related hypercalce-
mia unresponsive to hydration.
Hyperparathyroidism Corticosteroids are sometimes used as a long-term treat-
ment to suppress calcium release from bone in patients with
granulomatous disease, vitamin D intoxication, or hemato-
Metastatic cancer logic malignancies. The usual dose is hydrocortisone 3 mg/
Lymphoma kg/day. This treatment may take 1 to 2 weeks to produce an
Leukemia appreciable reduction in serum calcium.
Granulomatous disease The antineoplastic agent plicamycin (formerly called mith-
ramycin), a DNA-binding antibiotic and an RNA-synthesis
inhibitor, acutely reduces serum calcium by an unknown
Tuberculosis mechanism. It is given in small intravenous doses, 25 g/kg,
Fungal infection for 3 to 4 days. Calcium levels decrease within 48 hours and
Excessive dietary intake remain low for several days to weeks. Contraindications
Milk-alkali syndrome
include thrombocytopenia, coagulopathy or other bleeding
diatheses, and bone marrow suppression from any cause.
Vitamin A or D intoxication Plicamycin has significant renal and hepatic toxicity.
Thiazide diuretics Oral or intravenous phosphate supplements are sometimes
Immobilization used to form complexes with ionized calcium. Given intrave-
Endocrine abnormalities nously, these supplements may produce a precipitous decrease
in serum calcium, resulting in tetany, hypotension, and renal
failure. Therefore, phosphate supplementation is generally not
Adrenal insufficienc recommended.

Lawrence_Chap02.indd 48 7/21/2012 5:58:29 PM


Prognosis If the cause of hypercalcemia is treatable and the of 8 to 16 mEq of magnesium sulfate is administered, fol-
hypercalcemia itself is treated appropriately before neurologic lowed by intravenous infusion at a rate of 1 to 2 mEq/kg/day.
symptoms become severe, the patient should recover com- Concomitant or resulting deficiencies in other elements must
pletely. Many of the causes of hypercalcemia are life threaten- also be corrected, and adequate hydration must be maintained.
ing (e.g., metastatic cancer), and this prognosis determines the If the patient is in renal failure, extra care must be taken not to
outcome more that the hypercalcemia itself. overcorrect hypomagnesemia.
Prognosis Recovery from hypomagnesemia may be complete.
Magnesium The prognosis depends on the etiology, the severity of the defi-
Magnesium plays an important role in metabolism because it ciency and its symptoms, and the promptness of treatment.
is a cofactor for many enzymes. It also affects neuromuscular
function. At least one-half of the bodys total magnesium is Hypermagnesemia
in bone. Most of the remainder is intracellular. Less than 1% Clinically significant hypermagnesemia is rare, especially if
is extracellular. Magnesium is the most common intracellular renal function is normal.
divalent cation, and most intracellular magnesium is bound Etiology Hypermagnesemia can result from renal failure; any
to adenosine triphosphate. The average daily intake of mag- injury that causes rhabdomyolysis (e.g., crush injuries, severe
nesium is 15 to 30 mEq. Approximately 40% of the magne- burns); dehydration; severe metabolic acidosis; adrenal insuffi-
sium is absorbed, primarily in the jejunum and ileum, and it ciency; familial benign hypocalcuric hypercalcemia; or overdosage
is excreted primarily by the kidneys. A higher percentage of with magnesium salts in cathartics. In addition, in either mother or
intake is absorbed if body stores are deficient. The normal newborn, it can occur after treatment of eclampsia. It also occurs in
range of serum magnesium is 1.5 to 2.5 mg/dL. Normal kid- patients with renal failure who use magnesium-containing antac-
neys conserve magnesium when intake is low, but hypomagne- ids. Renal excretion is decreased in metabolic alkalosis.
semia develops if intake remains <0.3 mEq/kg/day. Presentation and Diagnosis Symptomatic hypermagnesemia
follows a progressive pattern, with increasing neuromuscular
Hypomagnesemia and central nervous system abnormalities as the serum level
Hypomagnesemia is common in surgical patients, particu- increases. Initial nausea is superseded by lethargy, weakness,
larly the elderly, who are often in a starvation state, experi- hypoventilation, and decreased deep-tendon reflexes. The
ence gastrointestinal loss, or have absorption defects. When condition then progresses to hypotension and bradycardia,
magnesium is deficient, losses of potassium and phosphorus, skeletal muscle paralysis, respiratory depression, coma, and
the other two major elements in cells, also occur. These ele- death. Diagnosis is made by testing serum values.
ments are expelled from the cell, and the cells decrease in Treatment Mild hypermagnesemia is treated with oral hydra-
size to maintain normal intracellular composition. Severe tion and by controlling magnesium intake (e.g., giving patients
hypomagnesemia also produces severe hypocalcemia by with renal failure nonmagnesium-containing antacids). Severe
decreasing PTH secretion and by an apparent skeletal resist- symptoms are reversed temporarily by intravenous calcium,
ance and an impaired renal response. and the magnesium excess is treated with hydration and diu-
Etiology The most common cause of hypomagnesemia is retics, or hemodialysis.
dietary deficiency combined with gastrointestinal loses (e.g., Prognosis Recovery from hypermagnesemia may be complete.
diarrhea, nasogastric suction) and deficiencies in other ele- The prognosis depends on the etiology, the severity of the defi-
ments. Other causes include chronic alcoholism (especially ciency and its symptoms, and the promptness of treatment.
during withdrawal), malabsorption (especially steatorrhea), Phosphate
acute pancreatitis, improperly constituted parenteral nutrition, Phosphorus is a component of all body tissues, and it partici-
and endocrine disorders. Hypomagnesemia also occurs as a pates in virtually all metabolic processes. In a normal adult,
side effect of many therapeutic drugs, particularly some diu- approximately 85% of phosphorus is bound in bone and 15%
retics, aminoglycosides, amphotericin, cyclosporine, cisplati- is distributed in other tissues. Less than 1% is extracellular.
num, insulin, and pentamidine. Athletes and pregnant woman The intestine, influenced by vitamin D, absorbs approximately
may be mildly hypomagnesemic. 70% of ingested soluble phosphorus, and a higher proportion
Presentation and Diagnosis The effects of magnesium defi- if dietary intake is low. The normal adult phosphorous require-
ciency are not immediate. Like calcium, the bodys other ment is 2 to 9 mg/kg/day. The amount of phosphorus excreted
major divalent cation, magnesium affects neuromuscular by normal kidneys is controlled by PTH and is proportional to
function. Symptoms develop insidiously, first as nonspecific the amount absorbed. The normal range of serum phosphate is
systemic symptoms that include nausea, vomiting, anorexia, 2.5 to 4.5 mg/dL. Circadian variation, mediated by the adrenal
weakness, and lethargy, then as neuromuscular symptoms cortex, produces the highest serum levels during the afternoon
that include muscle cramps, fasciculations, tetany, carpopedal and night and the lowest levels during the morning.
spasm, paresthesias, irritability, inattention and confusion, and
cardiac arrhythmias, along with other symptoms of associated Hypophosphatemia
hypokalemia and hypocalcemia. Hypophosphatemia is common in surgical patients. When
Diagnosis is made by testing serum values, which may be phosphorus is deficient, there are also losses of potassium and
normal, even in the presence of a deficiency in body magnesium. magnesium, the other two major elements in cells. These ele-
Treatment Primary attention must be given to correcting the ments are expelled from the cell, and the cells decrease in size
cause. If hypomagnesemia is mild and does not result from an to maintain normal intracellular composition.
absorptive defect, oral supplements are given. If it is moder- Etiology The causes of hypophosphatemia are categorized as
ate, then it is treated with intravenous magnesium sulfate at a (1) inadequate uptake as a result of inadequate dietary intake,
rate of 50 to100 mEq/day because the equivalent oral dose can malabsorption, gastrointestinal losses, prolonged antacid use,
cause diarrhea. If symptoms are severe, an intravenous bolus improperly constituted parenteral nutrition, or vitamin D

Lawrence_Chap02.indd 49 7/21/2012 5:58:29 PM


deficiency; (2) increased renal excretion as a result of diuretic Disorders of AcidBase Balance
use, hypervolemia, corticoid therapy, hyperaldosteronism, The management of acidbase disorders depends on prompt
syndrome of inappropriate secretion of antidiuretic hor- recognition and evaluation of the abnormalities involved. A
mone (SIADH), or hyperparathyroidism; or (3) compart- good clinician uses the history and physical examination to
mental shifts as a result of hormones, nutrients that stimulate determine the nature and the severity of the abnormalities
insulin release, treatment of diabetic ketoacidosis, recovery (Table 2-11). Data provided by an arterial blood gas and a
from hypometabolic states, rapidly growing malignancies, or serum bicarbonate concentration allow a correct diagnosis to
respiratory alkalosis. It is also seen in chronic alcoholism, in be made. Correction of the underlying disorder that has caused
burns, and after parathyroidectomy or renal transplantation. the acidbase disturbance is the ultimate goal. Identification
Occasionally, hypophosphatemia is the first clue to alcohol of the disorder allows for initiation of treatment. Acidbase
withdrawal in a hospitalized patient. status is defined by the plasma pH and by the conditions of the
Presentation and Diagnosis Severe phosphorous deficiency acidbase pairs that determine it. Under normal conditions,
causes anorexia, dizziness, osteomalacia, severe congestive the balance between these components is tightly controlled.
cardiomyopathy, proximal muscle weakness, visual defects, Within 95% confidence limits, the pH of the arterial blood is
ascending paralysis, hemolytic anemia, and respiratory fail- between 7.35 and 7.43. This is a delicate homeostatic system
ure. Leukocyte and erythrocyte malfunction, rhabdomyolysis, that is controlled acutely (minutes) by the lungs and chroni-
hypercalciuria, and severe hypocalcemia are also seen. Cen- cally (hours to days) by the kidneys.
tral nervous system dysfunction occurs and can progress to
seizures, coma, and death. If the hypophosphatemia is a result Overview
of vitamin D deficiency, metabolic acidosis may result from The pH disorders of blood can be grouped into two broad
reduced renal hydrogen excretion. categories, respiratory and metabolic. Respiratory acidbase
Diagnosis is made by testing serum values, but total body disorders are disorders of Paco2. Metabolic acidbase disor-
phosphate deficiency may exist, even in the face of elevated ders are disorders of bicarbonate. An arterial blood pH that is
serum values. Arterial blood gases, pH, and urine phosphate <7.35 signifies acidemia, while pH > 7.45 signifies alkalemia.
should be measured, along with serum potassium, calcium, The normal limits of Paco2 are 37 to 45 mm Hg. An arterial
and magnesium. Paco2 that is elevated above the normal range produces a res-
Treatment Severe hypophosphatemia should prompt an piratory acidosis. Respiratory alkalosis occurs if the Paco2 is
aggressive search for and treatment of cause. Phosphate salts below the normal range.
may be given orally or intravenously. Other associated elec- Bicarbonate concentration normally varies between 22 and
trolyte abnormalities must also be treated. Diuretics may be 26 mEq/L. A plasma HCO3 concentration that is <22 mEq/L
withdrawn. VIPomas should be surgically removed.
Prognosis Repletion of phosphorus corrects or decreases most
abnormalities. Respiratory failure may not be reversed com-
pletely, and the ultimate outcome is likely to depend on the TABLE 2-11 Simple Disorders of AcidBase
prognosis of the underlying deficiency. Balance, with Examples

Hyperphosphatemia Respiratory Alkalosis Metabolic Alkalosis

Hyperphosphatemia is relatively common in adults and is
seen even in the presence of total body phosphate deficiency. Congestive heart failure Chronic diarrhea
Etiology The causes of hyperphosphatemia are categorized as Cirrhosis Cushings syndrome
(1) decreased renal excretion as a result of renal insufficiency Fever Hyperaldosteronism
or failure, hyperthyroidism, hyperparathyroidism or pseudo- Hypermetabolic states Loop or thiazide diuretics
hypoparathyroidism, or adrenal insufficiency; (2) increased
intestinal absorption as a result of sarcoidosis or tuberculosis Hyperventilation Massive blood transfusion
(both of which produce vitamin D), or excess phosphate or Pregnancy Milk-alkali syndrome
vitamin D ingestion; (3) iatrogenic, as a result of intravenous Pulmonary embolus Vomiting
infusion of phosphate-containing fluids; or (4) shifts from the Sepsis
intracellular to the extracellular compartment as a result of
acidotic states, tumor lysis, hemolytic anemia, thyrotoxicosis, Respiratory Acidosis Metabolic Acidosis
or rhabdomyolysis. Chest cage hypofunction Anion gap
Presentation and Diagnosis Hyperphosphatemia is associated
Central nervous system depression Acid ingestion
with no symptoms, although in the presence of severe hyper-
calcemia, renal failure, or vitamin D intoxication, it may be Chronic obstructive pulmonary disease Advanced renal failure
accompanied by deposition of calcium phosphate in abnormal Drugs Hypotension
locations. It is diagnosed by testing serum values. Associated Morbid obesity Ketoacidosis
electrolyte abnormalities should also be identified and corrected. Pneumothorax Renal failure
Treatment Aluminum-based antacids decrease absorption by
Sleep apnea Sepsis
binding phosphate, and diuretics increase the rate of urinary
phosphate excretion. Dialysis is used in patients with renal fail- Status asthmaticus Nonanion gap
ure. It is often unnecessary to treat hyperphosphatemia, except Acute diarrhea
by correcting excess intake and addressing associated problems. Moderate renal failure
Prognosis The prognosis of hyperphosphatemia depends on Renal tubular acidosis
the cause.

Lawrence_Chap02.indd 50 7/21/2012 5:58:29 PM


is defined as metabolic acidosis. Metabolic alkalosis is pre- and ultimately coma can occur as a result of CO2 narcosis.
sent when the bicarbonate level is above normal (26 mEq/L). In combination with hypoxemia, cardiovascular dysfunction
Simple acidbase disorders occur when there is a primary can occur, which may result in cardiac arrest and death. In
change either in the bicarbonate concentration or in the Paco2 patients with chronic hypoventilation and respiratory acido-
with an appropriate (normal) secondary change in the other sis, the major threat is CO2 narcosis. This can occur with the
parameter, as illustrated in the following equation: administration of supplemental oxygen. In chronic compen-
sated respiratory acidosis, the stimulus to breathe is hypoxia,
+ HCO3 H 2 CO3 CO2 + H 2 O. not hydrogen ion concentration in arterial blood. By adding
oxygen, the stimulus to breathe is removed, and CO2 narcosis
Normally, the CO2 that is produced is eliminated rapidly by ensues. Rules 1 and 2 can be used to determine whether res-
the lungs. piratory changes are responsible for the acute acidotic state. If
Mixed acidbase disorders include all possible combina- the change in pH is greater than explained by rule 1, there is a
tions. For example, a patient may develop metabolic acido- component of metabolic derangement present. Likewise, using
sis and respiratory acidosis simultaneously. Another patient Rule 2, the contribution from the change in bicarbonate can be
may have a combination of respiratory alkalosis and meta- determined.
bolic acidosis. In clinical practice, the presence of an isolated Treatment Treatment of respiratory acidosis requires the
acidbase disorder is unusual. With normal kidney and lung identification and correction of the underlying cause of
function, compensation occurs. As a result, many disorders reduced alveolar ventilation while maintaining oxygena-
of acidbase are mixed. Two rules are helpful in assessing tion. This may be as simple as administering supplemental
the degree to which the respiratory or bicarbonate component oxygen, or by instituting mechanical ventilation or simply
contributes to the change in pH. improving pain control since many patients have enough
1. A change in Paco2 of 10 mm Hg is associated with a recip- postoperative pain that their breathing is inhibited, resulting
rocal change of 0.08 pH units. As the Paco2 goes up, the in decreased ventilation and subsequent hypercapnia. Acute
pH goes down. hypercapnia should not be overcorrected. Sudden decreases
2. A change in HCO3 of 10 mEq/L is associated with a direct in Paco2 cause rapid ionic shifts between cellular and ECF,
change of 0.15 pH units. As bicarbonate goes up, pH goes up. which can produce severe dysrhythmias. Abrupt decrease
in Paco2 below normal levels (for that patient) can cause
Acidosis cerebral vasoconstriction and decrease cerebral blood flow,
Regardless of the etiology, the consequences of acidemia particularly in patients with acute brain injury. The admin-
can be life threatening. At pH < 7.2, there is a decrease of istration of bicarbonate as the only treatment for respiratory
cardiac and peripheral vascular response to catecholamines acidosis is inappropriate.
including vasoactive drugs. As a result, cardiac function may
be depressed and lethal arrhythmias may occur. In addition,
Metabolic Acidosis
potassium is transported to the extracellular space, and can
Metabolic acidosis can be acute or chronic. One cause of
rise to clinically significant levels, resulting in dysrhythmias.
metabolic acidosis is loss of bicarbonate from the extracel-
Respiratory Acidosis lular space. This may be due to diarrhea, intestinal fistula,
Respiratory acidosis is the result of retention of CO2 because biliary fistula, or pancreatic fistula. Chronic bicarbonate
of pulmonary alveolar hypoventilation. It can be acute or losses occur with renal dysfunctions, ureterointestinal anas-
chronic. Acute causes are typically respiratory depression as tomosis, decreased mineralocorticoid activity, and the use of
a result of narcotics, sedatives, muscle relaxants, or anesthetic the diuretic acetazolamide, which is also a carbonic anhy-
agents. Decreased respiratory effort due to pain from surgi- drase inhibitor. In burn patients, the use of mafenide acetate,
cal incisions, or trauma, altered mechanics of the chest wall which is also a carbonic anhydrase inhibitor, can result in
due to rib fractures, can also cause hypoventilation. Pulmo- metabolic acidosis. Other losses of bicarbonate include ure-
nary injury including contusions and lacerations of the lung, terointestinal anastomosis and decreased mineralocorticoid
pneumonia, or pulmonary edema also result in hypoventila- activity. The second major cause of metabolic acidosis is an
tion due to an alteration in the ability to exchange gases at increased acid load. Lactic acidosis, one of the most com-
the alveolar level. Airway obstruction from a foreign body, mon causes of a high anion gap metabolic acidosis, occurs
misplaced or obstructed endotracheal tube, laryngospasm, with shock, whether hypovolemic, hemorrhagic, septic, or
or tracheal-bronchial injury can impair ventilation as well. cardiogenic, and is due to the production of lactic acid as
Acute hypoventilation can be rapidly fatal if not identified and the body responds to the insult with anaerobic metabolism
corrected. On the other hand, chronic respiratory acidosis is and/or increased accumulation in tissue of metabolites due
most often caused by advanced lung disease such as COPD. to reduced cellular clearance. Ketoacidosis that occurs with
This results in a compensated hypoventilation and can be well untreated hyperglycemia is another cause for metabolic aci-
tolerated. dosis, as is ingestion of toxins, including salicylates, metha-
Presentation and Diagnosis The acidbase disorder has a primary nol, and other toxins. Liver failure can result in metabolic
respiratory cause if the Paco2 is abnormal and the Paco2 and acidosis when the liver decompensates to the point where
pH change in opposite directions. The clinical consequences of lactate and citrate that are normally produced by the body
acute respiratory acidosis are caused by hypercapnia, and the cannot be metabolized. Likewise, renal failure can cause met-
accompanying hypoxia. Note hypoxia can be masked by increas- abolic acidosis when the kidney fails to retain bicarbonate as
ing the available inhaled oxygen concentration. With mild acute a result of injury to the tubules.
respiratory acidosis, restlessness and agitation may be present. Presentation and Diagnosis Metabolic acidosis is the primary
The patient may also be mildly hypertensive. With more disorder if the pH is abnormal and the pH and the Paco2
severe elevations of Paco2 levels, confusion, somnolence, change in the same direction. Respiratory compensation

Lawrence_Chap02.indd 51 7/21/2012 5:58:30 PM


occurs with both acute and chronic metabolic acidosis. Again, acidosis), hypoxia, fever, brain injury, sepsis, and liver failure
Rules 1 and 2 are useful in determining if the degree of that results in elevated serum ammonia. Hypocapnia is also
compensation explains the disorder. Determination of the common in patients who are mechanically ventilated. The
anion gap will help to distinguish the loss of bicarbonate compensatory mechanism for respiratory alkalosis is renal
from the presence of additional acids as the cause of meta- excretion of bicarbonate, which is slow, or limited in surgical
bolic acidosis. The anion gap is the difference between the patients who have increased aldosterone levels resulting in
serum sodium concentration and the sum of the bicarbonate sodium retention and associated limited bicarbonate excre-
and chloride concentrations in serum. tion. Only with chronic respiratory alkalosis is there time for
renal compensation.
Na + (Cl HCO3 ). Presentation and Diagnosis Acute respiratory alkalosis may
appear similar to hypocalcemia with paresthesias, carpo-
Normal anion gap is approximately 12 3 mEq/L. With loss of pedal spasm, and Chvosteks sign. Potassium, magnesium
bicarbonate, the chloride increases and the anion gap remains and calcium, and phosphate metabolism are all disturbed in
normal. With the addition of metabolic acids, the chloride lev- alkalotic states. The acute hypocarbia can also cause cer-
els do not increase and bicarbonate levels fall, thus causing an ebral vasoconstriction and decreased cerebral blood flow
anion gap. (1% to 3% for each 1 mm drop in PaCO2). The decreased
Treatment Identifying the underlying disorder causing meta- cerebral blood flow can be particularly dangerous in patients
bolic acidosis and correcting it expeditiously are critical. with acute brain injury, or atherosclerotic disease of cerebral
Hypovolemia must be corrected, bleeding must be stopped, blood vessels.
sepsis must be controlled, and/or cardiac function must be Treatment In the spontaneously breathing patient, the treat-
improved to improve tissue perfusion in order to satisfy cel- ment is aimed, as in respiratory acidosis, to correct the under-
lular metabolic needs. Administration of bicarbonate without lying cause of the hyperventilation. In the patients who are
correcting the underlying problem will not return the pH to mechanically ventilated, a decrease alveolar ventilation by
normal. In extreme life-threatening situation, such as when changing respiratory rate or tidal volume will correct the alka-
the patient is on vasopressors to maintain blood pressure, or losis caused by mechanical hyperventilation. Chronic respira-
when severe cardiac disturbances are present, the pH is <7.25, tory alkalosis usually is asymptomatic and does not require
and the patient has fully compensated by hyperventilating, treatment.
bicarbonate may be administered to raise the pH sufficiently
to allow catecholamines to act at their receptors. Similarly,
Metabolic Alkalosis
with diabetic ketoacidosis, treatment of the pHa with bicarbo-
Metabolic alkalosis occurs when the pH is elevated in
nate is of little value without concomitant administration of
association with an elevated serum bicarbonate level. It is
insulin and intravenous fluids.
one of the most common acidbase abnormalities in surgical
The amount of bicarbonate that may be needed to correct
patients. Renal and gastrointestinal losses of potassium and
the total body base deficit can be calculated as:
chloride result in hypochloremic, hypokalemic metabolic
mEq HCO3 needed = mEq/L HCO3 deficit alkalosis. The infusion of excess bicarbonate can also cause
(patient weight in kilograms
o 0.25). metabolic alkalosis. Also, the administration of loop diuret-
ics may result in a contraction of extracellular volume and
Rules 1 and 2 may be used to calculate the HCO3 deficit. It is metabolic alkalosis. Hypoventilation may allow for the accu-
advisable to replace no more than one-half of the calculated mulation of CO2 and correction of the metabolic alkalosis.
bicarbonate deficit in the first 3 to 4 hours, continuing with the The kidneys response to metabolic alkalosis initially results
additional bicarbonate over the next 12 to 14 hours. Too rapid in alkaline urine as bicarbonate is excreted. With hypochlo-
or overzealous administration of intravenous bicarbonate may remic, hypokalemic metabolic alkalosis, the loss of elec-
lead to cardiac irregularities, convulsions (which may not be trolytes and the kidneys mechanism of saving potassium,
evident if the patient is sedated and on a ventilator), meta- absorbing bicarbonate instead of chloride and excreting
bolic alkalosis, hypokalemia, impairment of oxygen delivery hydrogen ion will result in paradoxical aciduria. As the kid-
to cells from capillaries and symptomatic hyperosmolarity as ney reabsorbs the bicarbonate ion, the compensatory mecha-
a result of the infusion of excessive amounts of sodium. It is nism fails. The correction requires replacement of chloride
imperative that the underlying cause of the acidosis be treated and potassium ions.
while replacing the bicarbonate. Presentation and Diagnosis The clinical problems associated
with metabolic alkalosis are manifestations of hypochlo-
Alkalosis remia, hypokalemic, and intravascular volume deficiency.
Regardless of the cause, a pH more than 7.45 indicates an This may be caused by gastrointestinal or renal losses and
alkalosis is present. Alkalosis has clinical features specific to result in paralytic ileus, cardiac dysrhythmias, and digitalis
the etiology, whether metabolic or respiratory. toxicity.
Treatment The treatment of metabolic alkalosis requires
Respiratory Alkalosis replacement of electrolytes (particularly chloride and potas-
Respiratory alkalosis is present when an increase in pHa is sium) and of fluids specific to the type of loss, as well as
related to alveolar hyperventilation and a reduced PaCO2. control of ongoing losses. Once the kidney has adequate
This is common in surgical patients and may be caused by intravascular volume, and the electrolytes are replaced, the
apprehension, pain that does not impede respiratory effort kidney will again excrete bicarbonate. Most metabolic alka-
(usually in the young because pain in the elderly often losis is chloride responsive and can be identified by measur-
reduces alveolar ventilation and therefore causes a respiratory ing urinary chloride. In chloride-responsive alkalosis such as

Lawrence_Chap02.indd 52 7/21/2012 5:58:30 PM


in uncorrected gastric losses, the urine chloride will be low,

TABLE 2-12 Mixed AcidBase Disorders
<10 mEq/L. The treatment is administration of chloride as
a balanced salt solution, for example normal saline (0.9%
Disorder pH PaCO2 HCO2
NaCl). Chloride-unresponsive hypochloremic metabolic alka-
losis is characterized by urinary chloride that is >20 mEq/L. Metabolic acidosis + respiratory acidosis
This does not usually respond to chloride administration and Metabolic acidosis + respiratory alkalosis 
may require glucocorticoid administration even when the elec-
Metabolic alkalosis + respiratory acidosis 
trolytes are corrected.
Metabolic alkalosis + respiratory alkalosis
Acidbase disorders rarely occur in pure form. There are
compensatory mechanisms that quickly work to maintain to create mixed disorders (Table 2-12). Understanding the
homeostasis. Compensatory mechanisms alone will not cor- causes of the different acidbase disorders will allow correc-
rect the disorder to normal. The combination of metabolic and tion of the defect. Remember the essential treatment is correc-
respiratory causes of acidosis and alkalosis often intermingle tion of the underlying disorder.

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Lawrence_Chap02.indd 53 7/21/2012 5:58:32 PM


Questions A. Na+110 mEq/L, Cl90 mEq/L, K+2.8 mEq/L, CO220
Choose the best answer for each question.
B. Na+150 mEq/L, Cl120mEq/L, K+5.5 mEq/L, CO220
1. A 35-year-old man is admitted for a sigmoid colectomy due to mEq/L
repeated episodes of acute diverticulitis. He weighs 140 kg, but his C. Na+140 mEq/L, Cl110 mEq/L, K+4.0 mEq/L, CO226
ideal body weight is 80 kg. Which of the following body composi- mEq/L
tions should be used as a basis for calculating basic maintenance D. Na+120 mEq/L, Cl120 mEq/L, K+5.5 mEq/L, CO218
fluids for this patient? mEq/L
E. Na+135 mEq/L, Cl105 mEq/L, K+3.5 mEq/L, CO224
Total Body Intracellular Extracellular Blood mEq/L
Water (L) Water (L) Water (L) Volume (L)
4. A 30-year-old man is in the intensive care unit where he is being
A. 84 55 28 9.8
treated for injuries sustained in a motor vehicle crash. He sustains
B. 70 55 15 8.4
C. 56 35 21 8.4
multiple orthopedic injuries and a severe head injury. On hospital
D. 54 32 22 5.4
day 4, vital signs are BP120/70 mm Hg, pulse76/minute, and
E. 60 40 20 7.5 respiratory rate on a ventilator of 12/minute. His urine output is
20 mL/hour. Serum sodium is 120 mEq/L, BUN is 18 mg/dL, and
creatinine is 1 mg/dL. What is the most likely diagnosis?
2. A 46-year-old man is in the intensive care unit following surgery for
A. Water intoxication due to inappropriate fluid infusion
multiple gunshot wounds to the chest and abdomen sustained 2
B. Central diabetes insipidus
days ago. He has bilateral chest tubes inserted for hemopneumo-
C. Lab error
thoraces. Damage control surgery including packing his liver and
performing an ileostomy was done at that time. His urine output D. SIADH
has decreased to 90 mL over the past 4 hours. His temperature is E. Increased aldosterone secretion due to hypovolemia
38C, blood pressure (BP) 110/85 mm Hg, and pulse 100/minute.
5. A 40-year-old woman is admitted with a 3-day history of diarrhea.
What is the most likely cause for the drop in urine output?
She has a history of chronic renal insufficiency due to diabetic
A. Congestive heart failure
nephropathy. She is mildly acidotic. Serum potassium is 6.8 mEq/L.
B. Hypovolemia
An ECG shows peaked T waves. Which of the following is the most
C. Acute renal failure
appropriate initial treatment of the hyperkalemia?
D. Diabetes insipidus
A. Subcutaneous administration of 10 units of insulin plus 25 g of
E. Sepsis glucose over 5 minutes
B. Administration of a bicarbonate infusion or by injecting 45 mEq
3. A 65-year-old man is seen in the emergency department with a 5-day sodium bicarbonate intravenously over 5 minutes
history of nausea and vomiting. He has been drinking only water for C. Intravenous administration of sodium polystyrene sulfonate, a
the last 2 days. His BP is 100/75 mm Hg with a heart rate of 105/ cation-exchange resin, to bind extracellular potassium
minute. He has a distended abdomen with no bowel sounds but no D. Transferring the patient to a center with hemodialysis and peri-
signs of peritonitis. A diagnosis of a bowel obstruction is made after toneal dialysis capability
x-rays of the abdomen reveal distended loops of small bowel. Which E. Rapid intravenous infusion of 50 mL of 10% calcium gluconate
of the following abnormalities would you expect to find in this patient? under continuous ECG monitoring

Lawrence_Chap02.indd 54 7/21/2012 5:58:32 PM


Answers and Explanations a narrow pulse pressure and increased heart rate consistent with a
1. Answver: D low stroke volume and perhaps reduced cardiac output. The latter
could be due to a combination of an absolute hypovolemia and/or a
The composition of the body varies with lean body mass (muscle) and
relative hypovolemia if he is developing an abdominal compartment
the fat content. If one assumes that ideal body weight is related
syndrome, which could also contribute to decreasing urine output. The
to the theoretical young healthy male discussed in most textbooks
patient is relatively young to have congestive heart failure. Acute renal
where total body water is 60% of weight and intracellular volume is
failure would be possible but is unusual only 2 days after surgery.
60% of total body water, then for 80 kg, the patient would have 48 L
Diabetes insipidus would result in increased urine output. Sepsis or an
of total body water, 32 L of intracellular water, and 16 L of extracellular
inflammatory response syndrome would result in an increase in heart
water. Since fat is only about 10% water, the extra 60 kg of fat only
rate and a wider pulse pressure due to the vasodilation that occurs
adds 6 L of water. Therefore in this patient, total body water would only
as a result of the release of various cytokines. In this patient, treat-
be 54 L. Intracellular water changes little and therefore the ICF would
ment would begin by performing a detailed physical exam followed by
be about 32 L and the ECF about 22 L. Vascular volume for the 80-kg
increased fluid infusion.
weight would only be a little more than 6% of weight (6.3 0.4%) or
about 5 L. The additional 6 L of fat would add little to the blood volume
3. Answer: A
so 5.4 L total blood volume would be a close approximation.
The clinical significance of these estimations relates to numerous In a patient with a bowel obstruction who begins vomiting, the initial
clinical scenarios. For example, if one estimates that there is a serum acidbase abnormality would be a hypochloremic, hypokalemic meta-
sodium deficit of 10 mEq/L in this patient but assumes total body bolic alkalosis due to the loss of hydrogen ion, chloride, and potassium
water is 60% of total weight, the patient would get 10 84 L of total from the stomach. The bowel will continue to secrete fluid into the small
body water or 840 mEq of sodium instead of 10 54 L of total body intestine, which will initially lead to hypovolemia that is compounded by
water or 540 mEq of sodium. The extra and unnecessary 300 mEq of the loss of gastric fluid. This results in an increase in aldosterone, which
sodium is equivalent to 2 L of normal saline. will result in increased reabsorption of sodium and chloride from the
If one calculates total body water requirements for daily maintenance kidney, but since the vomiting results in a loss of chloride, eventually
using the standard 70-kg male as a reference, then the 140-kg male a reduction in chloride in the renal tubule will result in absorption of
would receive 35 mL/kg (Table 2-2) or about 4.9 L of fluid. However, bicarbonate with the sodium. The resulting alkalosis may be associ-
using ideal body weight for the calculation and adding only about 10% ated with a mild respiratory acidosis to compensate for the metabolic
for the increased fat content, the total fluid would instead be about 3 L. If acidosis. As the fluid sequestration in the small intestine increases,
the extra 1.9 L is given over 3 or 4 days and if the kidneys do not excrete hypovolemia increases, which increases ADH and stimulates thirst. The
this fluid due to numerous conditions such as syndrome of inappropriate kidneys reabsorb more water and sodium and the patient tries to drink
antidiuretic hormone (SIADH), the patient in 3 days is up almost 6 L that but in this case only tolerates water. This results in an increase in water
may not be visible in this obese patient. This increased total body water in relation to sodium in the extracellular fluid (even though both are
could result in a host of effects including peripheral edema, pleural effu- reduced compared to the normal state) and a hyponatremia occurs.
sions, and cardiac and pulmonary dysfunction; lead to subtherapeutic Now the patient has a hyponatremic, hypokalemic, hypochloremic met-
drug levels (since many drugs such as antibiotics have volumes of distri- abolic acidosis, which is compensated partly by a respiratory acidosis.
butions equivalent to extracellular or total body water); cause secondary As the hypovolemia progresses due to the sequestration of fluid in the
complications from each of these effects and overall delay in discharge intestine and perhaps into the peritoneal cavity, the patient may develop
from hospital; and increase costs. In other words, a more accurate a stage 2 shock state that results in a mild cellular acidosis, which
guesstimate using a similar thought process for patients decreases eventually causes a metabolic acidemia superimposed on the meta-
complications, reduces hospital stay, and reduces costs. bolic alkalemia. Hence, the final presenting electrolyte and acidbase
abnormality seen on the electrolytes in this patient is a hyponatremic,
2. Answer: B hypokalemic, hypochloremic metabolic acidemia. The first priority in the
The most common cause for a drop in urine output after surgery is treatment of this condition is to correct the hypovolemia, in this case
hypovolemia. This can be caused by inadequate fluid replacement to with normal saline since there is also a chloride deficit, and add potas-
correct the sequestration of fluid into the site(s) of injury, continuing sium to the fluids since the patient has a profound potassium deficit
blood loss, and stimulation of various endocrine responses including that may be slightly masked by a lower than normal pH. (See relation
an increase in aldosterone, which results in renal sodium retention and between acidosis and potassium in text.) Since the patient is stable
an increase in antidiuretic hormone (ADH), which result in reduced free without signs of peritonitis, there is time to correct the fluid and elec-
water clearance in the kidney. Atrial natriuretic factor may be inhibited trolyte disorders before taking the patient to surgery. Failure to cor-
due to the reduction in atrial volume and distention. The patient has rect before surgery could result in multiple complications including a

Lawrence_Chap02.indd 55 7/21/2012 5:58:33 PM


more profound hypotension and arrhythmias due to the low potassium. 5. Answer: A
In general, correction of vascular volume takes precedence followed Hyperkalemia <6 mEq/L or hyperkalemia without ECG abnormalities
by correction of acidbase and potassium abnormalities and finally usually needs minimal intervention other than stopping any potas-
correction of any other fluid and electrolyte problems. sium infusion, deciding if this increase in potassium is due to a sig-
nificant metabolic acidosis (since the potassium will increase at least
4. Answer: D 0.3 mEq/L for every 0.1 decrease in pH), checking to make sure the
Although water intoxication due to inappropriate fluids is possible, increased potassium was due to hemolysis of the blood sample, and
in this patient it is unlikely since he has normal renal function as monitoring the cardiac rhythm. If the patient has ECG evidence of
reflected by his BUN and creatinine. If he were given inappropriate peaked T waves, then prompt administration of 25 g of glucose plus
fluids, he would diurese the extra fluid. Central diabetes insipidus 10 units of insulin is recommended followed by hemodialysis if neces-
usually results in a marked increase in urine (free water) output and sary. If the T waves are higher than the R wave or if there is widening of
would result in an increase in sodium concentration. Laboratory error the QRS complex and a decrease in the P-wave amplitude, immediate
is always possible, and if there is any question of this possibility, the treatment is indicated with either infusion of 10 mL of 10% calcium
electrolytes should be rechecked prior to initiating therapy. Increased chloride over 10 minutes or 10 mL of calcium gluconate over 3 to 5
aldosterone secretion would result in sodium retention and therefore minutes. Calcium chloride freely dissociates upon infusion resulting in
would maintain serum sodium concentration. The most likely scenario 13 mEq of free calcium, whereas calcium carbonate results in only 4
is an increase in ADH, in this case due to the increase in intracranial mEq of free calcium. The remainder of the calcium is released as the
pressure due to the head injury. Since the patient has a wide pulse carbonate is metabolized. Intravenous infusion of 50 mEq or more of
pressure and normal output, he is at least euvolemic. Therefore, an sodium bicarbonate over 20 minutes may also be used. The amount
increase in ADH is inappropriate for the situation. If, however, the of bicarbonate infused is proportional to the degree of acidosis but is
patient had signs of decreased vascular volume including a narrow usually not used unless the pH is <7.20. Rapid increase in potassium
pulse pressure and increased heart rate, then the increased ADH such as occurs with sudden renal failure or rhabdomyolysis may be
secretion would be appropriate. lethal if not diagnosed and treated quickly.

Lawrence_Chap02.indd 56 7/21/2012 5:58:33 PM


1. Determine a patients protein and calorie requirements by 6. Discuss the effect of starvation, injury, and infection on a
estimation, with the Mifflin-St. Jeor equation, the Penn State patients metabolism, and describe how nutritional support
equation, and the Hamwi method, or with specific labora- must be altered.
tory tests. 7. List several indications each for enteral and parenteral
2. List at least four factors in a patients medical history and nutritional support.
physical examination that indicate malnutrition or risk for 8. Discuss the factors involved in choosing a route of nutritional
malnutrition. support.
3. Discuss the following objective assessments of nutritional 9. Describe the risks and benefits of enteral and parenteral
status: anthropometric measurements, biochemical blood nutritional support.
tests, immune function studies, and indirect calorimetry.
10. List at least four gastrointestinal, four mechanical, and four
4. List at least four water-soluble vitamins, three fat-soluble metabolic complications of enteral therapy, and describe
vitamins, and four trace elements that must be added to appropriate prevention or treatment of each.
long-term parenteral nutrition.
11. List four adverse sequelae of a total parenteral nutrition
5. Briefly describe the metabolic changes that occur in short- (TPN) catheter and four metabolic complications of TPN.
term and long-term starvation. Describe the appropriate treatment of each.

Surgeons care for patients who may have a compromised OVERVIEW OF METABOLISM
nutritional status and therefore an altered ability to heal
properly. The nutritional challenges for patients with surgi- Normal physiology relies on three essential substrates: carbo-
cal disease include anorexia, inanition, accelerated glucone- hydrates, proteins, and lipids, which provide both an energy
ogenesis, hyperglycemia, insulin resistance, and electrolyte source and the substrates for chemical building blocks.
and hormonal disturbances. Each of these can adversely Ideally, energy needs should be based on direct meas-
affect both response to surgery or injury and a patients abil- urement by calorimetry; however, this is labor intense and
ity to heal. The metabolic responses to stress, starvation, and impractical in most critically ill patients. Indirect calorimetry
sepsis include complex neuroendocrine and immunomodu- is the measurement of respiratory gas exchange in order to
latory responses that vary tremendously with the inciting make inference about cellular gas exchange, which equates
event. In the ideal situation, the bodys homeostatic response to metabolic rate and substrate utilization. The measured
would result in a coordinated effort to mobilize sufficient parameters of indirect calorimetry are oxygen consumption
nutrient substrates to maintain energy requirements, fight (VO2) and carbon dioxide production (VCO2). From these
infection, and provide for essential bodily functions. In measurements, respiratory quotient (RQ) and metabolic rate
reality, these metabolic alterations often can act at odds to can be calculated. Indirect calorimetry is valid only when
each other and result in a situation that places the patient the respiratory gas exchange and the cellular gas exchange
at increased risk of nutritional failure. This chapter reviews are equivalent. There are several limitations to using indirect
metabolism and the impact of stress on nutritional status and calorimetry; therefore, predictive equations are often used to
describes methods to identify patients at nutritional risk in estimate resting metabolic rate (RMR). With more than 200
order to direct nutritional therapy to achieve the best pos- predictive equations available, very few have been validated
sible outcomes. against indirect calorimetry.


Lawrence_Chap03.indd 57 7/21/2012 5:59:00 PM


TABLE 3-1 Validated Predictive Equations for TABLE 3-2 Hamwi Method for IBW
Estimating Energy Requirements
1. IBW in Pounds and Inches
Acutely Ill Patients and Obese PatientsNonventilated Men: 106 lb for the first 5 ft
Mifflin-St. Jeor Equation Plus 6 lb for every inch thereafter
Men: RMR = 5 + 10W + 6.25H 5A Women: 100 lb for the first 5 ft
Women: RMR = 161 + 10W + 6.25H 5A Plus 5 lb for every inch thereafter
Obese Patients (BMI > 30 kg/m2) 2. IBW in Kilograms and Meters
60%70% of target energy requirements (as predicted by above equations) Men: 48.1 kg for each 1.52 m
1114 kcal/kg/day actual body weight Plus 0.9 kg for every centimeter above 1.52 m
2225 kcal/kg/day ideal body weight Women: 45.5 kg for each 1.52 m
RMR = Resting metabolic rate in kilocalories/day Plus 1.1 kg for every centimeter above 1.52 m
W = weight in kilograms 10% can be added for a large body frame size or subtracted for a small body
H = height in centimeters frame size.
A = age in years 3. Body Mass Index (BMI)a
Critically Ill Ventilated Patients Weight (kg) height (m2)
Penn State Equation BMI BMI Classification Disease Risk
RMR via Penn State Equation (PSU)
<16 Proteinenergy malnutritiongrade III Very high
RMR (kcal/d) = MSJ (0.96) + Tmax (167) + VE (31) 6,212
1616.9 Proteinenergy malnutritiongrade II High
Modified PSU[m] Equation for BMI 30 kg/m2 and 60 yrs
1718.4 Proteinenergy malnutritiongrade I Moderate
RMR (kcal/d) = MSJ (0.71) + Tmax (85) + VE (64) 3,085
18.524.9 Normal Very low
BMR = basal metabolic rate calculated using the Mifflin-St. Jeor Equation
(using actual body weight) 2529.9 Overweight Low

VE = minute ventilation (L/min) 3034.9 Obesitygrade I Moderate

Tmax = maximum daily body temperature in previous 24 hr (C). 3539.9 Obesitygrade II High
40 Obesitygrade III Very high
Body Mass Index Classification and Interpretation

It is known that various conditions can increase metabolic

rate from 10% to 100% above basal metabolic rate (BMR)
(e.g., trauma, burns, pregnancy, lactation). However, predic- Complex carbohydrates form important components of cell
tive equations that add an activity and/or injury factor above wall glycoproteins and glycolipids, as well as the carbon
the RMR are not validated. The best-validated equations are backbone of lipid and nonessential amino acids. In addition,
listed in Table 3-1, correlating within 78% accuracy with met- the brain as well as red and white blood cells, are to a large
abolic rate measured by indirect calorimetry. Table 3-1 lists extent, obligate glucose tissues. Approximately 120 g/day
validated predictive equations for various types of patients. is necessary to maintain central nervous system (CNS) func-
RMR is more difficult to predict in the obese than in the tion. Glycogen stores are limited (180 g in a 70-kg person)
nonobese person as lean body mass and body cell mass are and are usually exhausted within 24 hours in the unfed state.
very difficult to measure clinically. Obesity adversely affects In the nonstressed state, the brain utilizes ketone bodies with
patient care, particularly in the critically ill, and increases the progressive starvation. The maximal glucose oxidation rate is
risk of comorbidities such as insulin resistance, sepsis, infec- 4 to 7 mg/kg/minute, roughly equivalent to 400 to 700 g/day
tions, deep venous thrombosis, and organ failure. Achieving in a 70-kg person. In the hypermetabolic patient, a large por-
some degree of weight loss may increase insulin sensitiv- tion of oxidized glucose is derived from amino acid substrates
ity, improve nursing care, and reduce risk of comorbidities. via gluconeogenesis yielding up to 2 to 3 mg/kg/minute of
Therefore, providing 60% to 70% of energy requirements in glucose. Exogenous insulin delivery can increase cellular glu-
this population promotes steady weight loss, while supple- cose uptake in critically ill patients; however, it is relatively
menting protein at a dose of 2.0 to 2.5 g/kg ideal body weight ineffective in improving glucose oxidation. In order to limit
per day should approximate protein requirements and neu- the diabetogenic response, glucose should comprise approxi-
tral nitrogen balance, allowing for adequate wound healing. mately 50% to 60% of total energy requirements, delivered at
Depending on the clinical condition, energy requirements for 3 to 4 mg/kg/minute. Supplemental insulin can then be used to
surgery patients range from 20 to 35 kcal/kg of ideal body maintain normoglycemia.
weight per day. Ideal body weight (IBW) can be calculated
using several formulas one of which is the Hamwi method, Protein Requirements
listed in Table 3-2.
Proteins provide 4.0 kcal/g and account for 20% to 30% of the
total daily caloric intake. Proteins and amino acids are essen-
Carbohydrate Requirements tial components of all living cells and are involved in virtu-
Carbohydrates largely in the form of glucose supply 3.4 kcal ally all bodily functions. All protein in the body is functional.
of energy/g. Glycogen is the principal storage form of glucose. In the nonstressed state, approximately 2.5% of total body

Lawrence_Chap03.indd 58 7/21/2012 5:59:01 PM


TABLE 3-3 Select Serum Proteins: Classification and Functions

Serum Protein Function Half-life Normal Range Interpreting Results


C-Reactive protein General marker of inflammation and 5 hr 0.28 mg/dL Synthesized by liver
infection Rises during inflammation and infection
Decreases when infection or inflammation resolves
Albumin Maintains plasma oncotic pressure, 21 days 3.55.0 mg/dL Routinely available
carrier for amino acids, zinc, Synthesized in liver; altered by liver disease
magnesium, calcium, free fatty Alterations occur in kidney disease with glomerular damage
acids, drugs Elevated in dehydration
Levels fall with protein-losing enteropathy; may be low in chronic,
long-term unstressed malnutrition
Negative acute-phase reactant, levels drop in inflammation, shock
Prealbumin Thyroxine transport, formation of 23 days 1838 mg/dL Synthesized in the liver
(transthyretin) complex with RBP Highly sensitive to dietary deprivation and refeeding
Elevated in renal dysfunction
Negative acute-phase reactant
Transferrin Iron-binding protein 8 days 202336 mg/dL Decreased levels when diet deficient in protein
Synthesized in liver; altered by liver disease
Elevated in iron deficiency; pregnancy; chronic blood loss
Low levels in chronic diseases, cirrhosis, nephritic syndrome, protein-losing
Negative acute-phase reactant
Retinol-binding Transports vitamin A; bound to 12 hr 26 mg/dL Highly sensitive to acute changes in protein malnutrition and dietary intake
protein prealbumin Elevated in renal failure
Decreased in vitamin A deficiency
Negative acute-phase reactant

protein is broken down and resynthesized every 24 hours. synthase, producing nitric oxide and citrulline. Nitric oxide is a
More than half of this turnover is accounted for by the daily ubiquitous molecule with significant roles in the maintenance
digestive process, hemoglobin turnover, muscle protein syn- of vascular tone, coagulation cascade, immunity, and GI tract
thesis, and maintenance of normal immune function. During function. While positive effects on wound healing are noted
metabolic stress, proteins are broken down into amino acids with arginine supplementation, arginine is controversial and not
and enter into the gluconeogenic pathway and used as a fuel recommended in severe sepsis, as it is believed to contribute to
source or form the basic structural elements of living cells. It hemodynamic instability via its conversion to nitric oxide.
is important to realize there is no protein storage per se and Pediatric amino acid solutions have altered amino acid
that any protein utilized for gluconeogenesis and acute-phase profiles from the adult solutions. This is because infants have
protein synthesis should be considered a loss of functional a number of immature enzymatic metabolic pathways, ren-
protein. Table 3-3 includes individual serum proteins, their dering certain amino acids considered nonessential for adults
half-life, normal range and function. essential in infants.
The amino acids glutamine and arginine deserve special
attention. Glutamine is the most abundant amino acid. It
comprises more than 50% of the free amino acid pool and Lipid Requirements
is synthesized in most tissues of the body. Glutamine is the Adipose tissue in the average 70-kg man contains approxi-
primary fuel source for the small intestine enterocytes. During mately 140,000 kcal and serves as the primary energy stor-
catabolic illness, glutamine uptake by the small intestine and age source for the body. Lipids are calorie dense, supplying
immunologically active cells can exceed glutamine synthesis on average 9.0 kcal/g and generally should account for 10%
and release from skeletal muscle, making glutamine a condi- to 30% of the total daily caloric load with a minimum of
tionally essential amino acid. Glutamine is a major contribu- 2% to 4% as essential fatty acids to prevent deficiency. Essen-
tor to homeostasis in the surgical population. tial fatty acids are required for the production of sterol-based
Arginine, like glutamine, is classified as a nonessential hormones including cortisol, gluconeogenic hormones, and
amino acid in unstressed conditions because the body syn- growth hormone, which are important in wound healing and
thesizes adequate arginine for normal maintenance of tissue the response to surgical stress. Lipids are the main component
metabolism, growth, and repair. Growth hormone, glucagon, in cellular and subcellular membranes. Linoleic and linolenic
prolactin, and insulin release are all increased with supple- acids are essential fatty acids that serve as precursors for pros-
mental arginine. Arginine is also the substrate for nitric oxide taglandin synthesis and are essential for cell signaling.

Lawrence_Chap03.indd 59 7/21/2012 5:59:01 PM


If patients are being supported with parenteral nutrition

TABLE 3-4 General Daily Parenteral Electrolyte
(PN), they should be monitored for tolerance of lipid deliv- and Mineral Recommendations
ery because long-chain triglyceride solutions may diminish
immune function, and cause hypertriglyceridemia. Complica-
Adults Infants and Children
tions may be minimized by infusing lipids continuously over
18 to 24 hours and at a rate not to exceed 0.1 g/kg/hour. Most Sodium 50250 mEq 24 mEq/kg
patients tolerate infusions of lipids when provided as an inter- Potassium 30200 mEq 23 mEq/kg
mittent or continuous infusion. Intravenous lipids in the US Chloride 50250 mEq 23 mEq/kg
are omega-6 fatty acids, considered to be immunosuppressive. Phosphate 1040 mmol 0.52 mmol/kg
It is acceptable not to give lipids during the first week of PN.
Once initiated, they can be given three times weekly to daily, Calcium 1020 mEq 13 mEq/kg
depending on the nutritional needs of the patient. They may be Magnesium 1030 mEq 0.250.5 mEq/kg
combined with the other PN nutrients in solution as part of a
total nutrient admixture (TNA) or given as a separate infusion.
There is a renewed interested in providing omega-3 fatty
acid containing nutrition therapy to patients, as they are con- cells. Iron is essential to produce hemoglobin and myoglobin,
sidered anti-inflammatory. Omega-3 fatty acids have been which is necessary for muscle iron storage, and cytochromes,
shown to be beneficial in critically ill patients as well as which are necessary for the oxidative production of cellular
patients with chronic inflammatory processes. The omega-3 energy. Vitamin K is essential for blood-clotting mechanism.
fatty acids eicosapentaenoic acid (EPA) and docosahexaenoic Trace element deficiencies of zinc, copper, manganese, and
acid (DHA) displace omega-6 fatty acids from the cell mem- selenium can lead to impaired wound healing, glucose metab-
branes of immune cells, thus reducing systemic inflammation olism, and protein sulfination. Surgical patients who require
through the production of alternative biologically less inflam- steroid medications and who have healing wounds should
matory prostaglandins (prostaglandin E3) and leukotrienes of receive supplemental Vitamin A to aid in collagen cross-
the 5-series. EPA and DHA (fish oils) have also been shown to linking. Recommended daily vitamin and trace element sup-
decrease neutrophil attachment and transepithelial migration plementation is shown in Table 3-4.
to modulate systemic and local inflammation, and they also
help to stabilize the myocardium and lower the incidence of Other Additives
cardiac arrhythmias. Additionally, they decrease the incidence For patients receiving PN, medications that are most frequently
of acute respiratory distress syndrome (ARDS), and reduce added include additional trace elements, histamine-2 receptor
the likelihood of sepsis. blockers, vitamin K, and regular insulin, although the latter is
not recommended unless glucose levels have stabilized.

Other Requirements Impact of Starvation and Stress

Fluid and Electrolytes During the first 24 to 72 hours of nonstressed starvation, basal
Surgical patients often receive large volumes of fluid periop- energy requirements are decreased and are supplied by liver
eratively. Typically, surgical patients are provided with intra- and muscle glycogen stores. With persistent starvation and
venous fluids until oral intake is resumed and tolerated to glycogen depletion, deamination of gluconeogenic amino
maintain fluid balance. The goals of fluid management include acids, such as alanine and glutamine, accounts for an increas-
maintenance of adequate hydration, tissue perfusion, and ingly greater percent of the total glucose production to meet
electrolyte balance. Insensible losses, measured losses (e.g., the preferential needs for glucose by the brain, CNS, and red
stool, urine, drainage, hemorrhage, open wounds), and altera- blood cells. Body proteins cannot serve as a long-term source
tions in fluid balance due to metabolic changes (e.g., fever, of fuel because of their structural and functional importance.
hyperthyroidism) or medical therapy (diuretics) must be care- Protein depletion in excess of 20% is not compatible with life.
fully considered When ordering nutritional replacement, one Fat mobilization with persistent starvation, likely resulting
must consider how to deliver maintenance, resuscitation, and from decreased insulin levels, inhibits lipase and allows for
replacement fluids and electrolytes. This can be done either intracellular hydrolysis of triglycerides. The liver only par-
separately from the nutritional requirements or combined with tially oxidizes most of the fatty acids it receives, so serum lev-
it. In the critically ill patient where fluid requirements can els of acetacetate, -hydroxybutyrate, and acetone increase.
fluctuate, it is recommended to provide the nutrition regimen These ketone bodies, released by the liver, can be oxidized
separately from the fluid requirements and then maximally to CO2 and H2O by tissues such as the kidney and muscles.
concentrate the nutrition regimen. Once the patient becomes The brain also converts to using ketoacids as an energy source
stable, the fluid, electrolyte, and nutrient requirements can be due to persistently low glucose levels. Utilization of ketone
combined. Typical adult maintenance electrolyte needs are bodies as an energy source decreases hepatic gluconeogen-
shown in Table 3-4. Careful monitoring of losses and serum esis and spares muscle protein. Although the brain and CNS
concentrations should be used to guide adjustments to sup- can convert to utilizing ketoacids for fuel during nonstressed
plemental replacement. starvation, these by-products of incomplete fatty acid metabo-
lism eventually become toxic. During unstressed starvation,
Vitamins and Minerals there is a general decrease in energy expenditure and a change
Vitamins and minerals are important for optimal postoperative in the insulinglucagon ratio to favor mobilization of stored
recovery. Vitamin C is an antioxidant, required for the synthe- fuels and minimize loss of lean body tissue.
sis of collagen, carnitine, and neurotransmitters and for the The metabolic response to injury or infection can classi-
immune-mediated and antibacterial functions of white blood cally be divided into the ebb and flow phase. The ebb phase

Lawrence_Chap03.indd 60 7/21/2012 5:59:01 PM


begins immediately after injury and typically lasts between however, they have not been validated to accurately assess
12 and 24 hours, but may last longer depending on the sever- acute nutritional risk.
ity of injury and adequacy of resuscitation. The ebb phase is An accurate height and body-weight measurement should
characterized by tissue hypoperfusion and a decrease in over- be obtained for all surgical patients to be used in calculating
all metabolism. Catecholamines are released to compensate BMI and IBW (Table 3-2). A nutrition-focused history can
for this, with norepinephrine being the primary mediator. reveal signs and symptoms of nutrient and vitamin deficien-
Released from peripheral nerves, norepinephrine binds to 1 cies or toxicities (Table 3-5). Many medications have nutri-
receptors in the heart and to alpha and 2 receptors in periph- tionally related side effects or increase nutrient requirements.
eral and splanchnic vascular beds. This results in increased Recent unexplained lean body mass weight loss of 10% over
cardiac contractility and heart rate and vasoconstriction in 2 to 6 months or 5% in 1 month and a BMI > 30 or <18 are
attempt to restore blood pressure, increase cardiac perfor- associated with increased postoperative complications. Albu-
mance and maximize venous return. min and total protein levels reflect long-term nutritional status
The flow phase encompasses the catabolic and anabolic and can be used as a simple marker for preoperative nutri-
phases. It is signaled by high cardiac output with restoration of tional status in nonhypermetabolic general surgical patients.
oxygen delivery and metabolic substrate. Although the dura- However, these levels can be affected by fluid shifts and in
tion of the flow phase depends on the severity of injury and these cases serum transferrin or prealbumin levels may be
illness, it typically peaks at 3 to 5 days and subsides by 7 to evaluated along with acute-phase proteins (e.g., C-reactive
10 days, merging with the anabolic phase over the next few protein [CRP]) to assist in delineation of an inflammatory
weeks. During this hypermetabolic phase, although insulin process versus poor nutritional status.
levels are elevated, high levels of catecholamines, glucagon, Every surgical procedure carries some risk of postoperative
and cortisol counteract most of its metabolic effects. This hor- complications. This risk correlates linearly with the magni-
monal imbalance results in mobilization of amino acids and tude and complexity of individual procedures. There is a linear
free fatty acids from peripheral muscles and adipose tissue. increase in complications in patients undergoing elective GI
Some of these released substrates are used for energy produc- surgery as preoperative albumin decreases from normal to levels
tion, either directly as glucose or through the liver as triglyc- below 2.0 g/dL/dL. Patients undergoing esophagectomy appear
eride. Other substrates contribute to the synthesis of proteins at risk if albumin drops below 3.75 g/dL/dL. Complications
in the liver, where humoral mediators increase production of increase in patients undergoing gastrectomy or pancreatic sur-
acute-phase reactants, and in the immune system for healing gery when preoperative albumin levels drop below 3.25 g/dL/
damaged tissues. The net result however is a significant loss dL. Patients undergoing elective colectomy have little increase
of protein, characterized by negative nitrogen balance and risk unless preoperative albumin levels drop below 2.5 g/dL.
decreased adipose stores, accompanied by enlarged extracel-
lular water compartments.
Hyperglycemia is a common occurrence during hypermet- OPTIONS FOR NUTRITIONAL THERAPY
abolic stress and results from the accelerated gluconeogenesis
and relative insulin resistance. This can become quite exagger- Patients unable to self-consume adequate nutrients orally (at
ated in patients with or without underlying diabetes. Glucose least 60% of nutritional needs), require adjunctive nutritional
control (e.g., blood glucose 80 to 150 mg/dL) is important in therapy in the form of either enteral nutrition (EN) or PN.
surgical patients to limit infectious complications, other mor-
bidities, and mortality. Enteral Nutrition
EN supplies either whole or partially digested nutrients to the
GI tract via a tube or via routine oral feeding. Table 3-6 lists
ASSESSMENT OF NUTRITIONAL STATUS the type of commonly used feeding tube access techniques
Patients with poor preoperative nutritional status are more for short-term and long-term enteral nutritional support. Criti-
likely to have increased morbidity and mortality postopera- cally ill patients best tolerate continuous infusion, with bolus
tively. It has been estimated that approximately 30% to 50% or intermittent infusion being reserved for stable patients
of hospitalized patients are malnourished. Since addressing requiring long-term enteral feeding.
malnutrition may result in improved outcomes, nutritional The GI tract not only functions to digest and absorb
assessment and intervention are necessary components of nutrients, fluid and electrolytes, but also is the bodys larg-
patient evaluation. est immunologic organ serving as a protective barrier against
intraluminal toxins and bacteria. Approximately 70% of the
Nutrition Risk Screening and Impact on bodys immunoglobulin-producing cells line the GI tract
with 80% of the bodys synthesized immunoglobulin being
Surgical Complications secreted here.
An appropriate history and physical examination remains a During severe physiologic stress, relative or absolute gut
primary nutritional assessment tool. Criteria to consider when ischemia can occur, leading to mucosal compromise and dis-
screening surgical patients for nutrition risk include magni- ruption of the guts barrier function and ultimate passage of
tude of the proposed surgical procedure, medications, body bacteria and toxins into the bloodstream or mesenteric lym-
mass index (BMI), recent weight changes, cachexia, changes phoid system. Animal studies reveal that enteral rather than
in diet or appetite, and serum visceral protein levels (e.g., PN maintains gut mucosal integrity and immune responsive-
albumin in the outpatient setting, prealbumin in the acute ness and prevents this gut-derived bacterial translocation.
care setting). Anthropometric measurements including vari- Enteral feeding remains the preferred route when the gut is
ous measures of muscle mass and circumference, and body functional. Studies suggest that providing at least 50% to
composition have been used to evaluate nutritional status; 65% of goal calories may be required to prevent increases in

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TABLE 3-5 Nutrient Deficiencies Revealed by Physical Examination

Suspected Nutrient Deficiency Physical Findings

Protein, calories Loss of weight, muscle mass, or fat stores; growth retardation; poor wound healing; infections
Protein, thiamin Edema (ankles and feet; rule out sodium and water retention, pregnancy, protein-losing enteropathy)
Obesity Excessive adipose tissue
Iron Anemia, fatigue
Protein, vitamin C, zinc Poor wound healing, pressure ulcers; cellophane appearance
Protein, thiamin Body edema; round swollen face (moon face)
Essential fatty acids, vitamin A, Xerosis (rule out environmental cause, lack of hygiene, aging, uremia, hypothyroidism), follicular hyperkeratosis, mosaic
pyridoxine dermatitis (plaques of skin in center, peeling at periphery on shins)
Vitamin C Slow wound healing, petechiae (especially perifollicular)
Niacin Pigmentation; desquamation of sun exposed areas
Zinc Delayed wound healing, acneiform rash, skin lesions, hair loss
Vitamin K or vitamin C Excessive bleeding, petechiae, ecchymoses; small red, purple, or black hemorrhagic spots
Iron Pallor; fatigue
Dehydration (fluid) Poor skin turgor
Excess beta carotene Yellow pigmentation of palms of hands with normal white sclera
Iron, folate, or vitamin B12 Pale conjunctivae (anemia)
Vitamin A Bitot spots, conjunctival xerosis, corneal xerosis, keratomalacia
Riboflavin, pyridoxine, niacin Redness, fissuring in corners of eyes
Thiamin, phosphorus Ophthalmoplegia
Hyperlipidemia Corneal arcus, xanthelasma
Protein Hair lacks shine, luster; flag sign; easily plucked with no pain
Vitamin C, copper Corkscrew hair; unemerged, coiled hairs
Protein, biotin, zinc Sparse
Riboflavin, niacin, pyridoxine Seborrhea on nasolabial area, nose bridge, eyebrows, and back of ears (rule out poor hygiene)
Iron Koilonychia (considered normal if seen on toenails only)
Protein Dull, lusterless with transverse ridging across nail plate
Vitamins A and C Pale, poor blanching, irregular, mottled
Protein, calories Bruising, bleeding
Vitamin C Splinter hemorrhages
Lips and Mouth
Niacin, riboflavin, pyridoxine Cheilosis, angular scars
Riboflavin, pyridoxine, niacin, iron Angular stomatitis
Riboflavin, niacin, folate, iron Atrophic filiform papillae
Vitamin B12 Glossitis
Zinc Taste atrophy
Riboflavin Magenta tongue
Excess sugar, vitamin C Edentia, caries
Fluorosis Mottled tooth enamel
Vitamin C Swollen, bleeding gums; receding

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TABLE 3-5 Nutrient Deficiencies Revealed by Physical Examination (Continued)

Suspected Nutrient Deficiency Physical Findings

Iodine Enlarged thyroid gland
Protein, bulimia Enlarged parotid glands (bilateral)
Excess fluid Venous distention, pulsations
Protein, calories Decreased muscle mass and strength, shortness of breath, fatigue, decreased pulmonary function
Cardiac system
Thiamine Heart failure
Gastrointestinal system
Protein, calories, zinc, vitamin C Poor wound healing
Protein Hepatomegaly
Urinary tract
Dehydration Dark, concentrated urine
Overhydration Light colored, diluted urine
Musculoskeletal system
Vitamin D, calcium Rickets, osteomalacia
Vitamin D Persistently open anterior fontanel (after age 18 months), craiotabes (softening of skull across back and sides before age 1 yr);
epiphyseal enlargement (painless) at wrist, knees, and ankles; pigeon chest and Harrison sulcus (horizontal depression on
lower chest border)
Protein Emaciation, muscle wasting, swelling, pain, pale hair patches
Vitamin C Swollen, painful joints
Thiamine Pain in thighs, calves
Nervous system
Protein Psychomotor changes (listless, apathetic), mental confusion
Vitamin B12, thiamine, vitamin B6 Weakness, confusion, depressed reflexes, paresthesias, sensory loss, calf tenderness
Niacin, vitamin B12 Dementia
Calcium, vitamin D, magnesium Tetany

intestinal permeability in burn and bone-marrow transplant Current nutrition guidelines recommend that EN should be
patients, to promote faster return of cognitive function in head started early, within the first 24 to 48 hours of ICU and hospi-
injury patients, and to improve outcome from immune-modu- tal admission. There is a window of opportunity that exists
lating enteral formulations in critically ill patients. in the first 24 to 72 hours following admission or the onset
of a hypermetabolic insult. Feedings started within this time
frame are associated with less gut permeability and dimin-
TABLE 3-6 Methods for Gaining Enteral ished activation and release of inflammatory cytokines. The
Feeding Access impact of early EN on patient outcome appears to be a dose-
dependent effect. Low rate feeding, often termed trickle or
Short-Term Access (<4 weeks) Long-Term Access (>4 weeks) trophic feeds (10 to 30 mL/hour), may be sufficient to pre-
Naso/oroenteric access Percutaneous feeding tube vent mucosal atrophy, but may be insufficient to achieve the
Spontaneous passage Percutaneous endoscopic
usual endpoints desired from EN therapy. If EN is unable to
gastrostomy (PEG)
meet 100% of energy requirements after 7 to 10 days, then
initiation of PN should be considered as to prevent excessive
Active passage Gastric/jejunal (PEG/J)
energy and protein deficits.
Bedside, assisted Direct jejunal (DPEJ) There are over 100 enteral formulations currently com-
Endoscopic Laparoscopic mercially available for a wide variety of clinical conditions,
Fluoroscopic Gastrostomy and they are constantly being reformulated. Enteral formula-
tions are classified as medical foods by the Food and Drug
Operative (passed in operating room) Jejunostomy
Administration and therefore do not undergo this regula-
Surgical tory control. Enteral formulas can be classified as standard,
Gastrostomy elemental, or specialized. Table 3-7 provides an overview of
Jejunostomy various categories of enteral formulas and specifies the types
of macronutrients and physical properties. The appropriate

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Lawrence_Chap03.indd 64
TABLE 3-7 Overview of Select Enteral Formulations

Formula Calories From Carbohydrate Calories From Calories Caloric Density mL for % Free Osmolality
Category Protein Sources Protein (%) Sources Carbohydrates (%) Fat Sources From Fat (%) (Calories/mL) 100% RDI Water (mOsmol/kg)
Oral supplements Sodium and calcium 1424 Corn syrup, sugar, sucrose, 4764 Corn oil, canola oil, soy oil, 2139 1.02.0 9462,000 7385 480870
caseinates, soy protein maltodextrin sunflower oil, safflower oil
Standard tube Sodium and calcium 1318 Corn syrup, maltodextrin 4557 Soy oil, corn oil, canola oil, MCT, 2939 1.02.0 8301,890 7785 270500
feedings caseinates, soy protein Fiber: soy fiber, guar gum, safflower oil
isolates oat fiber, FOS
High protein tube Sodium and calcium 2225 Hydrolyzed cornstarch, 3852 Canola oil, MCT, soybean oil, 2340 1.01.5 1,0002,000 7885 300490
feedings caseinates maltodextrin, sucrose, safflower oil
fructose, oat fiber, soy
fiber, guar gum
Elemental, Free amino acids, soy 1225 Hydrolyzed cornstarch, 3682 Soybean oil, safflower oil, 339 1.01.5 1,1502,000 7686 270650

semi- hydrolysates, hydro- maltodextrin, sucrose, canola oil, MCT, sunflower oil
elemental lyzed whey, hydrolyzed modified cornstarch
casein, hydrolyzed soy
Pulmonary Sodium and calcium 1720 Hydrolyzed cornstarch, 2740 Canola oil, soybean oil, MCT, 4055 1.5 9331,420 7679 330650
caseinates corn syrup, sucrose, corn oil, safflower oil, sardine
maltodextrin, sugar oil, borage oil
Renal Sodium and calcium 715 Corn syrup, sucrose, fruc- 4058 Corn oil, safflower oil, canola 3545 1.82.0 9471,000 7071 570700
caseinates tose, maltodextrin, sugar oil, MCT
Diabetic Sodium and calcium 1624 Maltodextrin, hydrolyzed 3440 Sunflower oil, soybean oil, 4049 1.01.06 1,0001,890 85 355450
caseinates, beef, milk cornstarch, fructose, canola oil, MCT, safflower oil or NA
protein, soy protein sucrose, guar gum, veg-
isolates etables, fruits, soy fiber
Immune modu- Sodium and calcium 2232 Hydrolyzed cornstarch, 3853 Canola oil, structured lipids; 2040 1.01.5 1,2502,000 7886 375550
lated caseinates, L-arginine, maltodextrin, soy fiber sunflower oil, fish oil, MCT
glutamine dipeptide,
Hepatic L-amino acids, whey 1115 Sucrose, maltodextrin, 5777 Soybean oil, MCT, canola oil, 1228 1.21.5 N/A1,000 7682 560690
modified cornstarch corn oil, lecithin
MCT, medium chain triglycerides
FOS, fructooligosaccharides
BCAA, branched chain amino acids

7/21/2012 5:59:02 PM

selection and administration of enteral formula requires a thor-

TABLE 3-8 Composition of Adult Parenteral
ough knowledge of physiology and pathophysiology of diges- Multivitamin and Micronutrient
tion and absorption. The physical form and quantity of each Products Available in the United States
nutrient may determine the extent of absorption of and tol-
erance to the formula (e.g., long-chain versus medium-chain Nutrient Dose Adult DRI
triglyceride). Disease-specific formulas have been developed Vitamins
for diabetes, renal failure, pulmonary, immune compromised,
Vitamin A (retinol) 1 mg (3,300 USP units) 700900 g
and hepatic disease. Although theoretically appealing, there
is lack of prospective, randomized controlled clinical trials Vitamin D (ergocalciferol 5 g (200 USP units) 515 g
supporting the purported indications for most specialized for- Vitamin E (DL--tocopheryl acetate) 10 mg (10 USP units) 15 mg
mulas, except for the immune formulas. Initiation of immune Vitamin K (phylloquinone) 150 g 90120 g
formulas perioperatively in GI surgery and trauma patients
Vitamin C (ascorbic acid) 200 mg 7590 mg
results in significantly decreased infections and infectious
complications. Folic acid 600 g 400 g
Niacinamide 40 mg 1416 mg
Riboflavin 3.6 mg 1.11.3 mg
Parenteral Nutrition Thiamin 3 mg 1.11.2 mg
PN is an intravenous infusion of a hyperosmolar solution, Vitamin B6 (pyridoxine) 6 mg 1.31.7 mg
which contains macronutrients (dextrose, protein, lipids),
Vitamin B12 (cyanocobalamin) 5 g 2.4 g
micronutrients, electrolytes, and fluids. PN is given via a cen-
tral venous catheter in order to accommodate the osmolarity Pantothenic acid 15 mg 5 mg
of PN. PN was first developed to provide nutrition to those Biotin 60 g 30 g
unable to take adequate nutrition via the GI tract. Diagno- Minerals
ses that commonly need PN include short bowel syndrome, Zinc 2.55 mg 811 mg
chronic malabsorption, bowel obstruction, prolonged ileus,
Copper 0.31.5 mg 0.9 mg
intractable diarrhea or vomiting, and high-output GI fistulas.
PN solutions can be infused continuously over 24 hours or Manganese 60180 g 1.82.3 mg
cycled over shorter intervals in stable patients. Chromium 1015 g 2035 g
PN increases the likelihood of hyperglycemia, even in Selenium 2080 g 55 g
nondiabetic patients. PN should not be initiated in someone
whose blood glucose is 300 mg/dL; blood glucose should be
treated and be between an acceptable range (80 to 150 mg/dL)
prior to initiating PN. Dextrose can be initiated at 150 to 250
g/day depending on the patients expected glucose tolerance of serum triglyceride levels <400 mg/dL is suggested during
and/or tolerance to prior dextrose infusions (e.g., IV dex- lipid infusion. For persistent or severe hypertriglyceridemia or
trose). If after 24 hours glycemic control is acceptable, then for patients with an egg allergy, safflower oil or any oil high in
the dextrose can be advanced to goal over the next 24 to 48 essential fatty acids can be administered enterally if tolerated
hours as tolerated. Capillary glucose measurements should be in attempt to alleviate the symptoms of essential fatty acid
obtainedthree to four times daily until the values are within deficiency, which develops in approximately 10 to 14 days
acceptable ranges for 2 consecutive days. Regular insulin in the absence of essential fatty acid provision (linoleic and
should be administered accordingly. Adding insulin to the PN linolenic acids).
solution should be delayed until the 24-hour insulin require- Most patients require daily multivitamin and mineral provi-
ment is stable and even then authors are not uniform that add- sion in their PN solution (Table 3-8). Some trace elements may
ing insulin to PN is advisable. need to be omitted in patients with liver failure (e.g., manga-
Protein can be provided at the targeted patient goal. Surgi- nese). Electrolytes are added based on the individual need of
cal patients typically require 1.5 to 2.0 g/day of protein due to each patient by evaluating their blood chemistries and medical
hypercatabolism and wound-healing needs. Protein may need therapies (e.g., dialysis) with guidelines provided in Table 3-4.
to be adjusted for patients with renal or liver failure. How-
ever, patients with dialysis have an increased protein need as
this therapy is also catabolic to the patient and therefore pro- Peripheral Parenteral Nutrition
tein requirements are typically no different. Hepatic failure is Peripheral parenteral nutrition (PPN) contains similar compo-
associated with cachexia, and therefore withholding protein nents to centrally infused PN, but macronutrients need to be
for these patients is not advised unless medical therapy is not provided at lower concentrations and more volume is required
successful in alleviating disease severity. because the solution osmolality needs to be 900 mOsm/L.
Lipids may be infused three to four times weekly or daily PPN is contraindicated in patients that cannot tolerate large
and for up to 24 hours, depending upon a patients nutritional volumes of fluid. PPN is indicated for only short periods
needs. Irrespective of the method of lipid delivery, either via (2 weeks) as it provides insufficient nutrients (800 to 1,200
TNA or as a separate infusion, maximal lipid infusion rates kcal/day). Generally, decisions to use PPN are based on
should not exceed 0.1 g/kg/hour. IV lipids in the United States energy demands, anticipated duration of use, and availability
are rich in omega-6 fatty acids and adverse effects associated of intravenous access. The use of PPN in severely malnour-
with large infusions include immunosuppression and hyper- ished is not indicated due to few suitable veins and insufficient
lipidemia. Lipid-based sedation such as propofol needs to be nutrient provision. Utilization of PPN has decreased with the
included in the lipid infusion rate calculation. Maintenance advent of peripherally inserted central catheters (PICC).

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Parenteral Nutrition: Advantages and Disadvantages Enteral Nutrition: Advantages and Disadvantages
PN offers an advantage in that a functional GI tract is not The proposed advantages of EN in surgical and critically
required. The parenteral route provides considerable ease in ill patients include attenuation of the metabolic response to
nutrient delivery, and studies show that nutritional require- stress, improved nitrogen balance, better glycemic control,
ments are more consistently met. The metabolic response to increased visceral protein synthesis, increased GI anastomotic
IV glucose differs from that of oral glucose. This is partially strength, and increased collagen deposition. Other benefits of
because the insulin-dependent hepatic uptake of glucose EN include stimulation of the gut-associated lymphoid tissue
from the portal vein during first-pass physiology is greater (GALT), decreased nosocomial infections, enhanced visceral
when glucose is provided orally. This results in less systemic blood flow, increased variety of nutrients for delivery, and
hyperglycemia and hyperinsulinemia. A meta-analysis com- decreased risk of GI bleeding. While few studies have shown a
paring EPN and PN concluded that plasma glucose concen- differential effect on mortality, EN has consistently resulted in
trations are lower during EN. Plasma glucose and insulin better outcomes by reducing infectious morbidity (generally
concentrations, glucose oxidation, carbon dioxide produc- pneumonia and central-line infections) in most patient popu-
tion, and minute ventilation increase in a linear relationship lations and specifically abdominal abscess in trauma patients.
with calories administered in PN. Prolonged infusion of Despite the benefits of EN over PN, it may not be feasible
high rates of glucose (>4 mg/kg/minute) results in de novo to provide adequate nutrition via the GI tract. GI access dif-
lipogenesis in the majority of critically ill patients. Other ficulties remain, and there is difficulty in achieving nutrient
known disadvantages of PN include increased infectious goals with up to 50% of patients being intolerant to enteral
complications and morbidity, liver complications (e.g., feedings. Complications of EN include jejunal necrosis, aspi-
biliary stasis, cholecystitis, liver fibrosis), bacteremia, and ration, diarrhea, and respiratory compromise. In addition,
gut mucosal atrophy. Table 3-9 lists metabolic complica- the formulas themselves can induce problems related to their
tions of PN. composition (Table 3-10).

TABLE 3-9 Metabolic Complications of PN

Complication Possible Cause Treatment

Hypovolemia Inadequate fluid provision, over diuresis Increase free-water delivery

Hypervolemia Excess fluid delivery, renal dysfunction, congestive heart failure, hepatic failure Fluid restriction, diuretics, dialysis
Hypokalemia Refeeding syndrome, inadequate potassium provision, increased losses Increase IV potassium
Hyperkalemia Renal dysfunction, too much potassium provision, metabolic acidosis, Decrease potassium intake, potassium binders, dialysis in extreme
potassium-sparing drugs cases
Hyponatremia Excessive fluid provision, nephritis, adrenal insufficiency, dilutional states Restrict fluid intake, increase sodium intake as indicated clinically
Hypernatremia Inadequate free-water provision, excessive sodium intake, excessive water Decrease sodium intake, replete free-water deficit
Hypoglycemia Abrupt discontinuation of PN, insulin overdose Dextrose delivery
Hyperglycemia Rapid infusion of large dextrose load, sepsis, pancreatitis, steroids, diabetes, Insulin, decrease dextrose as indicated
Hypertriglyceridemia Inability to clear lipid provision, sepsis, too much exogenous dextrose and insulin Decrease lipid volume provided, increase infusion time, hold lipids
provision, multisystem organ failure, medications altering fat absorption, up to 14 days to normalize levels
history of hyperlipidemia
Hypocalcemia Decreased vitamin D intake, hypoparathyroidism, citrate binding of calcium Calcium supplementation
resulting from excessive blood transfusion, hypoalbuminemia
Hypercalcemia Renal failure, tumor lysis syndrome, bone cancer, excess vitamin D delivery, Isotonic saline, inorganic phosphate supplementation, corticoster-
prolonged immobilization-stress hyperparathyroidism oids, mithramycin
Hypomagnesaemia Refeeding syndrome, alcoholism, diuretic use, increased losses, medications, Magnesium supplementation
diabetic ketoacidosis, chemotherapy
Hypermagnesemia Excessive magnesium provision, renal insufficiency Decease magnesium provision
Hypophosphatemia Refeeding syndrome, alcoholism, phosphate-binding antacids, dextrose infusion, Phosphate supplementation, discontinue phosphate binding antac-
overfeeding, secondary hyperparathyroidism, insulin therapy ids, avoid overfeeding, initiate dextrose delivery cautiously
Hyperphosphatemia Renal dysfunction, excessive provision Decrease phosphate delivery, phosphate binders
Prerenal azotemia Dehydration, excessive protein provision, inadequate nonprotein calorie provision Increase fluid intake, decrease protein delivery, increase nonprotein
with mobilization of endogenous proteins calories
Essential fatty acid Inadequate polyunsaturated long-chain fatty acid provision Provide lipids

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TABLE 3-10 Common Complications Associated with Enteral Feeding

Complication Possible Causes Corrective Measures


Obstructed feeding tube Crushed medications administered through tube Give medications as elixir
Formula coagulated in tube due to contact with acidic medium Flush tube with water before and after each medication
(gastric contents, medications) Use less viscous formula and a pump
Formula viscosity excessive for feeding tube Flush tube with water under pressure several times per day
Formula buildup inside tube
Hyperglycemia Metabolic stress, sepsis, trauma, Diabetes Mellitus Treat origin of stress and provide insulin needed to maintain BG
110150 mg/dL
Avoid excessive carbohydrate delivery
Altered serum electrolytes Inadequate electrolytes in formula Change formula
Refeeding syndrome Monitor electrolytes closely (K+, Mg2+, PO4) and replace as indicated
Dehydration Osmotic diarrhea caused by rapid infusion of hyperosmolar formula Avoid hyperosmolar formulas delivered into the small intestine
Excessive protein, electrolytes, or both Increase fluid provision or decrease protein and electrolytes
Inadequate free-water provision Ensure adequate free-water provision
Overhydration Excessive fluid intake Assess fluid intake; monitor daily fluid intake and output
Rapid refeeding in malnourished patient Monitor serum electrolytes, body weight daily; weight change >0.2 kg/
Cardiac, hepatic, or renal insufficiency day reflects decrease or increase of extracellular fluid
Increased extracellular mass catabolism causing loss of body cell Use calorically dense formula to decrease free-water provision
mass with subsequent potassium loss Diuretic therapy
Gradual weight loss Inadequate calories Ensure patient is receiving estimated calorie requirements
Malabsorption Adjust nutrient delivery as indicated based upon patient monitoring
Adjust nutrient composition or add PN if malabsorption of nutrients
Excessive weight gain Excess calories Rule out weight gain due to volume status
Volume overload Ensure patient receiving caloric needs
Visceral protein depletion Active inflammatory process Treat cause of inflammation
Inadequate calories or protein Adjust calorie and protein provision if inflammatory markers normal
Essential fatty acid Prolonged (>10 days) lack of sufficient lipid provision (LCT) Include at least 4% of daily caloric needs as essential fatty acids
Nausea and vomiting Excessive formula volume or rate of infusion Decrease rate of infusion or volume infused
Hyperosmolar formula infusion (especially in small intestine) Change to isotonic formula
Delayed gastric emptying Add prokinetic agent
Improper tube location Reposition tube if needed
Very cold formula provided Use polymeric formula as less offensive odor
Smell of enteral formulas Change to lower fat formula
Provide formula at room temperature
Diarrhea Too rapid infusion of formula Decrease rate infusion rate
Bolus feedings into small intestine Only continuous feeds into small bowel
Hyperosmolar formula infused Change to isotonic formula
Hyperosmolar medication infused Avoid hyperosmolar medications or dilute with water prior to giving
Altered GI anatomy or short bowel syndrome Change to hydrolyzed, free amino acid and MCT oil-containing formula
Malabsorption Use lactose-free formula
Lactose intolerance Check stool for pathogens and treat accordingly
GI bacterial overgrowth Consider prebiotics and/or probiotics
Antibiotic therapy
Vomiting and diarrhea Contamination Check sanitation of formula, equipment and assure proper handling


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TABLE 3-10 Common Complications Associated with Enteral Feeding (Continued)

Complication Possible Causes Corrective Measures

Abdominal distention, Rapid bolus or intermittent infusion with cold formula Administer formula at room temperature
bloating, cramping, gas Rapid infusion with syringe Infuse continuously and gradually advance to goal
Nutrient malabsorption or maldigestion Hydrolyzed formula, MCT containing, lactose free
Rapid administration of MCT Administer MCT gradually as tolerated
Constipation Lack of fiber Add fiber formula
Inadequate free water Stool softener
Fecal impaction, GI obstruction Assure adequate free water
Inadequate physical activity Rectal exam, digital disimpaction
Medications Increase physical therapy if able, turn patient
Aspiration or gastric reten- Altered gastric motility, diabetic gastroparesis, altered gag reflex, Postpyloric nutrient delivery with continuous infusion
tion of formula altered mental status Add prokinetic agent
Head of bed < 30 degrees Elevate HOB > 30 degrees if possible
Displaced feeding tube Verify feeding tube placement and reposition as needed
Ileus or hemodynamic instability For prolonged intolerance, may need PN
Medications that slow gastric emptying (opiates, anticholinergics) Evaluate medications and change if able
Gastric, vagotomy surgery

Parenteral Nutrition Therapy Indications factors, such as infection, uremia, cirrhosis, hepatitis, trauma,
Several organizations have developed practice guidelines to burns, hemorrhage, steroids, immunosuppressants, cimetidine,
identify appropriate and inappropriate indications for PN coumadin, general anesthesia, and surgery. Nonnutritional
(Table 3-11). PN should only be provided in those patients factors that affect TLC include hypoalbuminemia, metabolic
where enteral nutrient provision is not feasible for 7 or more stress, infection, cancer, and chronic diseases.
days. PN should only be initiated in patients who are hemo-
dynamically stable and who are able to tolerate the fluid vol- Nitrogen Balance Studies
ume, protein, carbohydrate, and IV lipid doses necessary to Nitrogen balance studies are used to evaluate the adequacy
provide adequate nutrient requirements. Malnourished surgi- of protein provision in order to reduce loss of muscle mass
cal patients benefit most if PN is provided for a minimum of in hospitalized patients. Nitrogen is released as the result of
7 to 10 days preoperatively and then continued throughout the metabolism of amino acids in proteins and is excreted in the
perioperative period. urine as free urea. Therefore, urine urea nitrogen concentra-
tion increases with increased catabolism or metabolism of
exogenous protein. In theory, by increasing exogenous pro-
ASSESSMENT OF NUTRITIONAL tein, endogenous protein losses will decrease. Nitrogen bal-
EFFECTIVENESS ance studies reflect the balance between exogenous nitrogen
intake and renal removal of nitrogen-containing compounds.
Catabolism to Anabolism Switch Nitrogen balance studies are not protein turnover studies,
Nutritional support does not convert a septic catabolic patient which require labeled (stable isotope) protein methods.
into an anabolic state. Numerous hormonal and inflammatory Measurement of nitrogen balance studies is most accurate
factors are present that limit the effectiveness of exogenously in patients who receive a defined nutrient intake such as those
administered nutritional substrates. Only the resolution of the with enteral or parenteral feeding. For nitrogen balance calcu-
underlying stress can reverse these effects. The switch from lations, amino acid products are generally assumed to be 16%
catabolism to anabolism is one of the signs that the hyper- nitrogen (6.25 g of protein = 1 g of nitrogen). Nitrogen balance
metabolic response of stress is resolving and the patient is is calculated by subtracting the excreted nitrogen (24-hour
improving. This is first noted by a shift from fluid retention to urine urea nitrogen [UUN] collection plus insensible losses)
diuresis and loss of edema, followed shortly by a rise in serum from the nitrogen intake provided in the nutrition therapy:
proteins and an increase in protein utilization. This is reflected
in a positive nitrogen balance. Nitrogen balance = (grams of protein or amino acid
intake/6.25) (UUN + 4)
Immune Competence A positive nitrogen balance in the range of 2 to 4 g of nitrogen
Malnutrition leads to a decline in immune function. Immune per day, indicating an anabolic state, is desired, but often dif-
competence as measured by delayed cutaneous hypersensitiv- ficult to achieve. Validity of nitrogen balance is affected by
ity (DCH) and total lymphocyte count (TLC) is reduced in severe nitrogen retention disorders (e.g., creatinine clearance
uncomplicated severe malnutrition. In hospitalized patients, <50 mL/minute, severe hepatic failure), massive diuresis,
DCH and TLC have limited value due to other intervening abnormal nitrogen losses through excessive diarrhea or large

Lawrence_Chap03.indd 68 7/21/2012 5:59:04 PM


TABLE 3-11 Indications and Contraindications for PN Therapy

Indications Consensus
Nonfunctional GI tract Obstruction, ileus
Distal to site of possible enteral access
Malnutrition awaiting surgery and need 7 days
Prolonged ileus (7 days) with poor nutritional status
Intractable vomiting or diarrhea
For losses >5001,000 mL/d
Unable to maintain adequate nutritional status
Short bowel syndrome
Inability to absorb adequate nutrients enterally
<60 cm small bowel may require indefinite provision
Inability to adequately utilize GI tract Slow progression of enteral feeding
Unable to provide at least 60% nutrient needs enterally for 7 days
Enterocutaneous Fistula
Fistula exhibits increased output with enteral feeding
High-output fistula (>200 mL/day)
Unable to safely gain enteral access
Patient at nutritional risk
Anticipated duration of need 7 days
Perioperative support Preoperative
Severely malnourished and EN not feasible
Provide for at least 57 days preoperatively
If severely malnourished and initiated preoperative, begin as soon as resuscitated
Provide if anticipate therapy to be for 7 days
Critical care Unable to gain enteral access
Resuscitated and hemodynamically stable
Expected to remain NPO 7 days
Severe pancreatitis If enteral feeding worsens condition
Provide if anticipate therapy to be for 7 days
No central venous access Safe access not achievable
EN as alternative therapy All means of providing EN not attempted
Well nourished, short duration No indication of nutrition risk
Anticipated need 7 days
Postoperative provision only If not provided preoperatively
Provide postoperatively only after 7 days of EN not being feasible
Grim prognosis when PN will be of no benefit End-of-life issues preclude nutrition support

draining wounds or fistulas, skin exfoliation as in burns, and albumin and transferrin for nutritional assessment and moni-
accuracy of protein and amino acid intake data. toring of hospitalized patients. Prealbumin is mostly syn-
thesized in the liver. During an anabolic state, it correlates
with positive nitrogen balance. The use of serum proteins for
Serum Proteins nutrition assessment assumes that decreased levels are solely
Because of the flaws with nitrogen balance studies, serum caused by malnutrition.
transport proteins listed in Table 3-3 (e.g., transferrin, and Aside from energy and protein intake affecting serum pro-
prealbumin) have been used to potentially identify adequacy tein levels, there are also multiple nonnutritional factors that
of nutrition intervention. All of these proteins have other alter their serum values. The acute-phase response to injury
functions separate from their use with nutrition assessment. is a systemic response to stress and inflammation. The liver
Because of its rapid turnover and simplicity of assessment, reprioritizes transport protein synthesis (e.g., albumin, preal-
serum prealbumin has historically been preferred over serum bumin) by downregulating their synthesis and upregulating

Lawrence_Chap03.indd 69 7/21/2012 5:59:04 PM


the synthesis of acute-phase proteins (e.g., CRP). Transport enterally is imperative. PN should be sequentially decreased
proteins become a marker of severity of illness and inflam- as the enteral intake and tolerance improves to avoid com-
mation, not malnutrition. Altering the nutritional plan when plications of overfeeding. PN may be discontinued once the
a prealbumin level is low and a CRP is high will not result in patient is tolerating approximately 60% to 75% of goal nutri-
improved nutritional status and may result in complications ents via the enteral route. For patients who are eating, PN may
of overfeeding. However, once the inflammation resolves and be reduced and discontinued over a 24- to 48-hour period. If
CRP levels decrease, then it may be reasonable to alter the PN is inadvertently but abruptly discontinued in patients who
nutritional plan if prealbumin levels remain low. In addition, are not eating, all insulin should be stopped and blood glu-
due to the long half-life of serum albumin and its depletion cose levels should be monitored for 30 to 120 minutes after
with large fluid volumes, it is not an accurate marker during discontinuation of PN. Based upon the blood glucose lev-
acute illness, but has been shown to be a good prognostic indi- els, appropriate therapy for hypoglycemia should be imple-
cator of surgical outcome when evaluated in the preoperative, mented. Previously, most clinicians advocated the immediate
ambulatory care setting. initiation of 10% dextrose in water (D10W) if PN was abruptly
discontinued, but most clinicians now find that it is unneces-
Other Biochemical Parameters sary and that patient monitoring is adequate. If PN was used
as a vehicle for medication or electrolyte administration, an
Other various laboratory assays exist that reflect a change in alternate plan should be made once it is discontinued.
nutrition status, tolerance, or response to nutrition therapy.
Electrolyte and micronutrients should be evaluated when
deficiencies or toxicities are suspected. Hepatic, renal, and NUTRITIONAL CONCERNS FOR PATIENTS
respiratory function strongly affects a patients dietary pre-
scription and should be included in the nutrition assessment UNDERGOING SURGERY
and monitoring process. Iron levels, iron transport proteins, Digestive Tract Surgery
hemoglobin, and hematocrit with indices may determine an
anemia of nutritional origin. Serum magnesium and calcium The digestive tract is a very metabolically active organ
vary inversely with albumin levels. Correction of total serum involved in digestion, absorption, and metabolism of many
levels of these elements should be made for serum albumin lev- nutrients; therefore, various surgical interventions involving
els. Currently, only calcium has an accepted correction value the GI tract can result in malabsorption and maldigestion lead-
calculated by the formula: Ca(true) = Ca(serum) + 0.8(Alb(normal) ing to nutritional deficiencies. Several examples of these are
Alb(actual)). Measurements of ionized calcium can also be used. included in Table 3-12. Understanding where nutrients are
In general total magnesium levels >1.5 mg/dL, even without absorbed in the intestinal tract will aid in determining which
albumin correction, rarely result in metabolic consequences. nutrient may become deficient postoperatively (Figure 3-1).
Improving nutritional status preoperatively is important for
optimal postoperative recovery.
Head and neck cancer surgery patients usually present for
Refeeding Syndrome surgery malnourished due to their disease state. Often, the
Patients with significant premorbid malnutrition may not tol- tumor inhibits the patients ability to chew and swallow nor-
erate either the acute volume increase or caloric load. Propor- mally. Preoperative treatment may involve radiation and/or
tional increases in carbohydrate-dependent electrolytes such chemotherapy to reduce tumor bulk. These therapies may
as magnesium and phosphorus, protein-dependent electrolytes
such as potassium, and volume-dependent electrolytes such as
sodium should be made as the macronutrients are increased.
This has been termed the refeeding syndrome. Refeeding syn- TABLE 3-12 Nutrition Consequences of
drome may be defined as a constellation of fluid, micronutri- Intestinal Surgery
ent, electrolyte, and vitamin imbalances that occur within the
first hours to days following nutrient infusion in a chronically Location Potential Consequence
starved patient. Refeeding syndrome can include hemolytic
Proximal small intestine Malabsorption of vitamins and minerals Calcium,
anemia, respiratory distress, paresthesias, tetany, and cardiac
magnesium, iron, Vitamins A, D
arrhythmias. Typical laboratory findings include hypoka-
lemia, hypophosphatemia, and hypomagnesemia. Reported Gastric bypass Proteincalorie malnutrition from malabsorption due to
risk factors for refeeding syndrome include alcoholism, ano- dumping, unavailability of bile acids and pancreatic
rexia nervosa, marasmus, rapid refeeding, and excessive dex- enzymes due to anastomotic changes
trose infusion. In these patients, dextrose should be limited Bezoar formation
initially to 100 to 150 g/day. In addition careful observation of Distal small intestine Malabsorption of vitamins and minerals Water soluble
potassium, magnesium, and phosphorous levels is necessary (folate, vitamins B12, B1, B2, C, pyridoxine)
as they may fall rapidly with refeeding. Proteincalorie malnutrition due to dumping
Fat malabsorption
Transition from Parenteral to Enteral Nutrition Bacterial overgrowth if ilealcecal valve resected
The goal in all patients is to transition from PN to EN, either Colon Fluid and electrolyte malabsorptionPotassium,
via tube feeding or orally. Before discontinuing PN, assurance sodium, chloride
that the patient is consuming and absorbing adequate nutrients

Lawrence_Chap03.indd 70 7/21/2012 5:59:04 PM



Duodenum Stomach
Calcium Water
Phosphorus Ethyl alcohol
Magnesium Copper
Iron Iodide
Copper Fluoride
Selenium Molybdenum
Thiamin Intrinsic factor
Folate Jejunum
Vitamins A, D, E, K Thiamin
Ileum Niacin
Water Pantothenate
Vitamin C Biotin
Folate Folate
Vitamin B12 Vitamin B6
Vitamin D Vitamin C
Vitamin K Vitamins A, D, E, K
Magnesium Calcium
Bile salts and acids Phosphorus
Iron zinc
Amino acids
Vitamin K FIGURE 3-1. Nutrient absorption in the
Di-, tripeptides
Biotin GI tract.

worsen the ability to swallow, so even though patients can capacity, with potential delayed gastric emptying and dump-
consume some liquids and soft foods, it is often not enough ing syndrome. Another option for reestablishing esophageal
to support nutritional needs. A long history of alcohol and continuity is by interposing a segment of colon or jejunum
tobacco use is commonly found among these patients, which between the distal esophageal remnant and the stomach, or
may also affect nutrient intake. Patients typically will require duodenum after subtotal gastrectomy. Complications follow-
nutrition therapy postoperatively as they may receive chem- ing this procedure include dysphagia, strictures, and leakage
otherapy and/or radiation therapy, which can further delay at the anastomotic site. These patients may be limited to a
return of adequate oral nutrient consumption. If the tumor size soft or liquid diet preoperatively due to dysphagia or stric-
permits, placement of a percutaneous endoscopic gastrostomy tures. If the patient is unable to consume adequate nutrients
(PEG) tube preoperatively can be performed for perioperative orally, then a nasoenteric feeding tube may be passed if fea-
EN therapy. Placing a PEG, open gastrostomy, or nasoenteric sible. A PEG tube is not indicated if a gastric pull-up proce-
feeding tube intraoperatively can be used postoperatively for dure is planned as the stomach is used to make the esophageal
EN therapy. Plans should be made as to how nutrition ther- conduit; thus, a hole resulting from a gastrostomy tube would
apy will be provided postoperatively to avoid the use of PN be contraindicated. Patients may require preoperative PN if
if feasible. the esophagus is obstructed. Intraoperatively, a jejunal feed-
ing tube may be placed to allow for postoperative EN therapy
Esophageal Surgery until adequate oral intake is achieved. If enteral access is not
obtained intraoperatively, then PN is indicted because patients
There are several medical conditions that affect the esophagus may not resume oral intake for 7 to 10 days.
and inhibit the ability to swallow. These conditions include
corrosive injuries and perforation, achalasia, gastroesophageal
reflux disease, and partial or full obstruction caused by cancer, Gastric Surgery
strictures, or congenital abnormalities. Usually, surgical inter- Any gastric surgical procedure carries a chance that malnu-
vention is required to correct the abnormality and involves trition can develop as a result of several postoperative con-
removal of a segment or the entire esophagus. The esophageal sequences (Table 3-13). Dietary modifications are a key
tract is then replaced with either the stomach (gastric pull-up) component of the medical therapy following these surgical
or the intestine (colonic/jejunal interposition). A gastric pull- procedures. Patients who have undergone gastric resection
up procedure results in displacement of the stomach in the including the pylorus have an increased gastric emptying rate.
thoracic cavity. This procedure results in a reduced stomach This can result in dumping syndrome (early vs. late) caused

Lawrence_Chap03.indd 71 7/21/2012 5:59:05 PM


for postgastrectomy patients who suffer from these symptoms.

TABLE 3-13 Potential Nutrition Related
Complications with Gastric Surgery
Oral supplements may be provided to increase nutrient intake,
but these need to be isotonic and should not contain simple
sugars. Unfortunately, many oral supplements do contain sim-
Procedure Potential Complications
ple sugars and are hyperosmolar; therefore, they are not well
Vagotomy Impairs proximal and distal motor function of the stomach tolerated postoperatively. As patients may become dehydrated
Total gastric and Digestion and emptying of solids are retarded
due to excessive diarrhea or vomiting, they should be discour-
truncal vagotomy
aged from drinking beverages with high simple sugar contents
Emptying of liquids is accelerated
(e.g., Gatorade, fruit juices). The World Health Organiza-
Total gastrectomy Early satiety, nausea, vomiting tion oral rehydration solution is the ideal beverage for these
Weight loss patients to consume. An ideal rehydration solution should con-
Inadequate bile acids and pancreatic enzymes availability tain water, sodium, potassium, bicarbonate, and small amounts
due to anastomotic changes of glucose to promote small intestinal water absorption and
Malabsorption replenish fluid losses. PN is only indicated if enteral access is
not available and the patient is malnourished and not able to
Proteincalorie malnutrition
tolerate adequate nutrients orally.
Anemia Anemia is a common consequence of gastric surgery.
Dumping syndrome Anemia can be a result of a deficiency or malabsorption of
Bezoar formation one or more nutrients, including iron, folate, and vitamin B12
Vitamin B12 deficiency (Table 3-15). Total gastrectomy and some subtotal gastrec-
Metabolic bone disease
tomy patients require periodic intramuscular vitamin B12 injec-
tions. Metabolic bone disease can also be a late complication
Subtotal gastrectomy Early satiety
of gastric surgery. In addition to consuming dietary calcium,
with vagotomy Delayed gastric emptying patients require calcium and vitamin D supplementation.
Rapid emptying of hypertonic fluids
Intestinal Surgery
If excessive lengths of intestine are removed, nutritional con-
sequences can arise depending on the location of resection
by rapid release of a hyperosmolar load into the small bowel. (Figure 3-1). Short bowel syndrome may occur if more than
This results in a constellation of symptoms: nausea, cramping, 50% of the small intestine is removed. This syndrome is char-
palpitations, sweating, weakness, hypotension, and diarrhea. acterized by severe diarrhea or steatorrhea, malabsorption,
Many patients will adapt to this after several weeks following and malnutrition. Often, the patient will require long-term
surgery, but there are those that may need to restrict their diet PN to maintain nutritional status and fluid and electrolyte
indefinitely. Table 3-14 lists recommended dietary modification balance.

TABLE 3-14 Postgastrectomy/Antidumping Diet

Principles of Diet

Postoperatively, some discomfort (gas, bloating, cramping) and diarrhea may occur. To reduce the likelihood of these symptoms, a healthy, nutritionally complete diet should be
followed. Each person may react to foods differently. Foods should be reintroduced into the diet slowly.
Diet Guidelines

1. Eat small, frequent meals per day.

2. Limit fluids to 4 ounces (1/2 cup) at a meal. Just enough to wash food down.
3. Drink remaining fluids at least 3040 min before and after meals.
4. Eat slowly and chew foods thoroughly.
5. Avoid extreme temperatures of foods.
6. Use seasonings and spices as tolerated (may want to avoid pepper, hot sauce).
7. Remain upright while eating and at least 30 min after eating.
8. Avoid simple sugars in foods and drinks.
Examples: fruit juice, Gatorade, PowerAde, Kool-Aid, sweet tea, sucrose, honey, jelly, corn syrup, cookies, pie, doughnuts.
9. Complex carbohydrates are unlimited. Example: Bread, pasta, rice, potatoes, vegetables
10. Include a protein containing food at each meal.
11. Limit fats (<30% of total calories).
Avoid fried foods, gravies, fat-containing sauces, mayonnaise, fatty meats (sausage, hot dogs, ribs), chips, biscuits, pancakes.
12. Milk and dairy products may not be tolerated due to lactose. Introduce these slowly in the diet if they were tolerated preoperatively. Lactose-free milk or soymilk is suggested.

Lawrence_Chap03.indd 72 7/21/2012 5:59:05 PM


TABLE 3-15 Nutrient Deficiencies Associated with Gastric Surgery

Deficiency Causes

Microcytic anemia Iron malabsorption or deficiency

Total and subtotal gastrectomy
Achlorhydria leads to insufficient
cleavage of iron from food to which its bound
reduction and solubilization of ferric iron to the ferrous form
BII more common as primary sites of absorption bypassed
Reduced intake of iron-rich foods due to intolerance and reduced gastric capacity
Supplementation: 325 mg ferrous sulfate twice daily with coadministration of vitamin C
Macrocytic anemia Folate, vitamin B12 deficiency, or anemia
Achlorhydria leads to insufficient liberation of vitamin B12 from protein foods it is bound
Decreased intrinsic factor leads to decreased binding of vitamin B12
Reduced intake of protein-rich foods due to intolerance and reduced gastric capacity
Intramuscular vitamin B12 monthly injections (1,500 g)
Metabolic bone disease Calcium deficiency or malabsorption
BII more common than BI procedure due to bypassing the duodenum and proximal jejunum
Rapid gastric emptying can reduce absorption
Fat malabsorption can lead to insoluble calcium soap formation
Vitamin D malabsorption may accompany fat malabsorption, which can impair calcium and phosphorous metabolism
Daily supplementation: 1,500 mg calcium, 800 IU vitamin D

Pancreaticoduodenectomy when diversion of fecal matter is necessary. These procedures

involve the creation of an artificial anus on the abdominal wall
In cases of ampullary, duodenal, and pancreatic malignancy, a
by incision into the colon or ileum and bringing it out to the
pancreaticoduodenectomy may be performed. This procedure
surface, forming a stoma. A pouch is placed externally over
is one of the most technically difficult and challenging GI
the stoma to collect the fecal matter. In general, patients with
surgeries and involves resecting the distal stomach, the distal
ostomies should eat regular diets. Foods that are gas form-
common bile duct, the pancreatic head, and the duodenum.
ing or difficult to digest may be avoided to reduce undesired
Three anastomoses must be performed: pancreatic duct to the
side effects. In the case of high-output ostomies (>800 mL/
GI tract, choledochojejunostomy, and gastrojejunostomy. The
day), patients may need to avoid hypertonic, simple-sugar
pylorus-sparing pancreaticoduodenectomy has become the
containing liquids and foods, fatty foods, and foods high in
preferred variation as it carries fewer postoperative nutritional
insoluble fiber to reduce outputs.
consequences. Common complications following these pro-
cedures include delayed gastric emptying, dumping syndrome
(if a nonpylorus-sparing procedure is performed), weight LOOKING AHEAD
loss, diabetes mellitus, and possible malabsorption due to pan-
creatic exocrine insufficiency. Nutrient guidelines following Nutritional assessment and support of surgical patients
these procedures are similar to those following a gastrectomy, impacts surgical outcome. With increased pressure to decrease
but also may include exogenous pancreatic enzyme replace- hospital stay and complications, nutritional status of patients
ment if exocrine dysfunction is suspected. is likely to become even more closely scrutinized by regula-
tory agencies, our hospitals, and payers. The role of PN in the
achievement of full nutritional support is undergoing renewed
Ileostomy and Colostomy interest and investigation, as is tailored enteral nutritional
An ileostomy or a colostomy may be required in the varie- support. Prevention of complications will likely become even
ties of intestinal lesions, obstruction, necrosis, or inflamma- more important, emphasizing the role and benefit of preopera-
tory bowel disease of the distal small intestine or colon or tive nutritional supplementation when possible.

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Lawrence_Chap03.indd 73 7/21/2012 5:59:05 PM


Questions A. Moderate risk for developing surgical complications
Choose the best answer for each question. B. Moderate risk for developing wound complications only
C. Low risk for developing surgical complications
1. A 27-year-old man is in the intensive care unit 24 hours after an
D. Cannot assess risk for surgical complications
automobile collision. He has a left pneumothorax, multiple broken
E. High risk for developing surgical complications
ribs, a ruptured spleen requiring splenectomy, a pelvic fracture, and
bilateral femur fractures. He is intubated. He has received 6 units
4. A 48-year-old woman is in the hospital because of nausea,
of PRBCs and is currently receiving IV fluids. Which one of the fol-
vomiting, and abdominal pain. She has a history of multiple
lowing best describes his metabolic response?
abdominal surgeries for small bowel obstruction. On admis-
A. Insulin is the major mediator of the stress response.
sion, she was quite thin with temporal and thenar muscle wast-
B. Glycogen stores can be used for 7 days. ing. Her albumin level was 1.7 g/dL. A nasogastric tube was
C. Energy expenditure is decreased by 30%. inserted and she has been receiving TPN for 2 days. You are
D. Hepatic reprioritization of protein synthesis favors acute-phase now called by her nurse because, in addition to nausea and
proteins. abdominal pain, shes begun to feel short of breath and have
E. Epinephrine and adrenocorticotropic hormone (ACTH) produc- tingling in her fingers. She suddenly goes into cardiac arrest.
tion are reduced.
Laboratory values now show potassium2.4 mEq/L, magne-
sium1.3 mEq/L, phosphorus1 mg/dL, and glucose350
2. A 66-year-old man is in the intensive care unit 10 days following
mg/dL. What nutritional complication may have resulted in this
colon resection for perforated diverticulitis. He has a history of
patients condition?
chronic obstructive pulmonary disease (COPD) and is unable to
A. Marasmus
wean from the ventilator. He has been maintained on total par-
enteral nutrition (TPN) and has started tube feeding. The most B. Refeeding syndrome
likely nutritional cause for failure to wean from the ventilator C. Overfeeding
would be D. Underfeeding
A. too much protein. E. Kwashiorkor
B. refeeding syndrome.
5. A 46-year-old man with an enterocutaneous fistula has been main-
C. underfeeding.
tained on TPN for several weeks. The fistula has healed and prior
D. overfeeding.
to removing the central line, the patient is given a unit of packed
E. hyperphosphatemia.
red blood cells through his central line for his chronic anemia. Two
hours into his red cell infusion, a rapid response is called when the
3. A 45-year-old man was admitted to the hospital 3 days ago with
nurse discovers the patient comatose and hypotensive. What is the
nausea and vomiting due to a gastric outlet obstruction. Further
most likely cause of the patients condition?
studies have confirmed a gastric cancer involving the antrum of the
stomach. He has a history of alcohol abuse and being homeless. A. Hypokalemia
The patient is thin and has temporal wasting and exposed ribs. B. Transfusion reaction
He has an albumin of 1.9 g/dL. A nasogastric tube was placed on C. Hypoglycemia
admission, and he was started on TPN. What is his surgical risk for D. Air embolus
perioperative complications? E. Catheter-related sepsis

Lawrence_Chap03.indd 74 7/21/2012 5:59:06 PM


Answers and Explanations surgical patients for nutritional risk include magnitude of the proce-
1. Answer: D dure, medications, recent weight changes, cachexia, changes in diet
or appetite, and serum albumin. (Assessment of Nutritional Status)
The injury stress response is mediated by the counter-regulatory hor-
mones, including ACTH, epinephrine, glucagon, and cortisol, along with the 4. Answer: B
proinflammatory cytokines such as interleukins 1 and 6. Insulin is dimin-
Refeeding syndrome occurs when chronically starved patients lose the
ished during this response. The stress response results in the marked
ability to tolerate acute changes in volume or caloric load. This results
increase of energy expenditure, which is proportional to the size of the
in a constellation of fluid, micronutrient, electrolyte, and vitamin imbal-
stress. Glycogen stores are rapidly depleted within 12 to 24 hours. Protein
ances within the first hours to days following nutrient infusion. These
synthesis in the liver is reprioritized to produce acute phase proteins.
patients are typically hypokalemic, hypophosphatemic, hypomagne-
2. Answer: D semic, and hyperglycemic. This may result in symptoms, including
Patients with COPD have difficulty weaning from the ventilator sec- hemolytic anemia, respiratory distress, paresthesias, tetany, and car-
ondary to CO2 retention. Feeding with both TPN and enteral feeding is diac arrhythmias including sudden cardiac death. (Complications of
likely to provide glucose loads far in excess of 4 g/kg/day, resulting in Initiating Nutritional Therapy)
lipogenesis. The respiratory quotient (RQ) for lipogenesis is 8.7, which
5. Answer: C
signifies a high CO2 production. This additional CO2 could make it very
difficult for a COPD patient to wean from the ventilator. (Parenteral When long-term infusion of highly concentrated glucose solutions is
Nutrition Advantages and Disadvantages) suddenly discontinued, the increased endogenous insulin levels pre-
cipitate hypoglycemia. A blood transfusion would be more likely to
3. Answer: E elevate rather than depress potassium levels. Transfusion reactions
Patients with a poor baseline nutritional status undergoing surgery cause fever, back pain, hemolysis, and hypotension, but not coma.
are more likely to have increased morbidity and mortality. There is The air embolus could cause both shock and unconsciousness and
a linear increase in complications in patients undergoing elective is unlikely to be associated with a blood transfusion. Catheter-related
gastrointestinal surgery as preoperative albumin decreases from sepsis could induce fever and hypotension, but not coma. (Transition
normal to levels below 2 g%. Criteria to consider when screening from Parenteral to Enteral Nutrition)

Lawrence_Chap03.indd 75 7/21/2012 5:59:06 PM

Surgical Bleeding: Bleeding
Disorders, Hypercoagulable States,
and Replacement Therapy in the
Surgical Patient

1. Using a patients physical examination and medical history, 5. Name the conditions that might lead to disseminated intra-
determine the likelihood and etiology of possible bleeding vascular coagulation (DIC).
disorders. 6. Describe the recommended component replacement ther-
2. Name five major etiologic factors that may lead to bleeding apy for the etiologic categories named in Objective 2, as well
disorders. as the definitive treatment for the underlying cause of each.
3. Describe the common laboratory tests that are used to 7. Describe the process of obtaining and transfusing blood, the
assess hemostatic competence, and explain how these symptoms of a transfusion reaction, and the diagnosis and
tests apply to the diagnosis of the conditions discussed in appropriate management of the different types of transfusion
Objective 2. reactions.
4. Identify the acute etiologic factors that might be responsible
for extensive bleeding in a patient who has received massive

Bleeding may occur during surgical procedures. Although THE HEMOSTATIC PROCESS
the volume of blood lost is usually not large enough to cre-
ate a major problem, certain operations are invariably asso- The hemostatic process involves an interaction between the
ciated with large blood losses that may impair the normal blood vessel wall, platelets, and the coagulation proteins.
hemostatic process. Additionally, some patients with con- After injury, hemostasis begins with a brief period (60 sec-
genital or acquired disorders of hemostasis require elective onds) of vasoconstriction by the vessels that have muscular
or emergency surgery. Therefore, surgeons must be prepared layers in their walls. This vasoconstriction in the region of
for significant blood losses that may have an adverse effect injury only controls blood loss for a brief time and cannot
on patient recovery, and they must be able to manage blood offer significant control of bleeding.
loss in their patients. In addition, surgeons must be knowl- The next step is mediated by platelets, which adhere to
edgeable about common bleeding disorders and causes of areas of vascular injury or to exposed subendothelial struc-
hypercoagulable states, the components of blood replace- tures (Figure 4-1). After adhesion, the platelets extrude
ment, and the problems associated with the transfusion of their contents, the most important of which is adenosine
blood products. diphosphate (ADP). As a result, platelet aggregation occurs.


Lawrence_Chap04.indd 76 7/21/2012 5:59:24 PM


Platelet adhesion to initiates the common pathway. The intrinsic (inside of the
subendothelial structures vessel) coagulation pathway requires factors XII, XI, IX,
of blood vessel wall
and VIII to interact and eventually convert factor X to Factor
Xa. The common coagulation pathway involves factors X,
Release of adenosine V, II (prothrombin), and I (fibrinogen). The end product of
diphosphate coagulation is fibrin, which has a weak clot-stabilizing abil-
ity. Factor XIII (fibrin-stabilizing factor) is required to create
Platelet aggregation fibrin of optimal strength (see Figure 4-2).
Bleeding may occur in the presence of a deficiency of any
of the factors of the coagulation pathways, except factor XII.
Formation of platelet Additionally, although normal hemostasis requires calcium,
aggregate (white thrombus)
hypocalcemia does not cause bleeding; it simply reduces
effective coagulation when it is very low.
Permanent thrombus
FIGURE 4-1. Platelets in the control of bleeding.
Detecting and correcting bleeding disorders before surgery is
the best way to avoid major bleeding problems during and
This platelet-to-platelet sticking causes the initial white after surgery. Therefore, a careful screening for bleeding risks
thrombus. The process from initial injury to the white (plate- is an essential part of the preoperative evaluation (Table 4-1).
let) thrombus occurs independently of the coagulation path-
ways; hemophiliacs, for example, can generate a normal white
thrombus. However, a more permanent thrombus is required History
for normal control of bleeding and eventual healing. This Obtaining a detailed bleeding history is the most important
more permanent thrombus is created through the formation step in evaluating patients for possible bleeding problems.
of fibrin. Patients should be asked if they have had prolonged bleeding
The coagulation pathways use various coagulation fac- after dental extractions, minor cuts, or previous operations; if
tors to generate fibrin, which stabilizes the white thrombus they have prolonged or frequent menses; if they have experi-
(Figure 4-2). The extrinsic (outside of the vessel) coagu- enced bruising after minor injury; or if they experience nose-
lation pathway begins with tissue thromboplastin, which bleeds. A history of bleeders in the family is also important
interacts with factor VII to convert factor X to factor Xa and to obtain. For the individual patient, a history of bleeding

Intrinsic Extrinsic
pathway pathway



IX thromboplastin

Measured by Measured by
activated partial prothrombin
X time
time V
Prothrombin Thrombin

Fibrinogen Fibrin (loose)

Measured by Measured
the thrombin XIII by urea
time clot
Fibrin (tight)

FIGURE 4-2. The coagulation pathways. Calcium and phospholipids from platelets are needed to permit the coagulation path-
ways to proceed at optimum rates. Activated factor XI in turn activates factor IX to become factor IXa. Factor IXa, in the presence
of factor VII, platelet phospholipids, and calcium, activates factor X. The rate of this reaction is greatly increased by the presence
of the platelet phospholipid. Coagulation pathways are tested as follows. Extrinsic pathway: measured by PT: monitor Coumadin
therapy. Intrinsic pathway: measured by aPTT: monitor heparin therapy.

Lawrence_Chap04.indd 77 7/21/2012 5:59:24 PM


to ethylenediaminetetraacetic acid (EDTA)-sensitive platelets,

TABLE 4-1 Preoperative Evaluation for
Bleeding and Clotting Disorders
which occurs in a small number of patients. For this reason,
very low platelet counts may need to be confirmed by manual
Study When Performed methods. Review of the peripheral blood smear provides a
reasonable estimate of platelet numbers and is recommended
History In all patients as part of routine preoperative for patients before surgery if any past history of abnormal
evaluation bleeding is known.
Physical examination As part of routine preoperative evaluation Platelets may be present in adequate numbers and yet
Laboratory studies: PT, aPTT, In patients with evidence of bleeding disorders
may not function appropriately (e.g., von Willebrand disease,
platelet count, bleeding time, or in whom excessive bleeding is antici-
chronic renal failure, qualitative platelet defects). In this case,
thrombin time pated because of the nature of the surgery
a platelet functionscreening test is prolonged, and platelet
aggregation done on platelet-rich plasma is abnormal.
aPTT, activated partial thromboplastin time; PT, prothrombin time.
Prothrombin Time
The PT measures the ability of the blood to form stable
thrombi. It evaluates the adequacy of factors VII, X, and V; pro-
problems is the most important preoperative information that thrombin; and fibrinogen (Figure 4-2), and both the extrinsic
predicts unexpected bleeding complications. A complete his- and common pathways. Its most common use is to monitor
tory must be obtained of all medications, both prescription and oral anticoagulation with warfarin (Coumadin). Today, PT is
over-the-counter, as these might induce or augment bleeding. reported with the international normalized ratio (INR). The
Special note must be made of the presence of anticoagulant INR system overcomes the problem of variable sensitivity by
medications such as aspirin, clopidogrel (Plavix), and warfa- standardizing the patients PT ration using the international
rin (Coumadin). This information is even more important than sensitivity index (ISI) of the particular thromboplastin. The ISI
laboratory tests. compares the locally used thromboplastin to an international
standard thromboplastin. Therefore, the INR is the PT ratio
that would have been obtained if the international standard had
Physical Examination been used, and provides reliable comparisons between labs.
The physical examination is less helpful than the history in Mastery of the use of the INR as tool for anticoagulation
assessing bleeding risk, because most patients with mild to therapy is important for physicians. Although most patients
moderate bleeding disorders do not have physical signs. The are adequately anticoagulated when the INR is between 2.0
examiner should seek signs of blood disorders, such as sple- and 3.0, certain patients, such as those with prosthetic heart
nomegaly, hepatomegaly, hemarthroses, petechiae, or ecchy- valves, require more intensive therapy that results in an INR
moses, which can be associated with bleeding disorders. of up to 3.5.
Petechiae and ecchymoses are typical of platelet disorders,
whereas hematomas are more typical of abnormalities in the Activated Partial Thromboplastin Time
coagulation pathways. The aPTT evaluates the adequacy of fibrinogen, prothrombin,
and factors V, VIII, IX, X, XI, and XII in the intrinsic and
Tests to Evaluate Hemostasis common pathways (see Figure 4-2). It is the most commonly
Platelet count, prothrombin time (PT), and activated used test to monitor the effectiveness of unfractionated hepa-
partial thromboplastin time (aPTT) should be determined rin therapy. The aPTT is normal in patients with factor VII
in patients who provide any history suggestive of a bleed- deficiency, but it is elevated during Coumadin therapy because
ing disorder as part of the routine preoperative evaluation to of reductions in factors II, IX, and X. The aPTT cannot be
exclude thrombocytopenia, a coagulation factor deficiency, or used to monitor most low molecular weight heparins (enoxa-
an acquired coagulation factor inhibitor. Certain other screen- parin and dalteparin).
ing tests, such as bleeding time, a platelet function test on
whole blood, or thrombin time, are indicated when the history Bleeding Time
or physical examination suggests a bleeding disorder. These The bleeding time test is conducted by making two standard
studies should be carried out as a part of preoperative screen- wounds (6 mm long, 1 mm deep) in the forearm of the patient
ing unless there has been a recent significant challenge to the with a spring-loaded lancet. The variation in the wound makes
patients hemostatic competence. Acquired bleeding disorders this test very technician dependent. The time from injury until
(e.g., thrombocytopenia) or acquired inhibitors against clot- the cessation of bleeding from both wounds is measured. A
ting factors can lead to a bleeding disorder in a previously normal bleeding time requires adequate numbers and function
hemostatically healthy person. These tests are relatively inex- of platelets and normal blood vessel walls. A normal bleeding
pensive and may potentially avoid unexpected bleeding and time range (in minutes) is established by each laboratory. The
the ensuing urgent need for transfusion of blood products. usual range is 5 to 10 minutes, but small variations are found
from laboratory to laboratory. A mild prolongation of bleed-
Platelet Count ing time may be caused by aging skin or long-term corticos-
The platelet count verifies that an adequate number of plate- teroid therapy. In both cases, senile ecchymoses may be seen,
lets are available in the circulation. Platelet counts are done by especially on the patients forearms.
automated methods in most institutions. However, automated A prolonged bleeding time is often associated with sig-
counters may not be accurate at platelet counts of <40,000. nificant bleeding at surgery. Bleeding time may be prolonged
Platelet counts may also be inaccurate if many red cell frag- by certain drugs (e.g., aspirin, or other nonsteroidal anti-
ments are present or in cases of pseudothrombocytopenia due inflammatory drugs [NSAIDs]). An abnormal bleeding time

Lawrence_Chap04.indd 78 7/21/2012 5:59:25 PM


in a patient without a history of associated drug use indicates of inheritance (e.g., males only as in hemophilia A or both
a potential bleeding disorder. A newly found prolonged bleed- males and females as in von Willebrand disease). The severity
ing time may be caused by any of the following disorders: of bleeding in response to prior trauma, such as surgery (e.g.,
1. Thrombocytopenia tonsillectomy or removal of wisdom teeth), is a very useful
2. Abnormal platelet function because of way to gauge the severity of the bleeding disorder: mild dis-
a. Medication (e.g., aspirin) orders may have very few manifestations of bleeding until
b. Dense granular disorders of platelets challenged by significant trauma. Other significant medical
3. von Willebrand disease (congenital or acquired) disorders can magnify bleeding risk. This is particularly true
of liver and kidney dysfunction.
The physical examination provides less information than
Whole Blood Platelet Function Testing
the thorough history in the evaluation of patients with bleed-
Many centers no longer provide the bleeding time as a method
ing history or acute event. Platelet disorders, either low
for the evaluation of platelet function. Testing of platelet
counts or dysfunction, will manifest similar physical findings.
function on citrated whole blood specimens is replacing the
Petechiae, which are pinhead-sized red spots on the skin or
bleeding time. The two most common instruments used are
mucous membranes that do not blanch on direct pressure,
1. PFA-100 (platelet function analyser-100). The basis of this are typical of thrombocytopenia (low platelets) or thrombo-
testing instrument is in vitro cessation of high shear blood cytopathies (disorders of platelet function). Ecchymoses are
flow by a platelet plug, the port closure time. An initial also seen in these same disorders but usually reflect a more
screening is done using a collagen/epinephrine port clo- severe disorder and reflect significant bleeding into skin or
sure time. If this time is prolonged, the collagen/ADP port mucous membranes. Coagulation factor deficiencies, on the
closure time is evaluated. This method can identify aspirin other hand, present with bleeding into joints (hemarthrosis)
suppression of platelet function-prolonged collagen/Epi and deep muscle bleeding (hematoma) as well as retroperito-
port closure and normal collagen/ADP port closure time. neal bleeding. On occasion, there may be GI or GU bleeding
Disorders of platelet function such as von Willebrand dis- in patients with coagulation factor deficiencies. The physical
ease lead to prolongation of both port closure times. examination may not be helpful in patients with mild bleeding
2. VerifyNow. This instrument bases the evaluation of plate- disorders. The site of bleeding may provide an indication of
let function on platelet aggregation. The instrument can be the etiology of the bleeding. Single-site bleeding is not usu-
designed to identify aspirin effect or clopidogrel effect on ally due to a bleeding disorder, whereas multisite bleeding is
platelets. more consistent with a bleeding disorder.
Neither testing instrument has yet gained complete accept- The following laboratory tests provide an adequate-enough
ance as a method of predicting excessive bleeding in a patient evaluation of the patients hemostatic competence to permit
during surgery. decisions to be made concerning the safety of proceeding with
Thrombin Time Platelet count and complete blood count (CBC)
The thrombin time evaluates fibrinogen-to-fibrin conversion Platelet function testing
with an external source of thrombin. Prolongation of thrombin aPTT
time can be caused by (1) low fibrinogen levels (hypofibrinogen- PT
emia); (2) abnormal fibrinogen (dysfibrinogenemia); (3) fibrin Fibrinogen level or thrombin clotting time
and fibrinogen split products; or (4) heparin (see Figure 4-2).
Thrombin time is used to evaluate disseminated intravascular
coagulation (DIC) and chronic liver disease. CAUSES OF EXCESSIVE SURGICAL BLEEDING
Most patients are hemostatically normal before they enter the
Presurgical Evaluation of Bleeding Risk operating room. However, in some patients with large blood
losses, generalized oozing is noted after a period of time. In
The medical history is the most important screening tool
addition, some operations (e.g., cardiopulmonary bypass,
in the assessment of the degree of bleeding risk in surgical
liver transplant surgery, prostate surgery, construction of port-
patients. The age of onset of bleeding/bruising will assist in
acaval shunts, trauma) are frequently associated with large
separating inherited from acquired bleeding disorders. Inher-
blood losses. These patients develop consumption of clotting
ited disorders usually present in childhood if they are severe;
factors and platelets, causing the syndrome of consumptive
mild inherited disorders may only manifest in adulthood, par-
coagulopathy or disseminated intravascular coagulopathy.
ticularly at the time of surgery or other trauma. The site(s) of
bleeding will provide clues concerning the underlying patho-
physiology of the patients bleeding disorder. Intracranial Preexisting Hemostatic Defects
bleeding may be associated with disorders of platelet function Preexisting hemostatic defects should be suspected when a
(e.g., von Willebrand disease) or thrombocytopenia, while prior history of bleeding exists or when abnormal bleeding
coagulation factor deficiencies usually present with intramus- begins within the first 30 minutes of the operative period.
cular or intra-articular bleeding and less frequently gastro-
intestinal (GI), genitourinary (GU) or intracranial bleeding. Congenital Bleeding Disorders
The medication history including all prescription and over- Congenital bleeding disorders, such as hemophilia and von
the-counter drugs must be thoroughly clarified in patients Willebrand disease, are uncommon. Mildly affected patients
suffering from bleeding events. The drug history must be all- may be asymptomatic. Type A hemophilia and von Wille-
inclusive even for drugs that are used sporadically. The family brand disease are both characterized by deficiencies of factor
history warrants particular attention in addressing the pattern VIII clotting activity (VIII), but there are differences in the

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TABLE 4-2 Congenital Bleeding Disorders TABLE 4-3 Causes of Acquired Bleeding
Hemophilia A Von Willebrand Disease
Advanced liver disease
Incidence 25 per 100,000 in U.S. 1% of U.S. population
Anticoagulation therapy
Pathophysiology Reduced or absent factor Reduced factor VIII activity
VIII activity. Factor VIII and von Willebrand Acquired thrombocytopenia
molecule is present. activity Platelet-inhibiting drugs
Site of bleeding Joints and intramuscular Mucocutaneous Uremia
Inheritance X-linked Autosomal dominant Over-the-counter medications, e.g., herbal supplements
Patients Only males Males and females DIC
Laboratory studies Prolonged aPTT Prolonged aPTT Primary/secondary fibrinolysis
Normal PT Normal PT
Normal platelet function Abnormal platelet function

may lead to clotting factor deficiencies, which can usually be

corrected with parenteral vitamin K. Cirrhosis may also cause
two disease processes (Table 4-2). Hemophilia is seen almost clotting factor deficiencies. These respond less well to vitamin
exclusively in males, and platelet function is normal. Von K. However, gastrointestinal bleeding in the patient who has cir-
Willebrand disease affects people of both sexes. In addition rhosis is usually caused by varices or gastritis rather than by a
to factor VIII deficiency, von Willebrand disease is associated coagulation defect.
with platelet dysfunction, which is diagnosed by decreased Anticoagulant therapy with heparin or oral anticoagulants
aggregation in response to ristocetin and is corrected by normal (e.g., Coumadin) leads to acquired bleeding disorders. Cou-
plasma. Von Willebrand disease is the most common inherited madin causes depression of the clotting activity of four coagu-
bleeding disorder. Although abnormal von Willebrand factor lation factors (II, VII, IX, and X). Because both the intrinsic
activity can be demonstrated in up to 1% of the population, the and extrinsic pathways are affected by Coumadin, both PT and
vast majority is asymptomatic with only 1 out of 10,000 show- aPTT are prolonged. Coumadin effect can be reversed with
ing any clinically significant signs. Von Willebrand factor has fresh frozen plasma (FFP) in an emergency or with vitamin
two principal functions: (1) carrier for factor VIII, preventing K. In cases of acute life-threatening hemorrhage (e.g., intrac-
destruction of factor VIII in the circulation and (2) support- ranial injury requiring emergent operation), recombinant acti-
ing platelet adhesion. Deficiency of von Willebrand activity vated factor VII has been successfully utilized to ameliorate
is corrected with cryoprecipitate infusions or desmopressin the effects of warfarin.
(DDAVP) therapy. Cryoprecipitate is a fraction of plasma that Heparin prolongs both aPTT and thrombin time. Heparin
contains von Willebrand factor, factor VIII clotting activity, (high molecular weight, or unfractionated heparin) works by
and fibrinogen. DDAVP is given as an intravenous infusion increasing the speed with which antithrombin III binds to and
or as nasal snuff. DDAVP is a hormone that, in addition to neutralizes factors IXa, Xa, Xia, XIIa, and thrombin. Heparin
other properties, leads to the release of von Willebrand factor effect can be reversed with protamine sulfate. A number of dif-
from its endothelial cell storage sites. Von Willebrand disease ferent low molecular weight heparins are available for use. It is
has multiple subtypes. Von Willebrand multimer studies must important to recognize the specifics of various low molecular
be done prior to using DDAVP, as this medication must not be weight heparin preparations when selecting an agent for clini-
used in some less common types of von Willebrand disease, cal use in specific settings. Low molecular weight heparin prep-
for example, type 2b. arations are more difficult to reverse with protamine sulfate.
Congenital platelet function disorders are uncommon and Acquired thrombocytopenia is caused by three mecha-
usually occur in patients who have a history of mucous mem- nisms: (1) decreased platelet production in the bone marrow
brane bleeding and easy bruising. Factor IX deficiency (e.g., (e.g., aplastic anemia); (2) increased destruction of platelets in
Christmas disease, hemophilia B) is seen only in males and the peripheral blood (e.g., idiopathic thrombocytopenia pur-
is less common (1 in 25,000 male births, about 3,300 cases pura [ITP], DIC, heparin-induced thrombocytopenia [HIT]);
in the United States) than type A hemophilia (1 in 5,000 to (3) splenic pooling in an enlarged spleen (e.g., cirrhosis); or
10,000 male births). Type A hemophilia is treated with puri- any combination of these three disorders (e.g., alcoholic liver
fied factor VIII products. Factor XI deficiency is found almost cirrhosis).
exclusively in Jewish patients. Platelet function disorders are most commonly associ-
ated with medications (e.g., aspirin, clopidogrel, other
Acquired Bleeding Disorders NSAIDs). Unlike other NSAIDs, however, aspirin induces
Acquired bleeding disorders are more common than congenital a defect that does not reverse; thus, patients should be
bleeding disorders and may have a variety of causes (Table 4-3). instructed to avoid aspirin for 1 week before elective sur-
Liver disease is a common cause of coagulation abnormalities. gery. Clopidogrel (Plavix), used commonly for platelet-
Inability of the liver to synthesize proteins leads to decreased lev- inhibiting effects, also has an irreversible effect on platelets.
els of prothrombin and factors V, VII, and X (but not VIII), which As with aspirin, clopidogrel should be stopped 7 to 10 days
may cause prolonged PT and aPTT. Alcohol ingestion may result before surgery.
in acute thrombocytopenia. Hypersplenism associated with sple- A second important cause of acquired platelet dysfunction
nomegaly may be associated with moderate thrombocytopenia is uremia. Patients who are uremic and are bleeding require
due to splenic pooling of the platelets. Obstructive jaundice dialysis before surgery to correct their platelet dysfunction.

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an increased risk of bleeding, particularly in patients who are

TABLE 4-4 Mechanism of Action and
Monitoring of Anticoagulants
taking vitamin K antagonists: dong quai (Angelica), garlic,
ginger, gingko biloba, ginseng, and St. Johns wort. Patients
Mechanism of Action Anticoagulant Laboratory Monitoring often fail to advise physicians about herbal supplements
because patients may not view them as medications.
Xa inhibition and thrombin Unfractionated aPTT or anti-Xa activity
inhibition heparin
Intraoperative Complications
Xa inhibition Low molecular Anti-Xa activity
weight heparin
Several common conditions contribute to bleeding during a
surgical procedure. Shock may cause or aggravate consump-
Production of inactive vitamin Warfarin INR
tive coagulopathy. Massive transfusion of stored packed red
Kdependent clotting
blood cells may lead to bleeding. This bleeding occurs after
factors IX, X, VII, II (1972)
rapid transfusion of 10 units or more of stored red blood cells
Xa inhibition Fondaparinux Anti-Xa activity over a 4- to 6-hour period. It is caused by low numbers of
Thrombin inhibition Lepirudin, aPTT platelets and by dilution of the clotting factors as a result of
argatroban the infusion of nonplasma fluids for volume support. For this
reason, transfusion of platelets, plasma, cryoprecipitate, and
calcium should be considered for patients receiving massive
transfusion of red blood cells.
Medication-Associated Bleeding Acute hemolytic blood transfusion reactions may lead to
Anticoagulants DIC. When a patient is under general anesthesia, there may
All anticoagulants carry the risk of inducing bleeding in any be no clues that incompatible blood has been infused until the
patient. The most common anticoagulants that are currently in onset of generalized bleeding as a result of DIC. The usual
use include vitamin K antagonist (Coumadin) and heparins, symptoms of an incompatible blood transfusion (e.g., agitation,
both unfractionated and low molecular weight. A new class of back pain) do not occur under general anesthesia. Hemoglobi-
anticoagulants, direct factor Xa inhibitors (Fondaparinux), is nuria and oliguria provide additional clinical evidence of DIC.
being used in specific settings but is likely to have expanded Intraoperative bleeding from needle holes, vascular suture
uses in the future. Direct thrombin inhibitors such as arga- lines, or extensive tissue dissection can often be controlled
troban, bivalirudin, and lepirudin have limited indications; in through the use of local hemostatic agents. These include gelatin
particular, these drugs are used to treat patients with HIT. sponge (e.g., Gelfoam), oxidized cellulose (Surgicel), collagen
Because of the increased risk of bleeding associated with sponge (Helistat), microfibrillar collagen (Avitene, Hemotene),
all anticoagulants, great care must be taken in using these topical thrombin (with or without topical cryoprecipitate), topi-
drugs (Table 4-4). cal e-aminocaproic acid (EACA), and topical aprotinin.
These medications must be used by knowledgeable practi-
tioners and in settings where monitoring is available. Heparin
in its unfractionated form can be monitored using the aPTT Postoperative Bleeding
or anti-Xa activity, while low molecular weight heparins can Fifty percent of postoperative bleeding is caused by inad-
be monitored, if needed, by only the anti-Xa activity. Anti-Xa equate hemostasis during surgery. Other causes of postopera-
inhibitors, such as Fondaparinux, are monitored using anti- tive bleeding include a number of possible causes. Residual
Xa activity. Direct thrombin inhibitors, such as lepirudin, are heparin that remains after cardiopulmonary or peripheral
monitored using the aPTT. vascular bypass surgery can cause significant oozing or overt
bleeding. Shock due to any cause that results in consumptive
Platelet-Inhibiting Drugs coagulopathy can lead to significant postoperative bleeding.
Drugs that inhibit platelet function fall into two groups. The first Altered liver function after partial hepatectomy often is asso-
group consists of drugs that irreversibly inhibit platelet function. ciated with bleeding. If a large portion of the liver is removed,
This group of drugs includes aspirin and clopidogrel (Plavix). the remaining liver may need 3 to 5 days to increase its pro-
When patients are taking these drugs and surgery is planned, the duction of clotting factors sufficiently to support hemostasis.
drug(s) must be stopped 7 to 10 days before planned surgery. If Acquired deficiency of the vitamin Kdependent clotting
the surgery is required as an emergency, transfusion of platelets factors (II, VII, IX, and X) can develop in patients who are
may be required to permit adequate hemostasis. The second poorly nourished and are receiving antibiotics. Supplementa-
group of drugs that can also alter platelet function does so by tion with vitamin K in postoperative patients who are not able
reversible inhibition of platelet function. The more commonly to adequately nourish themselves is essential to avoid devel-
used drugs in this group include dipyridamole and abciximab. oping these clotting factor deficiencies. Factor XIII deficiency
The platelet-inhibiting effect of these drugs disappears rapidly is an uncommon disorder but must be considered as a possible
and usually permits surgery to proceed promptly. cause for delayed postoperative bleeding. In this case, bleed-
Great care must be exercised in the use of anticoagulants ing occurs 3 to 5 days after surgery. The diagnosis of this defi-
and platelet-inhibiting agents. All medications used by the ciency is confirmed by a factor XIII assay.
patient must be chosen with caution to ensure no adverse drug
interactions occur.
Disseminated Intravascular Coagulation
Over-the-Counter Medications In any patient with postoperative bleeding, the possibility of
Over-the-counter medications used by patients may cause DIC must be considered as a possible cause. This is particu-
bleeding. This is particularly true of herbal supplements. The larly true if there is severe infection or shock. As the name
following herbal supplements are known to be associated with DIC suggests, it is characterized by intravascular coagulation

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and thrombosis that is diffuse rather than localized at the site which is rich in urokinase. It also occurs in patients with severe
of injury. This process results in the systemic deposition of liver failure. Very rare disorders of inhibitors of the fibrinolytic
plateletfibrin microthrombi that cause diffuse tissue injury. pathway (e.g., congenital deficiencies of 2-antiplasmin) can
Some clotting factors may be consumed in sufficient amounts also cause primary fibrinolysis. Treatment of these disorders
to eventually lead to diffuse bleeding. DIC may be acute or is best accomplished by eliminating the precipitating cause
clinically asymptomatic and chronic. The etiology of DIC may such as discontinuing lytic therapy. Since the half-life of lytic
be any of the following: (1) the release of tissue debris into agents is short (in minutes), bleeding usually stops rapidly.
the bloodstream after trauma or an obstetric catastrophe; (2) If primary fibrinolysis becomes severe, EACA can be
the introduction of intravascular aggregations of platelets as a used for therapy. This drug must be used cautiously because
result of the activation of platelets by various materials, includ- it blocks the fibrinolytic pathway and may predispose the
ing ADP and thrombin (which may explain the occurrence of patient to thrombotic events.
DIC in patients with severe septicemia or immune complex Secondary fibrinolysis is most often seen in response to
disease); (3) extensive endothelial damage, which denudes the DIC. The coagulation pathway is activated, followed by the
vascular wall and stimulates coagulation and platelet adhesion fibrinolytic pathway. Manifestations of this activation in labo-
(as seen in patients with widespread burns or vasculitis); (4) ratory tests include hypofibrinogenemia and the presence of
hypotension that leads to stasis and prevents the normal circu- fibrin split products and positive d-dimers. As the DIC is cor-
lating inhibitors of coagulation from reaching the sites of the rected, the secondary fibrinolysis resolves.
microthrombi; (5) blockage of the reticuloendothelial system;
(6) some types of operations that involve the prostate, lung, or Hypercoagulable States in the Surgical Patient
malignant tumors; (7) severe liver disease; and (8) brain trauma
or surgery may lead to DIC as the brain is rich in thromboplas- Thromboembolism may occur for a number of reasons during
tin, which activates clotting if released into the circulation. the course of surgery and in the postoperative period (Table 4-5).
The diagnosis of DIC is established by the detection of Both congenital and acquired disorders can put surgical patients
diminished levels of coagulation factors and platelets. The at risk for venous thromboembolism (VTE). The evaluation of
following laboratory results may be useful in diagnosing DIC: patients for surgery must include an assessment of the degree
(1) prolonged APTT; (2) prolonged PT; (3) hypofibrinogen- of risk the patient has for a VTE event. Virtually all surgery
emia; (4) thrombocytopenia; and (5) the presence of fibrin and carries varying degrees of risk for VTE from minimal to highly
fibrinogen split (FDP) products and positive d-dimers. The significant. A number of steps are essential in the assessment of
presence of fibrin and fibrinogen split products is caused by the degree of risk in a patient.
activation of the fibrinolytic pathway in response to activation The most important first step in the assessment of VTE risk
of the clotting pathway. The d-dimer is a product of fibrin is the medical history of the patient. The information to be
digestion by the fibrinolytic process. obtained should address the following points. Has the patient
The most important aspect of the treatment of DIC is to suffered a VTE event before the age of 40 years or had an
remove the precipitating factors (e.g., treating septicemia). If unprovoked VTE event at any age? A recurrent VTE event at
DIC is severe, replacement of coagulation factors is required any age can be a harbinger of a hypercoagulable state as can a
to correct the coagulation defect. Cryoprecipitate is the best thrombosis occurring at an unusual site (e.g., mesenteric vein
method to replace a profound fibrinogen deficit. Platelet trans- thrombosis). Perhaps one of the most important points in the
fusions may also be required. FFP is useful to replace other history is the family history, which can provide helpful clues
deficits that are identified, but it must be used judiciously if about the risks for VTE in any patient. A significant positive
volume overload is a potential problem. The use of heparin family history can guide one to evaluate patients for inherited
to treat DIC is controversial. In rare cases, the coagulation hypercoagulable risk factors.
must be inhibited with heparin or with drug therapy to pre-
vent platelet aggregation. There is no conclusive evidence that TABLE 4-5 Differential Diagnosis of
using heparin alters the outcome of DIC. Because antithrom- Hypercoagulable States by Site of
bin III is consumed during DIC, the use of heparin as an Thrombosis
anticoagulant may be severely compromised. Large trials are
under way to evaluate the benefit of using antithrombin III Arterial Thrombosis
concentrates and protein C concentrates as part of the treat- (e.g., Myocardial Infarction) Venous Thrombosis (e.g., VTE)
ment of DIC. Preliminary data from some trials are promising.
Common: Antiphospholipid syndrome Common: Factor V Leiden
Prothrombin 20210 mutation Prothrombin 20210
Bleeding Disorders Caused by Increased HIT Syndrome Protein C deficiency
Fibrinolysis Uncommon: Elevated PAI-1 activity Protein S deficiency
Postsurgical bleeding may also be caused by disorders leading Hyperhomocysteinemia Antithrombin deficiency
to increased fibrinolysis.
t-PA Deficiency Uncommon: Hyperhomocysteinemia
Primary fibrinolysis is a disorder that occurs when the
fibrinolytic pathway is activated leading to the production Anomalous coronary arteries Factor XII deficiency
of plasmin without antecedent activation of the coagulation Vasculitis Trauma
pathways. Most commonly, primary fibrinolysis occurs after Immobilization
fibrinolytic therapy with drugs such as tissue plasminogen
Pregnancy, oral contraceptive
activator (tPA), which are used to lyse coronary artery or
therapy, or hormone replacement
peripheral artery thromboses. Primary fibrinolysis is also seen
in conjunction with surgical procedures on the prostate gland,

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A positive history for thrombosis associated with preg-

TABLE 4-6 Initial Laboratory Evaluation
nancy, oral contraceptives, or hormone replacement therapy of Hypercoagulable States
should alert practitioners to the possibility of an underlying
hypercoagulable state. The specific complications of preg-
nancy that one must address in the history include recurrent APCR ratio; if positive request factor V Leiden study
fetal loss, fetal growth retardation, preeclampsia, or eclamp- Antiphospholipid antibody panel
sia. Each of these disorders can be an indicator of any underly- Antithrombin activity
ing hypercoagulable state. Protein C activity
Associated disease states such as malignancy, autoimmune
Protein S activity
disorders, and chronic inflammatory state can magnify the
risk for VTE, particularly if there is an underlying hyperco- Fasting homocysteine
agulable state. Prothrombin 20210 study
Circumstantial risk factors that add to a patients risk for Von Willebrand activity
VTE include advancing age, pregnancy, immobilization, and Factor VIII clotting activity
trauma of any type including the planned surgery procedure.
In addition, obesity is a significant risk factor for VTE, and
as the amount of obesity in the United States continues to
escalate, the risk for VTE in these patients will also. Interest- fibrinogen, von Willebrand factor, and factor VIII, which may
ingly, non-O blood group type blood does add to the patients occur in response to the stress of severe illness or trauma, have
risk for VTE, likely due to the associated higher levels of von been associated with an increased incidence of VTE. Platelet
Willebrand factor and factor VIII. counts >1,000 103/mm3 (1,000 109/L) may be seen in a
An unexplained prolonged aPTT may herald the presence small number of patients who have had a splenectomy particu-
of an antiphospholipid antibody that may be associated with larly in the immediate postoperative period. Very high platelet
an increased risk for VTE in some patients. Thus the aPTT is a counts are also associated with essential thrombocythemia, a
very useful part of the patients preoperative evaluation. myeloproliferative disorder.
The antiphospholipid antibody syndrome is an autoim-
Congenital Disorders mune disorder that may be associated with other autoimmune
Congenital disorders associated with hypercoagulable states disorders or may develop in otherwise healthy people. The
are diagnosed more frequently than in years past. They must diagnostic criteria include a documented thrombotic event
be considered as possible risk factors for VTE in anyone and/or pregnancy-associated morbidity and two positive
with a positive family history or in patients presenting with a antiphospholipid antibody tests done at least 12 weeks apart.
thrombosis at a young age (under 30 years of age). The most Some cases of chronic DIC, as can be seen associated with
common cause of congenital hypercoagulable states is acti- malignancies, may present as a VTE.
vated protein C resistance (APCR). The most common cause HIT is the development of a low platelet count associated
of APCR is the factor V Leiden mutation. Activated protein with the administration of heparin, in either its unfractionated
C binds to and neutralizes factors VIII and V, thus acting to or low molecular weight form. HIT predisposes to throm-
regulate the rate at which the intrinsic and common pathways bosis. In a patient receiving heparin who develops a new or
proceed. Genetically abnormal factor V (factor V Leiden) worsening thrombosis and a falling platelet count, HIT should
lacks the binding site for activated protein C; thus, factor V be suspected and heparin stopped immediately. Most patients
cannot be neutralized. Patients with factor V Leiden abnor- do not develop sufficient thrombocytopenia to cause bleed-
mality are predisposed to thromboembolic events. Additional ing. Recent (within 3 months) prior exposure to heparin may
causes of congenital hypercoagulable states include deficien- accelerate the process. The most common manifestations
cies of antithrombin III and proteins C and S. Protein C is of HIT are arterial thrombosis causing strokes, myocardial
present in the plasma in an inactive form. When thrombin is infarctions, leg ischemia, and venous thrombosis causing deep
attached to thrombomodulin on the endothelial cell surface, vein thrombosis (DVT) or pulmonary embolism. The diag-
protein C is activated. Protein S functions as a catalyst to this nosis is considered when the clinical scenario is compatible
activation. Activated protein C has two functions: (1) as an with HIT. The diagnosis is suggested with an enzyme-linked
anticoagulant (as described earlier) and (2) as an inducer of immunosorbent assay (ELISA), which detects circulating
fibrinolysis. Hyperhomocysteinemia may also be associated antibodies. However, this has a high false-positive rate and
with an increased risk of thrombosis. Some patients with must be confirmed by a serotonin release assay (SRA). Since
hyperhomocysteinemia are found to have gene defects (e.g., HIT predisposes to new thrombotic events, in addition to
MTHFR 6771). Prothrombin 20210 is an additional cause of discontinuing heparin, it is necessary to anticoagulate these
a congenital hypercoagulable state (Table 4-6). patients. Warfarin is contraindicated as it may cause skin gan-
grene (Coumadin-induced skin necrosis due to low protein
Acquired Hypercoagulable States C activity). Anticoagulation for a patient with confirmed or
Acquired hypercoagulable states may result from a number of suspected HIT requires using one of the following thrombin
possible causes, which may include one or more of the follow- inhibitors: argatroban, lepirudin, or danaparoid.
ing. Decreased production of naturally occurring anticoagu-
lants, protein C and S, or antithrombin may occur in patients Management of Hypercoagulable States
with significant liver disease. Therapy for hypercoagulable states is primarily directed at (1)
Ineffective fibrinolysis secondary to reduced or defective interfering with the coagulation pathways (with heparin, Cou-
plasminogen may also be present in patients with advanced madin, or both); (2) interfering with platelet function (with
liver disease. Very high levels of clotting factors, especially aspirin, clopidogrel, or other platelet-inhibiting drugs); and

Lawrence_Chap04.indd 83 7/21/2012 5:59:25 PM


(3) treating hyperhomocysteinemia (with folic acid, vitamin The platelet-poor plasma fraction is frozen and stored as
B12, and other B vitamins). Therapy must be individualized both FFP. It can be stored frozen for up to 12 months. Alternately,
to the patient and to the site and severity of the thromboembo- the platelet-poor plasma fraction can be further fractionated
lism. Great caution must be exercised when using warfarin in into cryoprecipitate and/or other plasma fractions or specific
patients with protein C deficiency. These patients may develop coagulation factors. Cryoprecipitate is rich in factor VIII and
Coumadin-induced skin necrosis if a long overlap period with fibrinogen. It can also be stored frozen for up to 12 months.
heparin is not performed. This long overlap allows metabolism
of all vitamin Kdependent proteins to reach a steady state. The
duration of anticoagulation therapy requires careful considera- Blood Component Therapy
tion, and the risks and benefits of protracted anticoagulation Typing and Cross-Matching of Blood Components
therapy must be weighed against potential benefits. There are over 600 known red blood cell antigens organized
During the perioperative period, therapy for patients with a into 22 blood groups systems. Most of these antigens are
history of thromboembolism and a documented hypercoagu- minor and are not involved in immunologic transfusion reac-
lable state must be planned carefully by both the surgeon and tions. Only two groups have immunologic relevance: the ABO
the hematologist. Low-dose heparin (5,000 international units and Rhesus groups. Both of these antigen groups are routinely
[IUs]), subcutaneously administered, provides adequate pro- identified for blood transfusions. An individuals ABO type is
tection from thromboembolism for short periods without com- genetically determined and falls into one of four blood types
promising surgical hemostasis. Alternatively, low molecular depending upon the presence or absence of two antigens: A
weight heparin prophylaxis may be used. For patients with and B. Type A only has the A antigen. Type B has only the B
a documented hematologic risk factor for thrombosis (e.g., antigen. Type AB has both antigens, and type O has neither
APCR) who have never had a thromboembolic event, prophy- antigen. Type O is the most common, and type AB is the least
laxis with pneumatic compression boots or low-dose hepa- common. An individual must receive ABO-matched blood,
rin is adequate. DVT prophylaxis is also covered in detail in and ABO incompatibilities are the most common cause of
Chapter 1, Perioperative Management of the Surgical Patient. fatal transfusion reactions.
The Rhesus, or Rh antigen system, is also clinically impor-
tant in matching blood for transfusion. There are over 50 Rh
BLOOD REPLACEMENT THERAPY antigens, but only D antigen testing is performed. If an indi-
vidual has the D antigen on the surface of red blood cells,
Collection, Separation, and Storage this person is Rh positive. If an individual does not have the
of Blood Products antigen, he/she is Rh negative.
The vast majority of the blood products used in the United Cross-matching is performed after A/B/Rh matching and
States are collected from volunteer donors in hospitals, com- is a process where serum from the recipient is mixed with the
munity donation centers, and blood banks. Blood is typically red blood cells from the donor. Antibodies in recipient serum
collected from these donation centers as whole blood. The to donor red cells will cause a positive crossmatch and pre-
volume of a donated unit of whole blood is approximately 450 clude transfusion of those donor cells to this recipient.
mL. This donated whole blood is initially stored in citrate
phosphatedextrose (CPD) solution. There are few civilian Transfusion of Red Blood Cells
indications for transfusion of whole blood. A more efficient Red blood cell transfusions are available as (1) whole blood,
use of donated blood is to separate whole blood into com- (2) packed red blood cells, (3) washed red blood cells, (4)
ponents and transfuse these individual components based on leukoreduced red blood cells, and (5) divided or pediatric unit
specific indications. Whole blood is separated into (1) red red blood cells. As stated above, there are no firm current
cells, (2) white cells, (3) platelets, and (4) plasma. Plasma is indications for transfusion of whole blood with the exception
then often further separated into cryoprecipitate and specific of the need for massive transfusion or need for life-saving
clotting factor concentrates (for instance factor VII). transfusion when component therapy is not available. Washed
Whole blood is collected into a bag containing the anti- red cells are washed with saline to remove plasma, and leu-
coagulant CPD solution using a closed sterile system. A koreduced red cells are filtered to remove leukocytes. Both of
centrifuge is used to separate the platelet-rich plasma from these preparations are used to transfuse red cells to patients
the packed red cells into a separate container. A storage life who have had hypersensitivity or nonhemolytic febrile trans-
extender (typically a crystalloid solution containing dextrose, fusion reactions to ordinary packed red blood cells, and for
sodium, adenine, and mannitol) is added to the packed cells, transplant patients. Pediatric unit red blood cells are adult
and the packed cells are frozen. units that have been divided and concentrated into a smaller
The platelet-plasma suspension is rich in platelets and volume. The result is that a pediatric or divided unit will
has a volume of about 200 mL. Platelet concentrate is then increase the hematocrit to the same degree in a child as in an
obtained by recentrifuging the platelet-plasma suspension adult when corrected for the childs weight and the volume
at a higher speed resulting in a concentration of platelets transfused.
that are then resuspended in a small volume of plasma. Gen- Transfusion of packed red cells is indicated when the red
erally, four to six adult platelet concentrates of the same blood cell mass is decreased (as reflected in the hemoglobin
blood type are pooled together to provide an adequate dose concentration and/or hematocrit level) with subsequent com-
of platelets. Many centers provide single donor pheresis promise of oxygen delivery to tissues and organs. The deci-
platelet transfusion, which is equivalent to six platelet con- sion to transfuse and the amount of blood to be transfused is
centrate packs. Platelets are stored at room temperature and multifactorial and must be individualized based on a number
require continuous gentle agitation. They can be stored for a of factors including (1) the reason for anemia; (2) the degree
maximum of 5 days. and acuity/chronicity of anemia; (3) underlying medical

Lawrence_Chap04.indd 84 7/21/2012 5:59:26 PM


conditions, particularly cardiac, pulmonary, and renal disease; Transfusion of Platelets

(4) anticipated future transfusion requirements; and (5) hemo- Platelet transfusion is indicated for patients who have clini-
dynamic instability. cal coagulopathy and either an absolute thrombocytopenia
Packed red blood cells are typically stored frozen between or a relative thrombocytopenia due to platelet dysfunction.
1C and 6C. The frozen cells have a shelf life of approxi- Platelet dysfunction often occurs as a result of medical con-
mately 42 days. During this period of time, there is a gradual ditions, such as renal failure, or as a result of medications
but progressive reduction in red cell viability. Red cells stored such as NSAIDs and clopidogrel (Plavix). Patients with
for 5 weeks have a 70% viability. Ideally, transfused red cells normal platelet function typically do not experience clinical
survive in recipient circulation for 5 to 6 weeks. Metabolism bleeding until the absolute platelet count drops to 30,000 to
during frozen storage causes an increase in both potassium and 50,000 platelets/L and often even lower than this. In con-
hydrogen ion concentration, resulting in an acidic pH level for trast, patients with dysfunctional platelets will often manifest
the transfusion solution. Additionally, leukocytes and platelets clinical bleeding with platelet counts in the normal range.
within the packed red cell suspension become nonfunctional Additional information regarding the need for platelet trans-
within hours of freezing. There is some evidence that transfu- fusion can be obtained from a bleeding time or whole blood
sion of red cells stored for more than 21 days may not be as platelet function testing. A bleeding time at least twice the
effective as transfusion of red cells stored for a shorter time. normal limit generally indicates need for platelet transfusion.
One unit of packed red blood cells contains about 200 mL Platelet suspensions contain some plasma and few red blood
of red cells and 30 mL of plasma in a total volume of about cells or leukocytes. Once received, platelets must be adminis-
310 mL. The hematocrit of a typical unit of packed red blood tered within 4 hours. The therapeutic effect of platelet trans-
cells is approximately 57%. Transfusion of one unit of packed fusion depends upon the patients pathologic state, existing
red cells into an average 70-kg person can be expected to raise platelet count, level of platelet function, weight of the patient,
the hematocrit by 3% and the hemoglobin concentration by and number of platelet concentrates transfused. The absolute
1 g/dL. rise in platelet count is also variable. A typical transfusion of
six platelets concentrates can be expected to raise the platelet
Transfusion Triggers count by approximately 50,000 to 100,000 platelets/L.
Clinical experience with Jehovahs Witness and other popu-
lations who refuse blood transfusions has demonstrated the Clinical Use of Recombinant factor VII
safety of relatively low hematocrits and hemoglobin concen- Recombinant activated factor VII (rFVIIa) was initially devel-
trations. A large clinical trial demonstrated that transfusing oped for use in hemophiliac patients. Factor VII binds to tissue
at a hemoglobin concentration of 7 g/dL was as least as safe factor and becomes activated. It then subsequently activates
as transfusing at 10 g/dL. Numerous retrospective studies in the extrinsic clotting pathway. It has a rapid onset and short
a variety of patient populations have found an association duration of action. Evidence is growing that rFVIIa may also
between blood transfusion and poor patient outcome. Numer- correct some factor deficiencies and clinical bleeding caused
ous other studies are in progress to define the appropriate by consumptive coagulopathies, such as those associated with
transfusion trigger. At this point in time, arbitrary transfusion massive transfusions in association with trauma and surgery.
triggers cannot be justified based on numeric value alone. The Although larger trials are lacking, case reports and series have
decision to transfuse must be made based on individual physi- demonstrated efficacy and safety in a variety of indications
ologic need and clinical circumstances. and at a variety of doses. Most clinicians reserve rFVIIa for
the most dire and refractory medical and surgical bleeding
Transfusion of Fresh Frozen Plasma emergencies. Clinical trials using rFVIIa in trauma, intracra-
FFP is the platelet-poor plasma removed from whole blood. nial bleeding, liver surgery, and spine surgery are ongoing.
It is typically stored frozen and thawed just prior to use. FFP
contains all of the required coagulation factors in physiologic Clinical Management of Hemophilia and
concentrations (note: the coagulation factors are not concen- von Willebrand Disease
trated). FFP does not contain red cells, leukocytes, or plate- As previously discussed, von Willebrand disease is the most
lets. FFP does not require crossmatch prior to use, but donor common hereditary human coagulation disorder. It causes a
and recipient must be ABO compatible. Rh status is not con- complex coagulopathy arising from absolute or relative defi-
sidered. ciencies of von Willebrand factor. This factor, which is produced
Indications for transfusion of FFP include patients with by endothelial cells and megakaryocytes, causes platelet adhe-
laboratory evidence of coagulation factor deficiency (e.g., sion and formation of the platelet plug. It also forms a complex
abnormally elevated PT or aPTT) with clinical bleeding or with factor VIII, facilitating its activity. Von Willebrand disease
need for an invasive procedure. Coagulation factor deficien- has several different pathologic subtypes. The classic syndrome
cies can result from dilutional coagulopathy following mas- is caused by a reduction in factor VIII activity. Clinical mani-
sive transfusion or resuscitation, congenital synthesis defects, festations include bruising, nosebleeds, bleeding gums, menor-
anticoagulant medications such as warfarin or heparin, liver rhagia, and muscle or joint bleeding. Most patients require no
disease, malnutrition, and other acquired disorders. treatment. However, patients undergoing surgery or actively
Thawed FFP should be used as soon as possible and within bleeding may require intervention. Typically, the therapeutic
24 hours. One unit of FFP is approximately 225 mL in volume goal is to maintain serum levels of 25% to 50%, or 50 to 100 IU/
and can be expected to raise the level of individual coagula- dL, for hemostasis. Cryoprecipitate is the most reliable source of
tion factors by about 1%. The actual therapeutic effect of FFP von Willebrand factor and is transfused to maintain serum activ-
transfusion will depend upon the several factors including ity and clinical effect. The National Institutes of Health have
absolute level of coagulation factors, synthetic capacity, and published a clinical guide for the treatment of von Willebrand
ongoing losses. disease (http://www.nhlbi.nih.gov/guidelines/vwd/).

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Hemophilia A is a sex-linked hereditary coagulation

TABLE 4-7 Management of Transfusion Reactions
disorder characterized by reduction in factor VIII activity.
The disease affects males, and clinical manifestations include
Reaction Management
easy bruising and bleeding from minor injury. Particularly
troublesome are episodes involving bleeding into joints, mus- Minor transfusion reaction Fever, rash, urticaria Observation, antihista-
cles, gastrointestinal tract, and central nervous system. Many mines
patients with severe forms of the disease require regular trans- Major transfusion reaction Fever, chills, hypoten- Immediate cessation of
fusion of factor VIII. Additionally, patients with active bleed- sion, bleeding in transfusion, send the
ing, trauma, or surgery require additional transfusion. After previously dry areas, unit of blood back to
minor surgery or trauma, 20% factor VIII activity should be hemoglobinuria, the blood bank for
maintained. For more severe trauma or surgery, 50% to 75% decreased urine recrossmatch, volume
and even up to 90% of factor VIII activity should be main- output expanders, pressors
tained by transfusion. Traditionally, pooled plasma factor VIII (mannitol, Lasix)
has been transfused. More recently, recombinant factor VIII
has become available.

Complications of Blood Component Therapy Febrile reactions are probably the most common immuno-
Transfusion of blood and blood components is safe and effica- logic transfusion reactions. These reactions typically occur
cious when used for the correct indications. However, trans- as a result of antileukocyte antibodies. Symptoms and signs
fusion is not without risk. There are multiple potential side include fever, chills, and tachycardia. Hemodynamic instabil-
effects associated with transfusion. These can be divided into ity can occur in severe cases. Patients with minor reactions
(1) metabolic derangements, (2) immunologic reactions, (3) can be managed expectantly, and the therapy is largely sup-
infectious complications, (4) volume overload, and (5) pul- portive. The transfusion should be stopped. Pretreatment with
monary complications. There are also special considerations aspirin, antipyretics, and antihistamines can prevent future
when transfusing large amounts of blood products over a short reactions. Alternately, transfusion of leukocyte-reduced red
period of time, a massive transfusion. cells can also be effective.
Acute hemolytic reactions can vary in severity from minor
Metabolic Derangements to catastrophic. Most hemolytic reactions occur as a result of
Metabolic complications of transfusion therapy are typically a clerical error and transfusion of ABO-mismatched blood.
seen in the context of transfusion of large amounts of blood They can begin quickly with administration of as little as
products, or transfusion of older blood products, or both. Most 50 mL of donor blood. Symptoms include sensation of hot or
common are hypocalcemia, hyperkalemia, hypokalemia, and cold, flushing, chest pain, and low back pain. Signs include
hypothermia. fever, hypotension, tachycardia, hematuria, hemoglobinuria,
Hypocalcemia can be seen with rapid transfusion (>100 bleeding, and possibly acute renal failure. Successful man-
mL/minute) of citrated blood products. This can manifest agement of hemolytic transfusion reactions rests on early
as muscle tremors, ST segment prolongation, delayed T diagnosis and prompt intervention. The transfusion must be
waves, ultimately decreased cardiac output, and ventricular immediately stopped. The remaining transfusion blood and a
fibrillation. This can be avoided by transfusing slowly and/ sample of the patients blood are returned to the laboratory for
or by administering calcium as intravenous supplementa- retyping and crossmatching. Transfused and patient blood is
tion. Supplementation rarely requires >1 g of intravenous also sent for culture to differentiate from contamination (see
calcium. below). Care is primarily supportive. Hemodynamic instabil-
Both hyperkalemia and hypokalemia can be seen by the fol- ity is treated with volume expansion and pressors, if neces-
lowing mechanisms. The concentration of potassium in a unit sary. Some clinicians recommend administration of mannitol
of packed red cells is often 75 mmol/L or greater after 35 days and/or loop diuretics such as furosemide to maintain urine
of frozen storage. Massive rapid transfusion of >10 units of output. Severe renal failure may require hemodialysis.
packed red cells can result in hyperkalemia. Following trans- Graft versus host disease occurs when immunosuppressed
fusion, the infused potassium can be rapidly taken back up patients receive donor leukocytes in blood component therapy.
into red cells resulting in hypokalemia. These cells are unrecognized as foreign cells by the recipient,
Finally, rapid transfusion of multiple units of frozen blood and they mount an immune response against recipient tissues.
products can result in precipitation or worsening of hypother- Onset of symptoms is often delayed for weeks and includes
mia. A patient receiving multiple transfusions should receive fever, rash, liver dysfunction, and diarrhea. This can be pre-
the products though a fluid warmer, and the patients core tem- vented by using leukocyte-reduced red cells and/or irradiated
perature should be monitored closely. red cells.

Immunologic Transfusion Reactions Transmission of Infectious Agents

Although ABO and Rh compatibility testing and crossmatch- Transmission of infectious agents following transfusion is rare
ing can obviate some of the more serious transfusion reac- but not zero. Blood can transmit infections caused by bacteria,
tions, minor untested and unidentified antigens and antibodies viruses, and parasites.
can still precipitate immunologic reactions (Table 4-7). Immu- Platelets are the most likely blood component to transmit
nologic transfusion reactions include (1) febrile reactions, (2) bacterial microorganisms. Clinical manifestations include
acute and delayed hemolytic transfusion reactions, (3) throm- fever, chills, tachycardia, and possibly hypotension. It can be
bocytopenia, (4) anaphylactic shock, (5) urticaria, (6) graft difficult to differentiate bacterial infection from other trans-
versus host disease, and (7) immune suppression. fusion reactions. The transfusion must be stopped, the blood

Lawrence_Chap04.indd 86 7/21/2012 5:59:26 PM


tested as described above, and anti-infective and supportive electrolyte and acidbase derangements, hypothermia,
measures initiated. possibly disease transmission, and development of acute res-
Probably the most feared complication of transfusion of piratory distress syndrome (ARDS).
blood products is the transmission of viruses such as hepatitis Recent studies have focused on development and imple-
B and C and the human immunodeficiency virus (HIV). Care- mentation of massive transfusion protocols (MTPs) to simul-
ful screening of donors and testing of blood has resulted in taneously improve outcome and reduce the number of blood
reduction of viral transmission to very low levels. The risk of products transfused. One study demonstrated that transfu-
hepatitis B transmission is about 1 in every 200,000 transfu- sion of packed red blood cells, FFP, and platelets in a 1:1:1
sions, and for hepatitis C, about 1 in 2 million transfusions. ratio resulted in a significant decrease in 24-hour mortality
Likewise, the risk of HIV transmission is about 1 in 2 million in trauma patients. Other studies have confirmed these results
transfusions. and have also demonstrated decreased use of packed red cells,
FFP, and platelets.
Transfusion-Related Acute Lung Injury Key features of an effective MTP include (1) activation of
Transfusion-related acute lung injury (TRALI) occurs in about protocol early in the patients clinical course, (2) automatic
1 out of every 5,000 transfusions. It can occur with transfusion delivery of red cells, FFP, and platelets in a 1:1:1 ratio, and
of any blood component, but is most common with transfu- (3) early use of rFVIIa in some studies. Proper use of an MTP
sions that contain plasma, such as FFP or platelets. TRALI should result in increased survival and decreased use of blood
is characterized by noncardiogenic pulmonary edema follow- products.
ing transfusion. The inciting event in TRALI is unknown, but
likely immunologic. Onset of pulmonary edema and respira- Blood Substitutes
tory insufficiency is generally within 1 to 2 hours of begin-
ning the transfusion, but it can happen up to 6 hours after a Blood substitutes, also known as artificial blood, can be
transfusion. Recently, a delayed TRALI syndrome has been divided into two broad categories based on intended function:
recognized, in which onset may be delayed up to 72 hours volume expanders and oxygen carriers. Volume expanders are
after transfusion. Treatment of TRALI is supportive. Patients inert and are used to increase blood volume. Volume expand-
usually require intubation and mechanical ventilation. The ers may be crystalloid based, such as Lactated Ringers solu-
pulmonary edema is due to pulmonary vascular mechanics tion, or colloid-based, such as hydroxyethyl starch. Volume
and not fluid overload, so diuresis is not usually indicated. As expanders can be used to replace volume following blood loss,
the pathophysiology is thought to involve activation of host either as a substitute for blood if the blood loss is relatively
neutrophils by donor antibodies and cytokines, plasma-rich small, or as a replacement until packed red blood cells can be
components such as FFP are associated with an increased risk transfused, in the case of larger blood loss.
of TRALI. Preventive efforts are focused on limiting blood Oxygen carriers are either perfluorocarbon based or hemo-
donors associated with elevated anti-HLA antibodies such as globin based, depending upon the transport mechanism used.
multiparous women. Mortality is 5% to 10% for TRALI. Oxygen-carrying blood substitutes are potentially useful in a
number of settings and for a number of reasons including (1)
easy storage and long shelf life, (2) no viral transmission, (3)
Massive Transfusion potential use in battlefield and extreme scenarios, (4) immedi-
Massive transfusion has been variously defined as the admin- ate availability, and (5) may possibly be more cost-effective.
istration of >10 units of packed red blood cells in <24 hours, A recent multicenter trial of a hemoglobin-based oxygen-
administration of a patients total blood volume in <24 hours, carrying blood substitute reported equivalent safety and
or transfusion of more than one-half of a patients blood vol- efficacy to packed red cells when used in emergent trauma
ume in 1 hour. Complications of massive transfusion include situations. However, the Food and Drug Administration
dilutional coagulopathy as a result of decreased levels of clot- (FDA) declined approval of this substitute due to safety con-
ting factors and platelets, oxygen transport abnormalities, cerns, and the product is not currently in production.

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Lawrence_Chap04.indd 87 7/21/2012 5:59:26 PM


Questions 3. A 50-year-old man is started on IV heparin for a peripheral arterial
Choose the best answer for each question. thrombosis. Three days later, it is noted that his platelet count has
dropped from 200 to 35. What is the next best step in management?
1. A 26-year-old man is brought to the emergency department (ED) A. Discontinue heparin and administer lepirudin
after being stabbed in the left arm in a fight. Brisk bleeding
B. Continue heparin and administer argatroban
from the wound was controlled by the EMTs with a pressure
C. Discontinue heparin and administer aspirin
bandage. Fifteen minutes later in the emergency depart-
D. Discontinue heparin and administer Coumadin
ment, the bandage is removed and only slight oozing is noted.
E. Continue heparin and administer a platelet transfusion
The most likely mechanism for decreased bleeding at this
time is
4. A patient is scheduled to undergo open abdominal aortic aneurysm
A. platelet activation and aggregation.
repair. During preoperative testing, it is determined that his blood
B. activation of the extrinsic coagulation cascade pathway. type is B negative. This means
C. activation of prothrombin to thrombin. A. he has circulating antibodies to Rh antigens.
D. activation of the intrinsic coagulation cascade pathway. B. he has circulating antibodies to A antigens.
E. local peripheral vascular vasoconstriction. C. he has circulating antibodies to B antigens.
D. he has no circulating antibodies to ABO antigens.
2. A 55-year-old woman is scheduled for a craniotomy to remove a
E. his red blood cells have A antigens.
brain tumor. She has a history of hypertension and hypercholes-
terolemia, and she underwent coronary artery angioplasty with a
5. A 65-year-old woman with severe symptomatic anemia secondary
stent placed 6 months ago. Current medications include enalapril,
to chronic renal disease is being transfused with packed red blood
pravastatin, and clopidogrel. Which one of the following would most
cells. A couple of minutes into the transfusion, she complains of back
likely be prolonged?
pain, chest pain, and shortness of breath. The most likely diagnosis is
A. Activated partial thromboplastin time (APTT)
A. transfusion-related acute lung injury (TRALI).
B. Bleeding time
B. delayed hemolytic transfusion reaction.
C. Prothrombin time (PT)
C. acute hemolytic transfusion reaction.
D. Thrombin time
D. transfusion-related volume overload.
E. Activated clotting time (ACT)
E. transfusion-related hyperkalemia.

Lawrence_Chap04.indd 88 7/21/2012 5:59:26 PM


Answers and Explanations with an alternative agent such as argatroban, lepirudin, or danaparoid.
1. Answer: E In this setting, starting Coumadin without starting one of these alterna-
tive agents is contraindicated as the initiation of Coumadin therapy is
Hemostasis involves the blood vessel wall, platelets, and the coagula-
associated with a transient hypercoagulable state.
tion cascade leading to fibrin deposition. After injury, local vasocon-
striction is the first hemostatic process to occur. This is followed by 4. Answer: B
platelet adherence, activation, and aggregation. Finally, the coagula- Multiple blood cell antigens exist; however, the ABO and Rh antigens
tion cascade leads to the deposition of fibrin. are most clinically relevant. A person with blood type B means his
2. Answer: B red cells have the B antigen. His plasma will have antibodies to the A
antigen. In patients who are Rh negative, they will not have circulat-
Clopidogrel is a platelet-inhibitor medication that is often used after
ing antibodies to the Rh antigens unless they have been previously
the placement of intravascular stents to prevent thrombosis. Like
exposed (e.g., during pregnancy of an Rh-negative mother with an
aminopsalicylic acid (ASA), clopidogrel is nonreversible; therefore, it
Rh-positive fetus). Hence, in this case, although he is Rh negative, he
should be stopped 7 to 10 days before surgery if normal coagula-
will not have circulating Rh antibodies.
tion is required. Prolonged bleeding time is associated with platelet
dysfunction. The APTT (intrinsic and common pathways), PT (extrinsic 5. Answer: C
and common pathway), and thrombin time (formation of fibrin from Acute hemolytic transfusion reactions are usually caused by clerical
fibrinogen) evaluate specific aspects of the coagulation cascade. error resulting in the administration of ABO mismatched blood. Host
3. Answer: A antibodies bind to antigens in donor red blood cells resulting in hemo-
lysis. This may result in renal failure and shock. Patients complain of
Heparin-induced thrombocytopenia (HIT) is a hypercoagulable state
shortness of breath, chest pain, and back pain. The most appropriate
manifest by arterial and venous thromboses. HIT occurs as a result
course of action is to stop the transfusion, provide supportive therapy,
of antibody formation to heparinplatelet complexes and results in
and have the blood rechecked. TRALI usually occurs after completion
thrombocytopenia due to intravascular platelet activation and aggrega-
of transfusions. Volume overload and hyperkalemia are unlikely only
tion. There is no indication for platelet transfusion. It can occur due to
minutes into a transfusion.
administration of any type of heparin. Patients must be anticoagulated

Lawrence_Chap04.indd 89 7/21/2012 5:59:26 PM

Shock: Cell Metabolic Failure in
Critical Illness

1. Define shock, and list the two primary mechanisms that may to determine which of the two primary mechanisms is the
cause cellular malfunction consistent with shock. predominant cause of shock in an individual patient.
2. List the etiologies of these primary mechanisms that are 4. Describe the interrelation between the two primary mecha-
responsible for shock. nisms of shock as a cause of cellular injury.
3. List the clinical information (i.e., history, physical examina- 5. Describe the general principles of management that diminish
tion, diagnostic tests, hemodynamic parameters) that helps cellular injury from the primary mechanisms of shock.

Traditional descriptions of shock often use systolic hypoten- oxygen delivery. The recognition that the primary toxins of
sion (<90 mm Hg) as the defining variable. According to this cellular injury are endogenous (the products of tissue injury
criterion, classification schemes that use categories such as or the consequent inflammatory response) rather than exog-
hypovolemic/hemorrhagic, septic, cardiogenic, and neuro- enous (endotoxin) emerged primarily over the last three dec-
genic shock are common and imply that evidence of an altered ades. Tissue injury and the associated inflammatory response
circulation is sufficient to make the diagnosis. However, certain result in the production or activation of cellular molecules
etiologies of hypotension (i.e., neurogenic vasodilation after (i.e., cytokines, superoxide radicals, prostaglandins, adhesion
spinal cord injury) do not necessarily cause cellular or organ molecules) that promote local cellular activation, tissue repair,
injury. In addition, cellular and organ injury may develop with- and host defenses. However, sometimes this local response
out hypotension reaching 90 mm Hg. Therefore, definitions of incites similar responses in cells that are distant from the
shock based on the circulatory measurement of systolic blood primary insult. The result is systemic inflammation that can
pressure are potentially misleading and narrow in scope. cause organ malfunction and shock.
A broader definition is that shock is a condition in which Simultaneously, during the last two decades, experimen-
total body cellular metabolism is malfunctional. This con- tal and clinical studies showed that these two mechanisms of
cept dates back to 1872 when S.D. Gross described shock cellular injury are not competitive or exclusive, but are most
as a rude unhinging of the machinery of life. When treated often additive during shock states. Simply stated, hypoperfu-
aggressively, this cellular metabolic dysfunction, the rude sion begets inflammation, and inflammation begets hypoperfu-
unhinging, is reversible. When allowed to continue, however, sion. The clinician must be alert to this association and must
shock results in cellular death, organ damage, and the eventual approach each patient who has the manifestations of total body
death of the individual. cellular malfunction with the dual goals of carefully assessing
During the 20th century, many theories were developed to circulation for oxygen delivery and the state of inflammation
explain this cellular injury and death (i.e., disorders of circu- for cell toxicity. Restoring excellent circulation and treating
lation, disorders of the nervous system, toxemia). By 1950, severe inflammation are the primary tenets for managing the
two competing theories were predominant: (1) shock is sec- patient with shock.
ondary to inadequate oxygen delivery; (2) shock is secondary This chapter describes the pathophysiology that links
to a toxic cellular insult that can progress even when suffi- hypoperfusion with inflammation, provides clinical guide-
cient oxygen is delivered. Such conditions as severe hemor- lines for recognizing hypoperfusion and severe inflamma-
rhage and cardiac malfunction (i.e., hypoperfusion) were tion, and outlines management strategies that can limit these
recognized throughout the century as etiologies of inadequate mechanisms of cellular injury.


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TABLE 5-1 Hemodynamic and Oxygen Delivery Variables

Item Definition Normal

CVP Central venous pressure; CVP = RAP; in the absence of tricuspid valve disease, CVP = RVEDP 515 mm Hg
LAP Left atrial pressure; in the absence of mitral valve disease, LAP = LVEDP 515 mm Hg
PAOP Pulmonary capillary occlusion pressure; PAOP = LAP, except sometimes with high PEEP levels 515 mm Hg
MAP Mean arterial pressure, mm Hg; MAP = DP + 1/3 (SP DP) 8090 mm Hg
CI Cardiac index; CI = CO/m BSA 2.53.5 L/min/m2 BSA
SI Stroke index; SI = SV/m BSA 3540 mL/beat/m2
SVR Systemic vascular resistance; SVR = (MAP CVP) 80/CO 1,0001,500 dyne-s/cm5
PVR Pulmonary vascular resistance; PVR = (MAP PAOP) 80/CO 100400 dyne-s/cm5
Cao2 Arterial oxygen content (vol%); CaO2 = 1.39 Hgb Sao2 + (PaO2 0.0031) 20 vol%
CVO2V Mixed venous oxygen content (vol%); CVO2 = 1.39 Hgb SVO2 + (PVO2 0.0031) 15 vol%
C(a v) o2 Arterial venous O2 content difference; C(a v)o2 = Ca o2 CVO2 (vol%) 3.54.5 vol%
O2D O2 delivery; O2D = CO Cao2 10; 10 = factor to convert mL O2/100 mL blood to mL O2/L blood 9001,200 mL/min
O2C O2 consumption; O2C = (CaO2 CVO2) CO 10 250 mL/min
BSA, body surface area (m2); CO,_cardiac output; DP, diastolic pressure; LVEDP, left ventricular end-diastolic pressure; PaO2, PAOP, pulmonary artery occlusion pressure; _PEEP, positive end-expiratory
pressure, arterial PO2 (mm Hg); PV O2, mixed venous PO2; RAP, right atrial pressure; RVED, right ventricular end diastolic pressure; Sao2, arterial oxygen saturation (%); SV O2, mixed venous oxygen
saturation; SP, systolic pressure; SV, stroke volume.

NORMAL PHYSIOLOGY OF CIRCULATION allows the measurement of pressure (typi cally measured as
central venous pressure [CVP] for the right side of the heart and
AND INFLAMMATION pulmonary capillary wedge or pulmonary artery occlusion pres-
The main function of circulation is to deliver oxygen to the sure [PAOP] for the left side of the heart) to estimate volume.
capillaries. The determinants of total body oxygen delivery are Ventricular afterload is determined primarily by the resist-
listed with other commonly measured or calculated hemody- ance to ventricular ejection that is present in either the pul-
namic variables in Table 5-1. As the formula for oxygen deliv- monary (pulmonary vascular resistance) or systemic arterial
ery shows, the pulmonary component is limited to providing tree (systemic vascular resistance). With constant preload,
adequate arterial oxygen saturation (90% saturation is usually increased afterload diminishes ventricular ejection, and
present when PaO2 60 mm Hg). This goal is usually read- decreased afterload augments ejection (see Figure 5-1).
ily achieved with modern respiratory therapy. Hemoglobin can Contractility is the force of contraction under conditions of a
be increased with the transfusion of red blood cells (RBCs), predetermined preload or afterload. Factors that may increase
but this strategy has limited applicability (see below). Usually, or decrease contractility are listed in Table 5-3. A change in
the most difficult component to treat is cardiac output. The contractility, like a change in afterload, results in a different
determinants of cardiac output are organized by both the vari- cardiac function curve (see Figure 5-1).
ables that affect ventricular function and the variables that The combined influence of increasing contractility and
affect venous return. Depending on clinical circumstances, decreasing afterload to improve ventricular function is also
sometimes it is more useful to use the logic associated with shown in Figure 5-1. Heart rate is directly proportional to car-
alterations in ventricular physiology to enhance circulation, diac output (not to cardiac muscle mechanics) until rapid rates
and sometimes it is more useful to use the logic associated with diminish ventricular filling during diastole.
alterations in venous return physiology. This logical applica-
tion of one circulatory physiology versus another (physio- Venous Return
logic) is described in more detail in the hypoperfusion section.
Venous return is described by the following formula:

Ventricular Physiology VR = (MSP CVP)/(RV + RA/19).

The major determinants of ventricular performance are listed in
Table 5-2. Preload is the magnitude of myocardial stretch, the
stimulus to muscle contraction that is described by the Frank- TABLE 5-2 Determinants of Ventricular Function
Starling mechanism (Figure 5-1), whereby increased stretch
leads to increased contraction until the muscle is overstretched
(commonly recognized clinically as congestive heart failure Preload
[CHF]; see the Hypoperfusion Section). Preload is most appro- Afterload
priately measured as end-diastolic volume. Because volume is Contractility
not easily measured clinically, the direct proportion between Heart rate
ventricular volume and ventricular end-diastolic pressure

Lawrence_Chap05.indd 91 7/21/2012 6:00:07 PM


TABLE 5-4 Factors That Alter Venous Return

SV Variables

Normal Increased Venous Return

V I Increased MSP
Increased vascular volume
V Increased vascular tone
External compression
Trendelenburg position (increased MSP in lower extremities and abdomen)
F Decreased CVP
D Negative pressure respiration
Decreased venous resistance
Dysfunction Decreased venous constriction
Diminished Venous Return

Decreased MSP
Increased CVP
FIGURE 5-1. Expected hemodynamic response in severe left ventricular
dysfunction to administration of diuretics (D), inotropic drugs (I), vasod