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Surgical
Decision Making
Sixth Edition
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Surgical
Decision Making
Sixth Edition
Robert C. McIntyre, Jr., MD, FACS
Professor and Chief
Division of GI, Trauma, and Endocrine Surgery
Vice Chair of Finance
Department of Surgery
University of Colorado School of Medicine
Aurora, Colorado
Richard D. Schulick, MD, MBA, FACS
Professor & Chair of the University of Colorado Department of Surgery
Director of the University of Colorado Cancer Center
The Aragón/Gonzalez-Gíustí Chair
University of Colorado School of Medicine
Aurora, Colorado
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1600 John F. Kennedy Blvd.
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Philadelphia, PA 19103-2899
SURGICAL DECISION MAKING, SIXTH EDITION ISBN: 978-0-323-52524-4
Copyright © 2020 by Elsevier, Inc. All rights reserved.
No part of this publication may be reproduced or transmitted in any form or by any means, electronic or
mechanical, including photocopying, recording, or any information storage and retrieval system, without
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This book and the individual contributions contained in it are protected under copyright by the Publisher
(other than as may be noted herein)
Notices
Practitioners and researchers must always rely on their own experience and knowledge in evaluating and
using any information, methods, compounds or experiments described herein. Because of rapid
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This book would not have been possible without the hard work and dedication of our
editorial assistant, Shelly Lange, who always “improves every life.”
Robert C. McIntyre, Jr.
Richard Schulick
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Contributors ix
ix
Minerva A. Romero Arenas, MD, MPH
Assistant Professor of General and Endocrine Surgery
Department of Surgery
The University of Texas Rio Grande Valley School of Medicine
Edinburg, Texas
Brett D. Arnoldo, MD
Professor and Interim Chief
General and Acute Care Surgery
University of Texas Southwestern Medical Center
Dallas, Texas
Juan A. Asensio, MD
Director of Trauma Center and Trauma Program
Creighton University Medical Center
Professor and Vice-Chairman of Surgery
Chief, Division of Trauma Surgery and Surgical Critical Care
Department of Surgery
Creighton University School of Medicine
Omaha, Nebraska
Chady Atallah, MD
Assistant Professor of Surgery
Department of Surgery
Johns Hopkins University School of Medicine
Baltimore, Maryland
Lori Baird, MD, MBA
Chief, Trauma, Surgical Critical Care, and Acute Care Surgery
Department of Surgery
University of Miami
Miami, Florida
Charles M. Balch, MD
Founding Editor-in-Chief Emeritus, Annals of Surgical
Oncology
Professor of Surgery
Department of Surgical Oncology
University of Texas MD Anderson Cancer Center
Houston, Texas
Carlton C. Barnett, Jr., MD, FACS
Chief, Surgical Oncology
Rocky Mountain Regional Veteran’s Affairs Medical Center
Professor
Division of Surgical Oncology
Department of Surgery
University of Colorado School of Medicine
Aurora, Colorado
Jad Abou-Khalil, MD, CM, MSc(Epid), FRCSC
Associate Professor of Surgery
Hepato-Biliary and Pancreatic Surgery Unit
Department of Surgery
University of Ottawa
Ottawa, Ontario
Anosheh Afghahi, MD, MPH
Assistant Professor
Division of Medical Oncology
Department of Medicine
University of Colorado School of Medicine
Aurora, Colorado
Gretchen Ahrendt, MD
Director, Diane O’Connor Thompson Breast Center
University of Colorado Hospital
Professor
Division of Surgical Oncology
Department of Surgery
University of Colorado School of Medicine
Aurora, Colorado
Nita Ahuja, MD, MBA, FACS
Surgeon-in-Chief, Yale New Haven Hospital
William H. Carmalt Professor and Chair of Surgery and
Oncology
Department of Surgery
Yale School of Medicine
New Haven, Connecticut
Maria B. Albuja-Cruz, MD, FACS
Assistant Professor
Division of GI, Trauma, and Endocrine Surgery
Department of Surgery
University of Colorado School of Medicine
Aurora, Colorado
Yewande Alimi, MD, MHS
Department of Surgery
MedStar Georgetown University Hospital
Washington, DC
Peter J. Allen, MD
Chief, Division of Surgical Oncology
Department of Surgery
Duke Cancer Institute
Duke University School of Medicine
Durham, North Carolina
Contributors
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x Contributors
Rachel E. Beard, MD
Assistant Professor
Rhode Island Hospital and the Lifespan Cancer Institute
Division of Hepatobiliary Surgery
Department of Surgery
Alpert Medical School of Brown University
Providence, Rhode Island
Daine Bennett, MD
Department of Surgery
University of Colorado School of Medicine
Aurora, Colorado
Walter L. Biffl, MD
Director, Trauma and Acute Care Surgery
N. Paul Whittier Chair of Trauma
Scripps Memorial Hospital La Jolla
La Jolla, California
James H. Black, III, MD, FACS
Associate Professor and Chief of Vascular Surgery and
Endovascular Therapy
The Johns Hopkins University School of Medicine
Baltimore, Maryland
Virginia Borges, MD, MMSc
Professor
Division of Medical Oncology
Department of Medicine
University of Colorado School of Medicine
Aurora, Colorado
Gregory M. Borst, MD
Trauma Acute Care Surgery
University of Colorado Health–Memorial Hospital
Colorado Springs, Colorado
Judy C. Boughey, MD
Professor of Surgery
Department of Surgery
Mayo Clinic College of Medicine
Rochester, Minnesota
Jason C. Brainard, MD
Associate Professor
Department of Anesthesiology
University of Colorado School of Medicine
Aurora, Colorado
Karen J. Brasel, MD, MPH
Professor and Program Director
Division of Trauma, Critical Care, and Acute Care Surgery
Department of Surgery
Oregon Health and Science University
Portland, Oregon
Brooke C. Bredbeck, MD
Department of Surgery
University of Michigan
Ann Arbor, Michigan
Robert E. Breeze, MD
Professor and Vice Chair
Department of Neurosurgery
University of Colorado School of Medicine
Aurora, Colorado
Murray F. Brennan, GNZM, MD
Benno C. Schmidt Chair in Clinical Oncology
Department of Surgery
Memorial Sloan Kettering Cancer Center
New York, New York
L.D. Britt, MD, MPH, DSc (Hon), FACS, FCCM
Henry Ford Professor and Edward J. Brickhouse Chairman
Department of Surgery
Eastern Virginia Medical School
Norfolk, Virginia
Clay Cothren Burlew, MD
Director, Surgical Intensive Care Unit
Denver Health Medical Center
Denver, Colorado
Professor
Division of GI, Trauma, and Endocrine Surgery
Department of Surgery
University of Colorado School of Medicine
Aurora, Colorado
John L. Cameron, MD
Alfred Blalock Distinguished Professor of Surgery
Department of Surgery
The Johns Hopkins University School of Medicine
Baltimore, Maryland
Eric M. Campion, MD
Assistant Professor
Denver Health Medical Center
Denver, Colorado
Division of GI, Trauma, and Endocrine Surgery
Department of Surgery
University of Colorado School of Medicine
Aurora, Colorado
DuyKhanh Pham. Ceppa, MD
Assistant Professor of Surgery
Division of Cardiothoracic Surgery
Department of Surgery
Indiana School of Medicine
Indianapolis, Indiana
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Contributors xi
Brandon C. Chapman, MD
Department of Surgery
University of Colorado School of Medicine
Aurora, Colorado
Akshay Pratap Chauhan, MBBS, MCh
Assistant Professor
Division of GI, Trauma, and Endocrine Surgery
Department of Surgery
University of Colorado School of Medicine
Aurora, Colorado
Tae Chong, MD
Associate Professor
Division of Plastic and Reconstructive Surgery
Department of Surgery
University of Colorado School of Medicine
Aurora, Colorado
Paul H. Chung, MD
Assistant Professor
Department of Urology
Jefferson University Hospitals
Philadelphia, Pennsylvania
David J. Ciesla, MD
Chief Trauma Acute Care Surgery
Tampa General Hospital
Professor and Division Chief
Division of Trauma & Acute Care Surgery
Department of Surgery
Morsani College of Medicine
University of South Florida
Tampa, Florida
Audra T. Clark, MD
Department of Surgery
University of Texas Southwestern Medical Center
Dallas, Texas
Joseph C. Cleveland, Jr., MD
Fred and Carol Grover Endowed Chair and Professor of
Surgery
Division of Cardiothoracic Surgery
Vice Chair of Faculty Affairs
Department of Surgery
University of Colorado School of Medicine
Aurora, Colorado
Kathryn E. Coan, MD
Assistant Professor
Department of General Surgery
Creighton Medical School
Phoenix, Arizona
Mitchell J. Cohen, MD
The Bruce M Rockwell Distinguished Chair in Trauma
Surgery
Denver Health Medical Center
Denver, Colorado
Professor and Vice Chair of Surgery
Division of GI, Trauma, and Endocrine Surgery
Department of Surgery
University of Colorado School of Medicine
Aurora, Colorado
Mary Condron, MD
Trauma and Acute Care Surgeon
Saint Charles Medical Center
Bend, Oregon
Michelle L. Cowan, MD
Assistant Professor
Division of GI, Trauma, and Endocrine Surgery
Department of Surgery
University of Colorado School of Medicine
Aurora, Colorado
Daniel Craig, MD
Department of Neurosurgery
University of Colorado School of Medicine
Aurora, Colorado
Chasen A. Croft, MD
Associate Professor of Surgery
Department of Surgery
University of Florida Health Science Center
Gainesville, Florida
Juliane Y. Cruz, MD
Department of Surgery
Huntington Hospital
Pasadena, California
Alan P. B. Dackiw, MD, PhD, MBA
Professor of Surgery
Department of Surgery
University of Texas Southwestern Medical Center
Dallas, Texas
Thomas A. D’Amico, MD
Professor
Division of Cardiovascular and Thoracic Surgery
Vice Chair
Department of Surgery
Duke University Medical Center
Durham, North Carolina
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xii Contributors
David R. Farley, MD
Professor of Surgery
Department of Surgery
Mayo Clinic College of Medicine
Rochester, New York
Stephanie Davis, MD
Department of Surgery
University of Colorado School of Medicine
Aurora, Colorado
Frederic W.-B. Deleyiannis, MD, MPhil, MPH
Professor
Division of Plastic and Reconstructive Surgery
Department of Surgery
University of Colorado School of Medicine
Aurora, Colorado
Ronald P. DeMatteo, MD, FACS
Vice Chair
Department of Surgery
Memorial Sloan Kettering Cancer Center
New York, New York
Rodrigo Donalisio de Silva, MD
Assistant Professor
Denver Health Medical Center
Denver, Colorado
Division of Urology
Department of Surgery
University of Colorado School of Medicine
Aurora, Colorado
Therese M. Duane, MD, MBA, CPE
Professor
Department of Surgery
John Peter Smith Health Network
Fort Worth, Texas
Linda A. Dultz, MD, MPH
Assistant Professor
Department of Surgery
University of Texas
Southwestern Dallas, Texas
Barish H. Edil, MD
Professor and Chair
John A. Schilling Chair in Surgery
Department of Surgery
University of Oklahoma College of Medicine
Oklahoma City, Oklahoma
Jonathan E. Efron, MD
Associate Professor of Surgery and Urology
Department of Surgery
The Johns Hopkins University School of Medicine
Baltimore, Maryland
Bryan A. Ehlert, MD
Assistant Professor
Division of Vascular Surgery
Department of Surgery
East Carolina University
Greenville, North Carolina
Oliver Fackelmayer, MD
Department of Surgery
University of Colorado School of Medicine
Aurora, Colorado
Josefina C. Farra, MD
Assistant Professor of Surgery
Department of Surgery
University of Miami
Miami, Florida
Carlos A. Fernandez, MD, FACS
Assistant Professor
Division of Trauma Surgery & Surgical Critical Care
Department of Surgery
Creighton University School of Medicine
Omaha, Nebraska
Lisa Ferrigno, MD, MPH
Assistant Professor
Division of GI, Trauma, and Endocrine Surgery
Department of Surgery
University of Colorado School of Medicine
Aurora, Colorado
Christina A. Finlayson, MD
Professor
Division of Surgical Oncology
Department of Surgery
University of Colorado School of Medicine
Aurora, Colorado
Yuman Fong, MD
Chairman
Department of Surgery
City of Hope Medical Center
Duarte, California
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Contributors xiii
Zhi Ven Fong, MD, MPH
Department of Surgery
Massachusetts General Hospital
Boston, Massachusetts
Charles J. Fox, MD
Chief of Vascular Surgery
Denver Health Medical Center
Denver, Colorado
Associate Professor of Surgery
Division of Vascular Surgery and Endovascular Therapy
Department of Surgery
University of Colorado School of Medicine
Aurora, Colorado
Richard Frazee, MD
Professor
Department of Surgery
Baylor Scott & White Healthcare
Texas A&M Health Science Center
Temple, Texas
David A. Fullerton, MD
John T. M. Wright Endowed Chair in Heart Valve Surgery
Professor and Head
Division of Cardiothoracic Surgery
Vice Chair of Research
Department of Surgery
University of Colorado School of Medicine
Aurora, Colorado
Csaba Gajdos, MD, FACS
Clinical Associate Professor
Buffalo Veterans Affairs Medical Center
Department of Surgery
University of Buffalo Jacobs School of Medicine and
Biomedical Sciences
Buffalo, New York
Maxx Gallegos, MD
Clinical Instructor
Department of Urology
Michigan State University
Detroit, Michigan
O. James Garden, CBE, BSc, MB ChB, MD, FRCSEd,
FRCPEd, FRSE, FRCSCan(hon), FRACS(hon),
FACS(hon), FRCS(hon), FCSHK(hon), FRCSI(hon)
Regius Professor of Clinical Surgery
Department of Clinical Surgery
University of Edinburgh
Royal Infirmary
Edinburgh, Great Britain
Fiona Gaunay, MD
Colon and Rectal Surgeon
Penn Medicine
Lancaster General Health
University of Pennsylvania Health System
Philadelphia, Pennsylvania
Susan L. Gearhart, MD
Associate Professor of Surgery
Department of Surgery
The Johns Hopkins University School of Medicine
Baltimore, Maryland
David A. Geller, MD, FACS
Richard L. Simmons Professor of Surgery
Chief, Division of Hepatobiliary and Pancreatic Surgery
Department of Surgery
University of Pittsburgh
Pittsburgh, Pennsylvania
Nicholas H. George
Department of Emergency Medicine
University of Maryland School of Medicine
Baltimore, Maryland
Jean-Francois H. Geschwind, MD
PreScience Labs LLC
Sepideh Gholami, MD
Assistant Professor
Division of Surgical Oncology
Department of Surgery
University of California, Davis
Sacramento, California
Alicia A. Heelan Gladden, MD
Department of Surgery
University of Colorado School of Medicine
Aurora, Colorado
Ana Gleisner, MD, PhD
Assistant Professor
Division of Surgical Oncology
Department of Surgery
University of Colorado School of Medicine
Aurora, Colorado
Rene Gonzalez, MD
Professor
Division of Medical Oncology
Department of Medicine
University of Colorado School of Medicine
Aurora, Colorado
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xiv Contributors
Karyn A. Goodman, MD
Professor
Department of Radiation Oncology
University of Colorado School of Medicine
Aurora, Colorado
Melissa A. Gorman, MD
Assistant Professor
Department of Orthopedics
University of Colorado School of Medicine
Aurora, Colorado
Patrick T. Hangge, MD
Department of Surgery
Mayo Clinic College of Medicine
Scottsdale, Arizona
Laura A. Harmon, MD
Assistant Professor
Division of GI, Trauma, and Endocrine Surgery
Department of Surgery
University of Colorado School of Medicine
Aurora, Colorado
Taryn Hassinger, MD
Department of Surgery
University of Virginia
Charlottesville, Virginia
Quinton M. Hatch, MD
Madigan Army Medical Center
Tacoma, Washington
Bryan R. Haugen, MD
Mary Rossick Kern and Jerome H. Kern Chair in Endocrine
Neoplasms Research
Professor and Head
Division of Endocrinology, Metabolism, and Diabetes
Department of Medicine
University of Colorado School of Medicine
Aurora, Colorado
Jin He, MD, PhD
Assistant Professor
Division of Surgical Oncology
Department of Surgery
The Johns Hopkins University School of Medicine
Baltimore, Maryland
Alexandra Heerdt, MD, MPH
Attending Surgeon, Breast Service
Department of Surgery
Memorial Sloan Kettering Cancer Center
Associate Professor of Surgery
Weill Cornell Medical School
New York, New York
Scott Helton, MD, FACS
Director Liver, Biliary, and Pancreas Surgery Center of
Excellence
Digestive Disease Institute
Virginia Mason Medical Center
Seattle, Washington
Thomas J. Herron, MD
Assistant Professor
Division of Trauma & Acute Care Surgery
Department of Surgery
Morsani College of Medicine
University of South Florida
Tampa, Florida
Vanessa P. Ho, MD, MPH
Assistant Professor of Surgery
Department of Surgery
Case Western Reserve University
Cleveland, Ohio
Maggie McQueen Hodges, MD, MPH
Department of Surgery
University of Colorado School of Medicine
Aurora, Colorado
Jordan R. H. Hoffman, MPH, MD
Fellow in Cardiothoracic Surgery
Division of Cardiothoracic Surgery
Department of Surgery
University of Colorado School of Medicine
Aurora, Colorado
Courtenay M. Holscher, MD
Department of Surgery
The Johns Hopkins University School of Medicine
Baltimore, Maryland
Tracy L. Hull, MD
Professor of Surgery
Department of Colon and Rectal Surgery
The Cleveland Clinic Foundation
Cleveland, Ohio
Jonathan B. Imran, MD
Department of Surgery
University of Texas Southwestern Medical Center
Dallas, Texas
Kenji Inaba, MD
Associate Professor of Surgery, Anesthesia, and Emergency
Medicine
Department of Surgery
University of Southern California
Los Angeles, California
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Contributors xv
William R. Jarnagin, MD
Chief, Hepatopancreatobiliary Service
Benno C. Schmidt Professor of Surgical Oncology
Memorial Sloan Kettering Cancer Center
Professor of Surgery
Weill Cornell Medical College
New York, New York
Eric K. Johnson, MD, FACS, FASCRS
Associate Professor of Surgery
MultiCare Colorectal Surgery
Uniformed Services University of the Health Sciences
Tacoma, Washington
Bobby L. Johnson III, MD
Instructor
Department of Surgery
University of Cincinnati College of Medicine
Cincinnati, OH
Edward L. Jones, MD, FACS
Assistant Professor
Rocky Mountain Regional Veteran’s Affairs Medical Center
Division of GI, Trauma, and Endocrine Surgery
Department of Surgery
University of Colorado School of Medicine
Aurora, Colorado
Teresa S. Jones, MD, FACS
Assistant Professor
Rocky Mountain Regional Veteran’s Affairs Medical Center
Division of GI, Trauma, and Endocrine Surgery
Department of Surgery
University of Colorado School of Medicine
Aurora, Colorado
Bellal A. Joseph, MD, FACS
Associate Professor of Surgery
Department of Surgery
Banner University Medical Center
Tucson, Arizona
Stephanie Joyce, MD
Surgical Critical Care Fellow
Department of Surgery
University of Colorado School of Medicine
Aurora, Colorado
Kyle J. Kalkwarf, MD
Assistant Professor
Division of Trauma and Acute Care Surgery
Department of Surgery
University of Arkansas for Medical Sciences
Little Rock, Arkansas
Amir Y. Kamel, PharmD, BCNSP
Clinical Specialist in Nutrition Support and Critical Care
University of Florida Health Shands Hospital
Clinical Assistant Professor
University of Florida College of Pharmacy
Gainesville, Florida
Farah Karipineni, MD, MPH
Endocrine Surgery Fellow
Division of Surgical Oncology
Department of Surgery
The Johns Hopkins University School of Medicine
Baltimore, Maryland
Howard S. Kaufman, MD, MBA
Chairman, Department of Surgery
Huntington Hospital
Medical Director, Huntington Hospital Cancer Center
Director of Colorectal Research Program,
Huntington Medical Research Institutes
Pasadena, California
Electron Kebebew, MD, FACS
Professor of Surgery
Chief, Division of General Surgery
Harry A. Oberhelman, Jr. And Mark L. Welton Professor
Program Leader, Endocrine Oncology Program
Department of Surgery and Stanford Cancer Institute
School of Medicine, Stanford University
Stanford, California
Abid D. Khan, MD
Trauma and Acute Care Surgeon
Department of Surgery
University of Colorado Health–Memorial Hospital
Colorado Springs, Colorado
David Khechoyan, MD
Assistant Professor
Division of Plastic and Reconstructive Surgery
Department of Surgery
University of Colorado School of Medicine
Aurora, Colorado
Fernando J. Kim, MD, MBA, FACS
Chief of Urology
Denver Health Medical Center
Denver, Colorado
Associate Professor
Division of Urology
University of Colorado School of Medicine
Aurora, Colorado
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xvi Contributors
Teresa S. Kim, MD
Assistant Professor
Division of General Surgery, Section of Surgical Oncology
Department of Surgery
University of Washington
Seattle, Washington
V. Suzanne Klimberg, MD, FACS
Professor and Director of Breast Cancer Program
Department of Surgery
Winthrop P. Rockefeller Cancer Institute
University of Arkansas
Little Rock, Arkansas
Patrick D. Kohtz, MD
Department of Surgery
University of Colorado School of Medicine
Aurora, Colorado
Rosemary A. Kozar, MD, PhD
Director of Translational Research
Associate Director of Shock Trauma Anesthesia Research
Center
R. Adams Cowley Shock Trauma Center
University of Maryland School of Medicine
Baltimore, Maryland
Rachel Kruer, PharmD
Clinical Pharmacist, ICU
The Johns Hopkins University School of Medicine
Baltimore, Maryland
Mustapha El Lakis, MD
Assistant Professor of Surgery
University of Pittsburg Medical Center
Seneca, Pennsylvania
Sepehr Lalezari, MD
Medical Staff
Department of Surgery
Good Samaritan Hospital
Los Angeles, California
Lung W. Lau, MD
Department of Surgery
Case Western Reserve University
Cleveland, OH
Harish Lavu, MD, FACS
Associate Professor
Chief, Section of Hepatopancreatobiliary Surgery
Department of Surgery
Thomas Jefferson University
Philadelphia, Pennsylvania
Ryan A. Lawless, MD
Assistant Professor
Denver Health Medical Center
Denver, Colorado
Division of GI, Trauma, and Endocrine Surgery
Department of Surgery
University of Colorado School of Medicine
Aurora, Colorado
John I. Lew, MD
Professor and Vice Chair of Surgery,
Chief of Endocrine Surgery
DeWitt Daughtry Department of Surgery
University of Miami Miller School of Medicine
Miami, Florida
Aaron Lewis, MD
Assistant Clinical Professor
Division of Surgical Oncology,
Department of Surgery
City of Hope National Medical Center
Duarte, California
Anne O. Lidor, MD, MPH, FACS
Professor
Department of Surgery
University of Wisconsin School of Medicine and Public
Health
Madison, Wisconsin
Keith D. Lillemoe, MD
Surgeon in Chief
Massachusetts General Hospital
HMS W. Gerald Austen Professor of Surgery
Harvard Medical School
Boston, Massachusetts
Gary Linkov, MD
Instructor
Otolaryngology—Head and Neck Surgery
Lewis Katz School of Medicine
Temple University Hospital
Philadelphia, Pennsylvania
Pamela A. Lipsett, MD, MHPE, MCCM
Warfield M. Firor Endowed Professorship in Surgery
Program Director, Residency in General Surgery and
Fellowship in Surgical Critical Care
Co-Director, Surgical Intensive Care Units
Assistant Dean of Assessment and Evaluation
The Johns Hopkins University School of Medicine
Baltimore, Maryland
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Contributors xvii
Tarik D. Madni, MD
Department of Surgery
University of Texas Southwestern Medical Center
Dallas, Texas
Gregory A. Magee, MD, MSc
Assistant Professor
Department of Surgery
University of Southern California
Los Angeles, California
David Mann, MD
Department of Neurosurgery
University of Colorado School of Medicine
Aurora, Colorado
David Mathes, MD
Professor and Chief
Division of Plastic and Reconstructive Surgery
Department of Surgery
University of Colorado School of Medicine
Aurora, Colorado
Sarah Mayson, MD
Assistant Professor
Division of Endocrinology, Metabolism, and Diabetes
Department of Medicine
University of Colorado School of Medicine
Aurora, Colorado
Martin D. McCarter, MD
Professor
Division of Surgical Oncology
Department of Surgery
University of Colorado School of Medicine
Aurora, Colorado
Ashley K. McCusker, MD, MSc
Trauma and Acute Care Surgery
University of Colorado Health–Memorial Hospital
Colorado Springs, Colorado
Robert C. McIntyre, Jr., MD, FACS
Professor and Chief
Division of GI, Trauma, and Endocrine Surgery
Vice Chair of Finance
Department of Surgery
University of Colorado School of Medicine
Aurora, Colorado
Travis J. McKenzie, MD
Division of Breast, Endocrine Metabolic and GI Surgery
Department of Surgery
Mayo Clinic College of Medicine
Rochester, Minnesota
Robert A. Meguid, MD, MPH/MSPH
Associate Professor
Division of Cardiothoracic Surgery
Department of Surgery
University of Colorado School of Medicine
Aurora, Colorado
Caleb Mentzer, DO
Department of Surgery
Ryder Trauma Center
Jackson Memorial Hospital
Miller School of Medicine of the University of Miami
Miami, Florida
Benjamin D. Medina, MD
Research Fellow
Department of Surgery
Memorial Sloan Kettering Cancer Center
New York, New York
John C. Messenger, MD
Professor
Division of Cardiology
Department of Medicine
University of Colorado School of Medicine
Aurora, Colorado
Bria Meyer, MD
Department of Surgery
University of Nebraska Medical Center
Omaha, Nebraska
Jordan D. Miller, DO
Assistant Professor
Division of Cardiothoracic Surgery
Department of Surgery
University of Kentucky
Lexington, Kentucky
John D. Mitchell, MD
Chief, General Thoracic Surgery
University of Colorado Hospital
Professor
Division of Cardiothoracic Surgery
Department of Surgery
University of Colorado School of Medicine
Aurora, Colorado
Damian James Mole, BMedSc, MBChB, PhD, FRCS
Honorary Consultant Surgeon
Department of Surgery
Senior Clinical Lecturer
MRC Centre for Inflammation Research
University of Edinburgh
Edinburgh, Great Britain
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xviii Contributors
Paul Nobert Montero, MD, FACS
Associate Professor
Division of GI, Trauma, and Endocrine Surgery
Department of Surgery
University of Colorado School of Medicine
Aurora, Colorado
Ernest E. Moore, MD
Director, Surgical Research
Denver Health Medical Center
Denver, Colorado
Professor
Division of GI, Trauma, and Endocrine Surgery
Vice Chair for Research
Department of Surgery
University of Colorado School of Medicine
Aurora, Colorado
Frederick A. Moore, MD
Professor and Chief
Division of Acute Care Surgery
Department of Surgery
University of Florida School of Medicine
Gainesville, Florida
Hunter Burroughs Moore, MD, PhD
Department of Surgery
University of Colorado School of Medicine
Aurora, Colorado
John T. Moore, MD
Associate Chief of Staff for Education
Rocky Mountain Regional Veteran’s Affairs Medical Center
Volunteer Clinical Faculty
Division of GI, Trauma, and Endocrine Surgery
Department of Surgery
Aurora, Colorado
Laura J. Moore, MD, FACS
Medical Director, Shock Trauma Intensive Care Unit
Texas Trauma Institute
Memorial Hermann Hospital
Texas Medical Center
Associate Professor
Chief of Surgical Critical Care
University of Texas Health Science Center
Houston, Texas
Eliza E. Moskowitz, MD
Department of Surgery
University of Colorado School of Medicine
Aurora, Colorado
Benedetto Mungo, MD
Department of Surgery
University of Colorado School of Medicine
Aurora, Colorado
Kenric M. Murayama, MD
Chair
Department of Surgery
John A. Burns School of Medicine
University of Hawaii at Manoa
Honolulu, Hawaii
Alexander P. Nagle, MD
Assistant Professor
Department of Surgery
Northwestern University Feinberg School of Medicine
Chicago, Illinois
Attila Nakeeb, MD
Professor
Department of Surgery
Indiana University of School of Medicine
Indianapolis, Indiana
Nicholas Namias, MD, MBA, FACS, FCCM
Medical Director
Ryder Trauma Center
Jackson Memorial Hospital
Chief, Division of Trauma and Acute Care Surgery
University of Miami Miller School of Medicine
Miami, Florida
Lena M. Napolitano, MD
Director, Trauma and Surgical Critical Care
Professor and Division Chief
Acute Care Surgery
Associate Chair
Department of Surgery
University of Michigan Health System
Ann Arbor, Michigan
Erinn Ogburn, MD
Department of Surgery
University of Kentucky
Lexington, Kentucky
Dmitry Oleynikov, MD, FACS
Chief of Gastrointestinal Minimally Invasive Surgery
Department of Surgery
University of Nebraska Medical Center
Omaha, Nebraska
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Contributors xix
Douglas M. Overbey, MD
Department of Surgery
University of Colorado School of Medicine
Aurora, Colorado
Alessandro Paniccia, MD
Department of Surgery
University of Colorado School of Medicine
Aurora, Colorado
Ian M. Paquette, MD
Associate Professor of Surgery
Department of Surgery
University of Cincinnati
Cincinnati, Ohio
Bruce C. Paton, MD
Director, The Given Institute
Aspen, Colorado
Emeritus Clinical Professor of Surgery
Department of Surgery
University of Colorado School of Medicine
Aurora, Colorado
Marco G. Patti, MD
Professor of Medicine and Surgery
Department of Medicine and Surgery
Center for Esophageal Diseases and Swallowing
University of North Carolina at Chapel Hill
Chapel Hill, North Carolina
Michael Patz, MD
Department of Anesthesiology
Mercy Regional Medical Center
Durango, Colorado
Erik Peltz, DO
Assistant Director, Trauma and Acute Care Surgery
University of Colorado Hospital
Assistant Professor
Division of GI, Trauma, and Endocrine Surgery
Department of Surgery
University of Colorado School of Medicine
Aurora, Colorado
Nancy Dugal Perrier, MD, FACS
Walter and Ruth Sterling Endowed Professor of Surgery
Surgical Oncology
University of Texas MD Anderson Cancer Center
Houston, Texas
Frederic Pieracci, MD, MPH
Associate Professor
Denver Health Medical Center
Denver, Colorado
Division of GI, Trauma, and Endocrine Surgery
Department of Surgery
University of Colorado School of Medicine
Aurora, Colorado
Amit Prabhakar, MD
Fellow
Anesthesiology and Critical Care Fellow
The Johns Hopkins University School of Medicine
Baltimore, Maryland
Sanjeev Puri, MD
Department of Surgery
University of Colorado School of Medicine
Aurora, Colorado
Jennifer M. Racz, MD
Assistant Professor of Surgery
Department of Surgery
Mayo Clinic College of Medicine
Rochester, Minnesota
Michael Radomski, MD
Trauma and Acute Care Surgery Fellow
Department of Surgery
Denver Health Medical Center
Denver, Colorado
University of Colorado School of Medicine
Aurora, Colorado
Christopher D. Raeburn, MD
Associate Professor
Division of GI, Trauma, and Endocrine Surgery
Department of Surgery
University of Colorado School of Medicine
Aurora, Colorado
Judi Ann Ramiscal, MD
Department of Surgery
University of Hawaii at Manoa
Honolulu, Hawaii
Bradley N. Reames, MD
Assistant Professor
Division of Surgical Oncology
Department of Surgery
University of Nebraska Medical Center
Omaha, Nebraska
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xx Contributors
T. Brett Reece, MD
Director, Thoracic Aortic Program
University of Colorado Hospital
Professor
Division of Cardiothoracic Surgery
Department of Surgery
University of Colorado School of Medicine
Aurora, Colorado
John A. Ridge, MD, PhD, FACS
Chief, Head and Neck Surgery
Professor and Vice-Chair, Department of Surgical Oncology
Louis Della Penna Family Chair in Head and Neck Oncology
Fox Chase Cancer Center Temple Health
Philadelphia, Pennsylvania
David Rivadeneira, MD, MBA, FACS, FASCRS
Director of Colorectal Surgery and Surgical Services
Huntington Hospital
Huntington, New York
Professor of Surgery
Hofstra University School of Medicine
Hempstead, New York
Amy Rivere, MD
Breast Surgical Oncologist
Ochsner Medical Center
New Orleans, Los Angeles
Tyler P. Robin, MD, PhD
Department of Radiation Oncology
University of Colorado Hospital
Aurora, Colorado
Thomas N. Robinson, MD, FACS
Chief of Surgery
Rocky Mountain Regional Veteran’s Affairs Medical Center
Professor
Division of GI, Trauma, Endocrine Surgery
Department of Surgery
University of Colorado School of Medicine
Aurora, Colorado
Stanley James Rogers, MD, FACS, FRCS
Professor
Department of Surgery
University of California, San Francisco
San Francisco, California
Martin D. Rosenthal, MD
Assistant Professor
Department of Surgery
University of Florida
Gainesville, Florida
Hai Nguyen Salfity, MD
Department of Surgery
Indiana University School of Medicine
Indianapolis, Indiana
Jason M. Samuels, MD
Department of Surgery
University of Colorado School of Medicine
Aurora, Colorado
Richard A. Santucci, MD
Specialist-in-Chief
Department of Urology
The Detroit Medical Center
Clinical Professor
Surgical Specialties
Michigan State College of Osteopathic Medicine
Detroit, Michigan
Robert G. Sawyer, MD
Professor and Chair
Department of Surgery
Western Michigan University Homer Stryker MD School of
Medicine
Kalamazoo, Michigan
Morgan Schellenberg, MD, MPH
Trauma/Critical Care Fellow
Trauma and Surgical Critical Care
Los Angeles USC Medical Center
Los Angeles, California
Todd R. Schlachter, MD
Assistant Professor
Department of Radiology and Biomedical Imaging
Yale University School of Medicine
New Haven, Connecticut
Francisco Schlottmann, MD, MPH
Department of Surgery
University of North Carolina
Chapel Hill, New Jersey
Jonathan A. Schoen, MD
Associate Professor
Division of GI, Trauma, and Endocrine Surgery
Department of Surgery
University of Colorado School of Medicine
Aurora, Colorado
Thomas J. Schroeppel, MD
Trauma Medical Director
Trauma and Acute Care Surgery
University of Colorado Health–Memorial Hospital
Colorado Springs, Colorado
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Contributors xxi
Michael Schweitzer, MD
Director, Johns Hopkins Center for Bariatric Surgery
Associate Professor of Surgery
The Johns Hopkins University School of Medicine
Baltimore, Maryland
Luke V. Selby
Department of Surgery
University of Colorado School of Medicine
Aurora, Colorado
Paulesh K. Shah, MD
Assistant Professor of Surgery
Department of Surgery
University of Maryland School of Medicine
Baltimore, Maryland
Eduardo Smith Singares, MD, FACS
Director SICU
University of Illinois Hospital and Health Sciences System
Chief, Division of Surgical Critical Care
Department of Surgery
University of Illinois College of Medicine at Chicago
Chicago, Illinois
Wayne Soong, MD, FCCP
Department of Anesthesiology
Rocky Mountain Regional Veteran’s Affairs Medical Center
Aurora, Colorado
Philip F. Stahel, MD
Professor of Orthopedics and Neurosurgery
Rocky Vista University College of Osteopathic Medicine
Parker, Colorado
Gregory Stettler, MD
Department of Surgery
University of Colorado School of Medicine
Aurora, Colorado
Lauren Steward, MD, MHSA, MPHS
Assistant Professor
Division of GI, Trauma, and Endocrine Surgery
Department of Surgery
University of Colorado School of Medicine
Aurora, Colorado
Gregory Van Stiegmann, MD
John H. and Cynthia H. Schultz Endowed Chair and Professor
Division of GI, Trauma, and Endocrine Surgery
Department of Surgery
University of Colorado School of Medicine
Aurora, Colorado
Jason W. Stoneback, MD
Chief, Orthopedic Trauma and Fracture Surgery
University of Colorado Hospital
Assistant Professor
Department of Orthopedics
University of Colorado School of Medicine
Aurora, Colorado
Andrea M. Stroud, MD, MS
Assistant Professor
Department of Surgery
Oregon Health & Science University
Portland, Oregon
Joshua J. Sumislawski, MD
Department of Surgery
University of Colorado School of Medicine
Aurora, Colorado
Jon S. Thompson, MD
Professor of Surgery
Department of Surgery
University of Nebraska Medical Center
Omaha, Nebraska
Robert J. Torphy, MD
Department of Surgery
University of Colorado School of Medicine
Aurora, Colorado
Becky B. T. King, MD
Department of Surgery
University of Colorado School of Medicine
Aurora, Colorado
Jennifer F. Tseng, MD, MPH
Chief of Surgery
Boston Medical Center
Chair
Department of Surgery
Boston University School of Medicine
Boston, Massachusetts
Anthony P. Tufaro, DDS, MD, FACS
Associate Professor
Department of Plastic and Reconstructive Surgery
Associate Professor
Department of Oncology
The Johns Hopkins University School of Medicine
Baltimore, Maryland
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xxii Contributors
John Twomey, MD
Retired Director, Burn Center
Department of Surgery
Hennepin County Medical Center
Minneapolis, Minnesota
Todd F. VanderHeiden, MD
Department of Orthopaedics
Denver Health Medical Center
Denver, CO
Associate Professor
University of Colorado School of Medicine
Aurora, Colorado
George C. Velmahos, MD, PhD, MSEdpel
Division Chief of Trauma, Emergency Surgery, and Surgical
Critical Care
Massachusetts General Hospital
Boston, Massachusetts
Catherine Velopulos, MD, MHS
Associate Professor
Division of GI, Trauma, and Endocrine Surgery
Department of Surgery
University of Colorado School of Medicine
Aurora, Colorado
Neil Venardos, MD
Division of Cardiothoracic Surgery
Department of Surgery
University of Colorado School of Medicine
Aurora, Colorado
Bryan B. Voelzke, MD, FACS
Spokane Urology
Spokane, Washington
Jon D. Vogel, MD
Director of Colorectal Surgery
University of Colorado Hospital
Associate Professor
Division of GI, Trauma, and Endocrine Surgery
Department of Surgery
University of Colorado School of Medicine
Aurora, Colorado
Anne Lambert Wagner, MD, FACS
Medical Director of the Burn Center
University of Colorado Hospital
Associate Professor
Division of GI, Trauma, and Endocrine Surgery
Department of Surgery
University of Colorado School of Medicine
Aurora, Colorado
Michel Wagner, MD, FACS
Assistant Professor
Division of Trauma Surgery and Surgical Critical Care
Department of Surgery
Creighton University
Omaha, Nebraska
Carrie D. Walsh, BA
Thomas Jefferson University
Philadelphia, Pennsylvania
Tracy S. Wang, MD, MPH
Professor
Chief, Section of Endocrine Surgery
Department of Surgery
Medical College of Wisconsin
Milwaukee, Wisconsin
Michael Weyant, MD
Professor
Division of Cardiothoracic Surgery
Department of Surgery
University of Colorado School of Medicine
Aurora, Colorado
Elizabeth C. Wick, MD
Associate Professor
Department of Surgery
The Johns Hopkins University School of Medicine
Baltimore, Maryland
Krzysztof Wikiel, MD
Assistant Professor of Surgery
Rocky Mountain Regional Veteran’s Affairs Medical Center
Aurora, Colorado
Arek Wiktor, MD, FACS
Assistant Director of the Burn Center
University of Colorado Hospital
Assistant Professor
Division of GI, Trauma, and Endocrine Surgery
Department of Surgery
University of Colorado School of Medicine
Aurora, Colorado
David J. Winchester, MD
Senior Attending
Department of Surgery
NorthShore University HealthSystem
Evanston, Illinois
Clinical Professor
Department of Surgery
University of Chicago
Chicago, Illinois
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Contributors xxiii
Steven E. Wolf, MD, FACS
Chief of Staff
Shriners Hospitals for Children - Galveston
Professor and Chief
JD and LH Jamail Distinguished Chair
Division of Burn and Trauma Surgery
Vice-Chairman, Finance
Department of Surgery
University of Texas Medical Branch,
Galveston, Texas
Franklin L. Wright, MD
Assistant Professor
Division of GI, Trauma, and Endocrine Surgery
Department of Surgery
University of Colorado School of Medicine
Aurora, Colorado
Charles J. Yeo, MD, FACS
Samuel D. Gross Professor and Chair
Department of Surgery
Sidney Kimmel Medical College at Thomas Jefferson
University
Philadelphia, Pennsylvania
Andrew J. Young, MD
Department of General Surgery
Naval Hospital Bremerton
Bremerton, Washington
Tonia M. Young-Fadok, MD
Professor of Surgery
Department of Surgery
Mayo Clinic College of Medicine
Phoenix, Arizona
Martha Zeiger, MD
S. Hurt Watts Professor and Chair
Department of Surgery
University of Virginia School of Medicine
Charlottesville, Virginia
Frank Z. Zhao, MD
Queen’s Medical Center
John A. Burns School of Medicine
University of Hawaii at Manoa
Honolulu, Hawaii
Brittany A. Zwischenberger, MD
Assistant Professor
Division of Cardiothoracic Surgery
Department of Surgery
Duke University
Durham, North Carolina
Joseph B. Zwischenberger, MD
Johnston-Wright Professor and Chair
Department of Surgery
University of Kentucky
Lexington, Kentucky
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xxv
variation (“I do it my way because of what I was taught
35 years ago”)
This sixth edition presupposes that surgeons will be the key
managers of many prevalent medical problems. The present
editors have added experts and expertise consistent with the
immense new knowledge that contributes to better (i.e., more
valuable) care for all of our patients. But these Surgical Decision
Making algorithms do not substitute for judgment. The humility
of Eiseman etal.’s preface to the third edition still stands:
Clinicians understandably resist the idea of reducing multifactorial decisions, which are subject to variations of the patient and the provider, to simple line drawings. A cookbook approach to problem solving cannot pos- sibly reflect the circumstances under which the surgeon exercises judgment. This book is not intended to prescribe behavior in every instance. It offers the reader an oppor-
tunity to follow the logic of an expert in selecting the best among many competing options of diagnosis and
treatment.
And I would argue that as the data and the complexities in
diagnostics and therapeutics have expanded, the need for simplic-
ity and default best-practice algorithms becomes even more
critical as a starting point for determining a continued optimiza-
tion of surgical care.
As one of my former colleagues at Geisinger stated, “This is
the stuff every surgical trainee should know if he or she is to
pass the specialty board exams.”
iii
Ben Eiseman and colleagues first conceived of best-practice
decision trees applied to prevalent surgical diagnoses and treat-
ments in the late 1970s.
i,ii
At that time, care pathways, bundled
care episodes, cost-effectiveness analysis for individual patients
or patient cohorts, and the transition from analog to digital
information flow were irrelevant. Or perhaps these ideas were
aspirations for a few forward-thinking clinicians, for a few
researchers interested in health policy and payment reform, and
for elite informaticians dealing largely with complicated datasets
not in the health-care universe.
Six editions later, Surgical Decision Making algorithms could
be viewed as having led the way, as a “forcing function” in
coalescing default best practice in an ever-more-complex popula-
tion of data. Surgical Decision Making has been and still is a
practical attempt to optimize the everyday management of
common surgical diseases.
Many of the dilemmas apparent at the inception of the series
are still present:
• How t c to a consensus on best practice in diagnostic
and therapeutic approaches
• How t continuously update clinical expertise with an
ever-expanding and dynamic basic and clinical research database
• How to define and update intermediate- and long-term quality
metrics
• And most importantly, how to balance the art and the science
of care without creating one of the popular false polarities in health care—cookbook medicine (one care template that fits all patients) versus “seat of the pants” individual
Preface
iii
Casale, A., Paulus, R., Selna, M., Doll, M., Bothe, A., McKinley, K.,
Berry, S., Da D., Gilfillan, R., Hamory, B., Steele, G. 2007. “Proven-
CareSM”: a provider-driven pay-for-performance program for acute
episodic car surgical care. Annals of Surgery 246 (4), 613–621.
i
Norton, L., Steele, G., Eiseman, B. 1978. Surgical Decision Making.
W.B. Saunders Company, Philadelphia.
ii
Eiseman, B Robinson, W., Steele, G. 1982. Follow-Up of the Cancer
Patient. Thieme-Stratton, New York.
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2
assumed to have CAD until proven otherwise. Routine preopera-
tive laboratory testing is not indicated unless the patient’s car-
diovascular comorbidities and/or the invasiveness of the operation
indicate it.
In patients with pulmonary disease and a recent change in
symptoms, preoperative chest x-ray is indicated to assess
for the presence of acute or progressive disease. Patients with
stable disease need not undergo chest x-ray. Pulmonary function
tests (PFTs) and arterial blood gases (ABGs) may be warranted
in patients with significant obstructive/reactive airway disease
undergoing thoracic or upper abdominal surgery but should
not be done in all patients. Spirometry may be helpful in a
patient with chronic obstructive pulmonary disease or asthma
if, after clinical assessment, it is uncertain whether the degree
of airflow obstruction has been optimally reduced. A partial
pressure of arterial carbon dioxide (PaCO
2) greater than 45  mm
Hg is a risk factor for pulmonary complications. Risk reduction
can include cessation of smoking for 8 weeks before operation,
airflow reduction with bronchodilators or steroids, elimination
of infection, and instruction on lung-expansion maneuvers.
CBC, liver function tests (LFTs), prothrombin time (PT),
international normalized ratio (INR), and partial throm-
boplastin time (PTT) are indicated in patients with a history of
advanced liver disease because these patients are at increased
risk for perioperative infections, hemorrhage, and wound
complications. It remains controversial whether diabetes mellitus
is an independent risk factor for perioperative complications,
unless it is poorly controlled. Thus checking the HgbA1c is
reasonable if the planned surgery would be delayed to optimize
glycemic control. Although mild to moderate malnutrition does
not affect perioperative complications, patients with severe
malnutrition may have significant anemia, electrolyte disturbances,
and coagulation defects. Severely malnourished patients undergo-
ing elective surgery may benefit from preoperative nutritional
support. Serum albumin level is a very reliable indicator of
increased operative risk.
Renal dysfunction predisposes to electrolyte disturbances,
which increase the risk for anesthetic complications and
perioperative arrhythmias. Thus assessment and normalization
of preoperative electrolyte abnormalities and anemia are
indicated.
A history of hematologic disorders such as anemia, throm-
bocytopenia, or bleeding tendency should be investigated.
Malignancy affects perioperative morbidity and warrants a search
for anemia, thrombocytopenia, and coagulation abnormalities
if this has not previously been completed.
A social history is important in identifying patients with a
significant history of alcohol or tobacco abuse. Identification
of liver disease in patients with a significant history of alcohol
abuse may permit medical optimization before elective surgery.
Cessation of smoking 4 weeks before surgery significantly reduces
perioperative pulmonary complications. Concern that stopping
smoking only a few weeks before surgery might worsen clinical
outcomes has not been found in recent studies, which show no
increase in complications. Routine preoperative laboratory testing
in patients with a history of alcohol or smoking use is not recom-
mended unless there is high suspicion of disease.
F
G
H
I
J
The estimated cost of preoperative testing in the United
States is between $3 billion and $18 billion each year. The
majority of these tests are unnecessary and do not change
perioperative morbidity or mortality or necessitate a change in
management. Additional testing to evaluate borderline or falsely
abnormal results further increases cost and, more important,
can lead to iatrogenic injury. Thus routine preoperative testing
should be avoided; instead, specific preoperative laboratory
evaluation should be performed to confirm or rule out medical
conditions that are likely to affect a patient’s perioperative course.
Laboratory testing within 6 months of the operative date is
acceptable if a patient’s medical history has not changed. A
thorough history and physical alone are 96% accurate in predicting
a patient’s fitness for surgery.
The magnitude and risk of the operative procedure should
be considered when determining the extent of preoperative
evaluation. Intracranial, thoracic, intraabdominal, and supra-
inguinal vascular operations are higher risk procedures. Multiple
studies, including two large randomized controlled trials, have
shown no difference in outcome between patients who underwent
routine versus no preoperative testing before low-risk ambulatory
surgery.
Asymptomatic patients without any comorbid disease who
can perform 4 metabolic equivalents (METS; e.g., walking,
golf, yard work) and are undergoing elective procedures need
no preoperative laboratory evaluation regardless of age. Abnormal
preoperative laboratory values in healthy, asymptomatic patients
do not predict postoperative adverse outcomes.
A basic metabolic panel (BMP) including electrolytes,
glucose, blood urea nitrogen, and creatinine is useful in
patients with seizure disorders because electrolyte abnormalities
may lower the seizure threshold during the perioperative period
and complicate antiseizure therapy. A history of stroke may
indicate a cardiac condition such as atrial fibrillation or simply
be a marker of systemic atherosclerotic disease; thus a complete
blood count (CBC), BMP, and electrocardiogram (ECG) should
be considered in those undergoing a high-risk procedure.
Patients with a known history of coronary artery disease
(CAD), and those with signs/symptoms or risk factors
indicative of CAD, may require further preoperative cardiac
evaluation (see Chapter 2, Preoperative Cardiac Evaluation).
Patients with evidence of peripheral vascular disease should be
A
B
C
D
E
Chapter 1
PREOPERATIVE
LABORATORY
EVALUATION
Stephanie Davis, MD, and
Christopher D. Raeburn, MD
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Chapter 1 ◆ Preoperative Laboratory Evaluation 2.e1
Abstract
A thorough history and physical alone are very accurate in
predicting a patient’s fitness for surgery. The majority of preopera-
tive tests are unnecessary and do not change perioperative
morbidity or mortality or necessitate a change in management.
Routine preoperative testing should be avoided; instead, specific
preoperative laboratory evaluation should be performed to
confirm or rule out medical conditions that are likely to affect
a patient’s perioperative course.
Keywords
preoperative risk
laboratory
surgery
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Chapter 1 ◆ Preoperative Laboratory Evaluation 3
A careful review of medications is important because certain
medications, such as anticoagulants and diuretics, may
increase the risk for perioperative morbidity. There are increasing
numbers of new oral anticoagulant (NOAC) medications available,
most of which do not have an accurate laboratory test to assess
the degree of anticoagulation effect. Thus it is important to
understand the indications for and half-life of these medications
to determine whether they should be held for surgery and if so,
for how long. Testing of renal function is important in determining
how long NOAC medication should be stopped before surgery.
For specific urologic procedures, a preoperative urinalysis
may be indicated. Alternatively, if a patient is complaining
of signs/symptoms that may indicate a urinary tract infection
(UTI), a urinalysis should be obtained.
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testing full blood count, electrolytes and urea, and pulmonary function
tests before elective surgery in patients with no apparent clinical
indication and in subgroups of patients with common comorbidities: a
systematic review of the clinical and cost-effective literature. Health
Technol Assess. 2012;16(50):1–159.
Matulis J, Liu S, Mecchella J, North F, Holmes A. Choosing wisely: a quality
improvement initiative to decrease unnecessary preoperative testing. BMJ
Qual Improv Rep. 2017;6(1).
Schein OD, Katz J, Bass EB, et al. The value of routine preoperative medical
testing before cataract surgery. Study of medical testing for cataract
surgery. N Engl J Med. 2000;342(3):168–175.
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4
Low-risk situations need no work-up in general. Perioperative
beta blockades should be continued in patients who have
been on beta blockers chronically. Conversely, beta blockers should
not be started on the day of surgery. In all other circumstances,
the initiation of beta blockers can be considered but must be
weighed as a risk–benefit ratio. The available clinical trials suggest
that starting beta blockers within 1 day of noncardiac surgery
is associated with a reduction in nonfatal myocardial infarction
(MI). However, the weight of evidence also suggests that this
benefit comes with an increased risk for stroke, death, hypotension,
and bradycardia. If a beta blockade is started, the dose must be
titrated to effect to avoid perioperative hypotension.
In general, patients with moderate or greater functional
capacity can proceed directly to surgery (metabolic equiva-
lents [METS] > 10, Class IIa recommendation; METS 4–10, Class
IIb recommendation).
Various noninvasive tests are now available for stress evalu-
ation. Stress testing can be from exercise, usually on a
treadmill with continuous electrocardiogram (ECG) monitoring,
or pharmacologic, as seen with dobutamine, dipyridamole, and
adenosine. Imaging studies, including echo and radionucleotide
studies (thallium, sesta-MIBI), reveal not only exercise capacity
but also the presence of previous MI and extent of reversible
ischemia. The choice of stressor and imaging techniques should
be determined in consultation with professionals who interpret
these tests and or institutional experience.
Although most would consider any abnormality on stress
imaging an indication for invasive testing, one may refer
to the appropriate clinical practice guidelines regarding the
appropriate indication for invasive testing. In general, revascu-
larization strategies should be based on standard indications as
outlined by the American College of Cardiology/American Heart
Association clinical practice guidelines for coronary revasculariza-
tion. Revascularization solely to reduce risk before noncardiac
surgery should not be performed.
Antiplatelet therapy arises from powerful medications that
reduce the risk for thrombosis in coronary stents. Although
aspirin fits into this category, the currently used medications
are much more effective in preventing thrombosis with the
correlated magnified risk for bleeding from intervention. Anti-
platelet therapy management perioperatively depends on various
characteristics, such as the urgency of the procedure, the bleeding
risk for the intervention, and the type of coronary stent. Most
important, if surgical delay will adversely affect patient outcome,
then operation must take precedence over stopping the antiplatelet
therapy. If the bleeding risk, in terms of either amount of bleeding
or adverse effects of bleeding, of the procedure is low, then there
may be little need for cessation of antiplatelet therapy. Given
the opportunity, the antiplatelet therapy should be continued
for at least 30 days with bare-metal stents or 1 year for drug-
eluting stents. Some patients with drug-eluting stents at low risk
for thrombosis may be able to hold antiplatelet therapy.
The optimal delay for therapy depends on the specific
medication. The length of delay should be explored specifi-
cally per the medication. The most commonly discussed is
clopidogrel, which should be held for a week. Other forms of
anticoagulation that should be considered to increased bleeding
D
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A careful history and physical examination, and prudent
evaluation of electrocardiograms and selected laboratory
tests, should be able to screen the majority of patients at risk
for noncardiac surgery. Important risk factors from the history
include increasing age (≥55 years), coronary artery disease (prior
myocardial infarction), history of prior cardiac revascularization—
either percutaneous coronary intervention or coronary artery
bypass grafting, history of heart failure, and prior stroke.
Numerous risk-prediction tools exist. The Revised Cardiac
Risk Index (RCRI), the American College of Surgeons
National Surgical Quality Improvement Program (NSQIP)
Myocardial Infarction and Cardiac Arrest (MICA) calculator,
and the American College of Surgeons NSQIP Risk Calculator
are three validated risk-prediction indices. Several caveats to the
universal implementation of risk calculators exist. Patients with
active major clinical predictors should be stabilized before surgery
(including unstable coronary syndromes such as ST-elevation
myocardial infarction [STEMI], non-ST-elevation myocardial
infarction [NSTEMI] or unstable angina, decompensated conges-
tive heart failure, significant arrhythmias, and severe valvular
disease). In the vast majority of cases, preoperative cardiac
evaluation should not delay or change plans for the primary
presenting problem. Finally, “cleared by cardiology” should never
substitute for good judgment and communication among surgeon,
anesthesiologist, and other treating physicians or allied health
providers.
Procedural risk has evolved into a combination of surgical
and patient characteristics in the current version of risk
modeling. This risk has also now become binary in definition,
with the two labels being low risk and elevated risk. Previous
versions of risk modeling had low-, intermediate-, and high-risk
categories. This has been simplified to low risk, meaning the
summative risk for the patient and the procedure predicts a risk
for a major adverse cardiac event (MACE) of <1%, whereas
elevated risk is any prediction of MACE ≥ 1%. This was simplified
because the recommendations for intermediate- and high-risk
stratification were similar. Examples of low-risk surgical proce-
dures include inguinal herniorrhaphy and procedures with
minimal fluid/volume shifts. Intraabdominal and intrathoracic
procedures are considered at elevated risk. Infrainguinal vascular
operations are elevated-risk procedures. Any emergent procedure
is considered as elevated risk. Because of the wide variety of
surgical procedures, it is difficult to absolutely classify many
procedures.
A
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Chapter 2
PREOPERATIVE
CARDIAC
EVALUATION
T. Brett Reece, MD, and
Joseph C. Cleveland, Jr., MD
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Chapter 2 ◆ Preoperative Cardiac Evaluation 4.e1
Keywords
preop evaluation
Abstract
The preoperative cardiac evaluation seeks to match patient and
procedural risks. In general, only patients with elevated risk and
low functional capacity need additional noninvasive imaging
prior to operation. All other patient risk and procedural risk
categories can proceed directly to operation.
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Chapter 2 ◆ Preoperative Cardiac Evaluation 5
risk (time for hold before at-risk surgery) are the medications
for treatment of atrial fibrillation, such as Coumadin (can be
reversed with fresh frozen plasma [FFP] or vitamin K), and
novel oral anticoagulants like rivaroxaban (Xarelto®, hold 1–3
days), apixaban (Eliquis®, hold 1–3 days), dabigatran (Pradaxa®,
hold 2–4 days), and edoxaban (Savaysa®, submitted to the U.S.
Food and Drug Administration [FDA]). All of these medications
are at least partially cleared by the kidneys, prolonging their
clearance in patients with renal insufficiency. Despite the short
half-lives, the bleeding risk from these medications within their
therapeutic windows can be considerable, which amplifies
the significance of the lack of reversal agent for these
medications.
REFERENCES
Fleisher LA, Fleischmann KE, Auerbach AD, et al. 2014 ACC/AHA guideline
on perioperative cardiovascular evaluation and management of patients
undergoing noncardiac surgery: a report of the American College of
History / physical exam / lab
Ischemic heart disease
Cerebrovascular disease
Congestive heart failure
Prior PCI
Prior CABG
Evaluate
preoperative
risk
Procedural risk
Low risk
Elevated risk/
low functional
capacity
Noninvasive study
Nuclear
echo
Coronary
angiogram
Normal
1, 2 vessel
CAD
Left main
3-vessel
CAD
PCI
CABG
Positive study
Moderate or high functional capacity
Negative study
O
p
e
r
a
t
i
o
n
C
B
D
A
E
G H
F
I
Cardiology/American Heart Association task force on practice guidelines.
J Am Coll Cardiol. 2014;64:e77–e137.
Fihn SD, Gardin JM, Abrams J, et al. 2012 ACCF/AHA/ACP/AATS/PCNA/
SCAI/STS guideline for the diagnosis and management of patients with
stable ischemic heart disease: a report of the American College of
Cardiology Foundation/American Heart Association Task Force on
Practice Guidelines, and the American College of Physicians, American
Association for Thoracic Surgery, Preventive Cardiovascular Nurses
Association, Society for Cardiovascular Angiography and Interventions,
and Society of Thoracic Surgeons. J Am Coll Cardiol. 2012;60:e44–e164.
Wijeysundera DN, Duncan D, Nkonde-Price C, et al. Perioperative beta
blockade in noncardiac surgery: a systematic review for the 2014
ACC/AHA guideline on perioperative cardiovascular evaluation and
management of patients undergoing noncardiac surgery: a report of the
American College of Cardiology/American Heart Association task force
on practice guidelines. Circulation. 2014;130:2246–2264.
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6
longer operations and operations involving general anesthesia
rather than regional anesthesia. These factors increase the risk
for development of postoperative pneumonia secondary to
chest wall pain or the inability to reliably ambulate in the early
postoperative period.
Because surgeons have special insight into the conduct of
an operation, we are uniquely situated to evaluate a patient
and identify concerns that could change the proposed surgical
plan. Evidence supporting the use of perioperative medical
consultation is inconsistent. Several studies have indicated that
medical consultation may be associated with inferior patient
outcomes and suboptimal resource utilization. Consequently,
the surgeon should remain at the forefront of perioperative
patient care.
Well-validated pulmonary-specific risk assessment tools exist
to help physicians determine which patients are at highest risk
for developing postoperative respiratory complications. Preopera-
tive risk stratification allows physicians to identify which patients
may benefit from further preoperative testing, additional preopera-
tive surgical optimization, and a more thorough discussion of
postoperative expectations and management.
The results of a preoperative history, physical examination,
review of relevant studies, and risk stratification help surgeons
identify patients who fall into the categories of low, moderate,
or high risk for postoperative pulmonary complications.
A patient deemed to be at low risk should not need additional
pulmonary-specific testing before an operation. Low-risk
variables include young patient age, normal room air oxygen
saturation, no history of recent respiratory infection, elective
operation, short procedural duration, and location of surgical
incision.
A patient who is considered moderate or high risk after
risk stratification should undergo additional pulmonary-
specific testing before proceeding with operative intervention.
In addition to obtaining a thorough history and physical
examination, preoperative pulmonary testing should include
laboratory studies, such as a complete blood count, serum
metabolic panel, serum albumin, and a posterior-anterior (PA)
and lateral chest radiograph (CXR).
Serum studies may help identify a pulmonary infection in a
patient with concerning symptoms and signs on history and
physical examination, anemia in a patient with unexplained
shortness of breath, and the presence of an underlying chronic
respiratory or metabolic acid–base disorder. Serum albumin may
identify patients with malnutrition, a known risk factor for
postoperative pulmonary complications. PA and lateral CXR
will evaluate the lung fields, chest wall, and mediastinal contour
in patients with concomitant medical conditions or a history of
tobacco use. Additionally, radiographs may help to refine a
diagnosis of preexisting infectious, inflammatory, neoplastic, and
anatomic abnormalities.
The results of routine preoperative assessment will further
stratify a patient into moderate or high risk.
Adjunct testing should be reserved for preoperative patients
with respiratory complaints when routine investigation is
unrevealing. Arterial blood gas (ABG) may identify respiratory
or metabolic acid–base disorders. Cross-sectional imaging, such
C
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Surgery and anesthesia involve the risk for postoperative pul-
monary complications (POPCs). The risk for POPCs depends
on patient, anesthetic, and surgical factors. The incidence is highly
variable in different studies and ranges from 2% to 40%. These
differences are likely due to variability in study design, definitions,
and patient population. Attributable mortality also ranges from
10% to 25%. Patients with POPC have increased intensive care
unit (ICU) admission, hospital length of stay, and hospital
readmission. POPCs include atelectasis, pneumonia, broncho-
spasm, tracheobronchitis, pleural effusion, pulmonary collapse,
acute lung injury, acute respiratory distress syndrome (ARDS),
prolonged mechanical ventilation, postoperative reintubation,
and respiratory failure. Annual costs attributable to POPCs are
$3.4 billion, with an average of $72,333 per patient. The highest
cost complication is respiratory failure with tracheostomy, which
averages $120,579.
A thorough history and physical examination are indicated
for all patients for whom operative intervention is being
considered. In addition to standard preoperative questioning,
respiratory symptoms should be addressed and further investi-
gated. Signs of underlying pulmonary disease found on the
physical examination should be well documented for future
reference.
In a systematic literature review, the American College of
Physicians identified several patient-related risk factors for
postoperative pulmonary complications. These risk factors include
advanced age, American Society of Anesthesiologist physical
status classification (ASA class), recent history of smoking,
abnormal imaging, limitations in functional status, active or
recent alcohol or tobacco use, presence of major comorbid medical
conditions, active cardiopulmonary disease, malnutrition defined
by acute fluctuations in weight, and the presence of impaired
sensorium (excluding stable chronic psychiatric or neurologic
conditions).
The risk for postoperative pulmonary complications is
increased by several procedural-related risk factors. Studies
indicate that the surgical site, type of operation, duration of
surgery, type of anesthesia used, and the possibility of an emergent
operation can all lead to increased risk for pulmonary
complications.
The risk for pulmonary complications is thought to be
highest after operations near the diaphragm, such as during
noncardiac thoracic surgery or upper gastrointestinal surgery.
Similarly, aortic surgery, neurosurgery, and head and neck surgery
also appear to increase the risk for postoperative pulmonary
complications. Other procedural-related risk factors include
A
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Chapter 3
PREOPERATIVE
PULMONARY
EVALUATION
Jordan R. H. Hoffman, MD, MPH, and
Robert A. Meguid, MD, MPH, FACS
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Chapter 3 ◆ Preoperative Pulmonary Evaluation 6.e1
Keywords
preoperative
pulmonary
evaluation
perioperative
work-up
lung
risk stratification
Abstract
Postoperative pulmonary complications are associated with poor
patient outcome, prolonged hospital stay and unplanned readmis-
sion. A thorough preoperative pulmonary work-up, including
a history and physical exam, as well as serum laboratory markers,
and dedicated chest imaging can help delineate which patients
are at higher risk for pulmonary complications. Additional
consideration should be made of the type, location and duration
of the planned operation. Risk stratification may help guide
preoperative optimization and decrease postoperative pulmonary
complications. Additionally, postoperative strategies exist to
decrease postoperative pulmonary complications.
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Chapter 3 ◆ Preoperative Pulmonary Evaluation 7
as a noncontrast or intravenous (IV) contrast chest computed
tomography (CT) scan, will evaluate the pulmonary parenchyma
and pulmonary vasculature and provide additional definition
of the chest wall or muscles of respiration. Spirometry will detect
restrictive or obstructive respiratory disorders and, with the
addition of diffusion capacity, can help identify impairment in
the transfer of gas across the pulmonary capillary-alveolar
membrane. Pulmonary function testing (PFT) should not be
considered a routine part of the preoperative pulmonary workup
for nonthoracic surgery. PFTs should be used sparingly to answer
very specific questions regarding a patient’s lung mechanics. As
such, PFT results should not be used to exclude a patient from
an operation but should be viewed as part of a patient’s total
clinical picture. A ventilation–perfusion (V/Q) scan may be
helpful in identifying pulmonary shunting or dead space. Results
of these investigations may further help to risk-stratify patients.
Moderate-risk patients fall into one of three categories: (1)
no abnormalities found on preoperative laboratory studies
or imaging, (2) laboratory studies or imaging abnormalities
indicative of disease processes that are unlikely to increase patient
risk for postoperative complications, and (3) laboratory studies
or imaging abnormalities indicative of disease processes that are
modifiable with preoperative optimization. The first and second
categories of patients may proceed to surgery without further
pulmonary-specific testing. The third category of patients will
benefit from further preoperative optimization, which may help
minimize the risk for postoperative pulmonary complications.
High-risk patients have abnormal, irreversible preoperative
findings placing them at prohibitive surgical risk. In the
event of emergency surgery, every attempt should be made to
optimize preoperative pulmonary function. In addition, aggressive
postoperative measures to minimize pulmonary morbidity should
be instituted early. Consideration should be given to nonoperative
management in patients deemed high risk.
H
I
Prevention of postoperative pulmonary complications begins
before a patient entering the operating room. Preoperative
smoking cessation has been shown to have dramatic effects on
postoperative pulmonary recovery. Patients should be encouraged
to abstain from smoking before an operation. Although data are
conflicting regarding the optimal length of time between smoking
cessation and surgery, most clinicians agree that there is benefit
to even a short duration of cigarette abstinence, such as 2 weeks
before an operation. If time permits, smoking cessation should
be encouraged for at least 8 weeks before surgery. Patients with
stable asthma or chronic obstructive pulmonary disease (COPD)
should be medically optimized. Oral glucocorticoids should be
weaned to an acceptable level. Patients should be evaluated and
treated for obstructive sleep apnea (OSA) before elective opera-
tions. Enrolling patients in preoperative pulmonary rehabilitation
programs should be considered when an operation can be safely
delayed for several months. Consideration should be given to
delaying an elective operation in patients with active, or recent,
upper or lower respiratory tract infections. Active respiratory
tract infections can cause difficulty oxygenating or ventilating,
postoperative bronchospasm, postoperative tussis leading to
increased intraabdominal pressure, inability to clear secretions,
superimposed bacterial pneumonia, and ARDS. Because of this,
most authors agree that an elective operation should be delayed
during the acute phase of a respiratory tract infection, or at least
2 weeks. Some clinicians will postpone operative intervention
for greater than 2 weeks depending on the likelihood of postopera-
tive pulmonary complications after an operation. Last, patients
should be given education on the importance of minimizing
postoperative pulmonary complications. Smoking cessation,
medication adherence, initiation or continuation of aerobic
exercise programs, and breathing exercises should all be
encouraged.
For patients proceeding to operative intervention, several
intraoperative interventions have been demonstrated to
J
K
Patient-related risks
-Age
-Pulmonary symptoms
-Functional and general
health status
-Tobacco use history
-Medical comorbidities
Procedural risks
-Surgical site
-Type of operation
-Duration of surgery
-Type of anesthesia
-Emergent procedure
“Low” risk
“Moderate” or “high” risk
Pulmonary specific testing
-PA and lateral CXR
-Laboratory studies
Adjunct testing
-ABG
-Cross-sectional imaging
-Spirometry and diffusion
capacity
-Ventilation/perfusion (V/Q)
scan
Abnormal (“high” risk)
Normal (“moderate” risk)
Perioperative optimization
-Optimize medications
-Preoperative incentive
spirometer use
-Smoking cessation
-Evaluation and treatment of
OSA
-Preoperative pulmonary
rehabilitation
-Patient education
-Delay operation
Proceed to surgery
-Anesthetic strategy
-Minimally invasive
approach
-Avoid or reverse
neuromuscular
blockade
-Minimize procedure
duration
Consider non-operative
management
Postoperative considerations
-Early mobilization & frequent
ambulation
-HOB > 30°
-Aspiration precautions
-Adequate pain control
-Incentive spirometer/flutter
valve use
-VTE prophylaxis
Preoperative Pulmonary Evaluation
Perioperative risk assessment
C
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F
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H
J
K
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8 Part I ◆ Perioperative Care
evidence suggests continuing prophylactic anticoagulation beyond
the primary hospitalization for further VTE risk reduction in
select populations.
CONCLUSIONS
Successful care of the surgical patient is a rewarding endeavor
and begins weeks to months before any operative intervention
is undertaken. The surgeon is ideally suited to address all aspects
of perioperative medical and surgical care. Given the nature of
our long-term commitment to a patient considering an operation,
surgeons will remain at the helm when a patient is being prepared
for an operation.
REFERENCES
American Society of Anesthesiologists Task Force on Perioperative
Management of Patients with Obstructive Sleep Apnea. Practice
guidelines for the perioperative management of patients with
obstructive sleep apnea: an updated report by the American Society of
Anesthesiologists task force on perioperative management of patients
with obstructive sleep apnea. Anesthesiology. 2014;120(2):268–286.
Auerbach AD, et al. Opportunity missed: medical consultation, resource use,
and quality of care of patients undergoing major surgery. Arch Intern
Med. 2007;167(21):2338–2344.
Bergqvist D, et al. Duration of prophylaxis against venous thromboembolism
with enoxaparin after surgery for cancer. N Engl J Med. 2002;346(13):
975.
Bilimoria KY, et al. Development and evaluation of the universal ACS NSQIP
surgical risk calculator: a decision aid and informed consent tool for
patients and surgeons. J Am Coll Surg. 2013;217:833–842.
Brooks-Brunn JA. Predictors of postoperative pulmonary complications
following abdominal surgery. Chest. 1997;111(3):564.
Canet J, et al. Prediction of postoperative pulmonary complications in a
population-based surgical cohort. Anesthesiology. 2010;113(6):1338–1350.
Grosse-Sundrup M, et al. Intermediate acting non-depolarizing
neuromuscular blocking agents and risk of postoperative respiratory
complications: prospective propensity score matched cohort study. BMJ.
2012;345(6329).
Hausman MS, et al. Regional versus general anesthesia in surgical patients
with chronic obstructive pulmonary disease: does avoiding general
anesthesia reduce the risk of postoperative complications? Anesth Analg.
2015;12(6):1405.
Mastracci TM, et al. Effect of preoperative smoking cessation interventions
on postoperative complications. J Am Coll Surg. 2011;212(6):1094.
Meguid RA, et al. Surgical risk preoperative assessment system (SURPAS): III.
Preoperative prediction of adverse outcomes with eight predictor
variables. Annals Surg. 2016;264(1):23–31.
Qaseem A, et al. Risk assessment for and strategies to reduce perioperative
pulmonary complications for patients undergoing noncardiothoracic
surgery: a guideline from the American College of Physicians. Ann Intern
Med. 2006;144(8):575.
Rodgers A, et al. Reduction of postoperative mortality and morbidity with
epidural or spinal anaesthesia: results from overview of randomised trials.
BMJ. 2000;321(7525):1493.
Smetana GW, et al. Preoperative pulmonary risk stratification for
noncardiothoracic surgery: systematic review for the American College of
Physicians. Ann Intern Med. 2006;144(8):581.
Wijeysundera DN, et al. Outcomes and processes of care related to
preoperative medical consultation. Arch Intern Med. 2010;170(15):1365.
decrease the risk for postoperative pulmonary complications.
Minimizing the duration of an operation by choosing a less
aggressive surgical approach has been shown to reduce postopera-
tive pneumonia in moderate- to high-risk patients. Conflicting
data exist regarding the use of regional versus general anesthesia
and its effect on postoperative pulmonary outcomes. When
feasible, a spinal, epidural, or regional anesthetic strategy should
be used for high-risk surgical patients. Similarly, minimally
invasive surgical options should also be considered in high-risk
patients. Last, neuromuscular blockade should be used sparingly
and should be completely reversed before extubation.
Consideration should be given to nonoperative management
in patients deemed at high risk for developing postoperative
pulmonary complications.
The immediate postoperative period is characterized by an
assault on the respiratory system. After major abdominal
or thoracic surgery, patients typically experience a reduction in
lung volumes for several weeks to months. Inadequate postopera-
tive pain control can cause a restrictive pattern of breathing.
Splinting, in conjunction with the possibility of diaphragm
dysfunction, particularly after noncardiac thoracic surgery,
increases patient risk for atelectasis, aspiration, and pneumonia.
This risk is compounded by postoperative opioid use, which
depresses respiratory drive.
Strategies to increase patient lung volumes and respiratory
drive will attenuate much of the possibility for postoperative
pulmonary morbidity. Measures aimed at minimizing aspiration
and pneumonia, including elevation of the head of the bed (HOB)
to at least 30 degrees above horizontal, early mobilization and
frequent ambulation, and avoidance of the use of nasogastric
tubes, should be instituted. A routine and progressively more
frequent ambulation schedule should be instituted and empha-
sized by everyone on the multidisciplinary care team. The benefit
of incentive spirometer use in the postoperative period is debated.
However, an incentive spirometer for deep breathing should be
provided to all postoperative patients. Counseling on the impor-
tance of accurate use and frequency should be provided and
reinforced daily. Adjuncts to narcotic pain control should be
provided to minimize respiratory depression while maintaining
an adequate level of pain control to prevent respiratory splinting.
These adjuncts include scheduled nonopioid pain medications,
placement of ice and local anesthetic–infused patches over the
operative site, centrally acting gamma-aminobutyric acid (GABA)
analogs, and liberal use of local anesthetic injection before, during,
and after an operation.
Last, early prophylactic subcutaneous anticoagulation in con-
junction with intermittent lower-extremity compression minimizes
the risk for venous thromboembolic (VTE) disease. Mounting
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10
to take into consideration that the patient’s hematocrit can affect
platelet function. The optimal hematocrit for platelets to function
is 30%. This occurs through margination, a process in which
the red blood cells push platelets to the periphery of vessels.
The prothrombin time (PT), more commonly referred to
as the international normalized ratio (INR), and activated
partial thromboplastin time (PTT) are often used as first-line
screening for bleeding risk. The PT was originally designed to
measure the effects of warfarin or detect liver disease and the
PTT to identify hemophilia A/B. However, these plasma-based
assays reflect circulating levels of clotting factors in the extrinsic
and intrinsic clotting pathways and thus do not represent the
physiology of hemostasis in accordance with the now accepted
cell-based concept of clotting. Consequently, changes in INR
and PTT are relatively nonspecific when applied beyond the
measurement of hereditary coagulation abnormalities and medi-
cally induced anticoagulation.
Fibrinogen plays a critical role in hemostasis because it is
the precursor to fibrin, which binds platelets. Fibrinogen
is an acute-phase reactant, and levels are generally preserved
even with liver failure. Low levels of fibrinogen are a result of
massive blood loss, consumption, dilution, hyperfibrinolysis, or
sustained metabolic acidosis. A fibrinogen level, measured by
the Clauss assay, of less than 150  mg/dL is usually the threshold
for treating active bleeding. Viscoelastic assays also have specific
tests that can measure fibrinogen activity (TEG functional
fibrinogen and ROTEM FIBTEM). Fibrinogen deficiency in the
United States is treated with cryoprecipitate, whereas in Europe,
a recombinant fibrinogen product is available.
D-Dimers are a clinical assay to measure degradation
products of fibrinolysis. Although an elevated level of
D-dimer is concerning for overactivation of the fibrinolytic system
(hyperfibrinolysis), this is a nonspecific finding. Any tissue injury
related to operative interventions will elevate levels. As a result,
they hold limited utility in the postoperative surgical patient.
However, in certain circumstances, such as obstetrics and septic
patients in the intensive care unit, a rising D-dimer level with
concurrent fibrinogen depletion is concerning for disseminated
intravascular coagulation, warranting further work-up. The
treatment for this pathology is to treat the underlying cause and
not give an antifibrinolytic.
Thromboelastography (TEG) or rotational thromboelas-
tometry (ROTEM) are gaining prominence in the assessment
of surgical bleeding because these devices reflect the individual
components of the cell-based concept of hemostasis. Current
indications primarily involve the assessment of abnormalities
in the clotting cascade during active blood product replacement
for significant bleeding. Measurements provided by TEG can
guide ongoing transfusion needs. Specifically, an elevated activated
clotting time (ACT > 128 secs) indicates the need for coagulation
factors, and thus FFP should be administered. If the angle of
the TEG tracing is decreased (<65 degrees), cryoprecipitate is
given. If the maximal amplitude of clot is diminished (<55 mm),
platelets should be administered. If the LY 30 is >5%, fibrinolysis
is elevated, and tranexamic acid should be considered.
Platelet mapping refers to a category of studies that assess
the strength of the platelet plug and the contribution by a
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The first step to identifying potential bleeding abnormalities
is a thorough history and physical examination. Patients
who report prior episodes of significant bleeding after surgical,
endoscopic, or dental procedures are likely to have underlying
coagulation abnormalities. A history of easy bruising, petechia,
gingival bleeding, epistaxis, hemarthrosis, and heavy menstrual
flow in women also suggests an underlying bleeding disorder.
Similarly, patients with a family history of hospitalizations second-
ary to life-threatening bleeding should arouse concern. Chronic
renal and liver disease, malnutrition, leukemia, and autoimmune
disorders are risk factors for surgical bleeding. Finally, the patient’s
prescribed medications, specifically, any oral anticoagulant or
antiplatelet therapy, should be reviewed, and the most recent
time of ingestion is critical. However, the most important step
in a patient with a potential bleeding disorder is to determine
if the patient is actively bleeding and needs an immediate
intervention. Mechanical control of major bleeding is a priority,
and waiting for coagulation results before taking the patient for
definitive care will not benefit the patient. In this clinical scenario
of a massive transfusion, the blood bank needs to be alerted,
and early blood-based product resuscitation is needed. Conversely,
preemptive transfusions in a hemodynamically stable patient
with a presumed coagulation abnormality can be lethal. The
decision to transfuse blood products into a patient in preparation
for the operating room should be goal directed, with a laboratory-
based assay with a defined threshold for each blood product
administered that is coordinated with the timing of the operative
intervention.
A complete blood count (CBC) provides a gross measurement
of the patient’s circulating cellular components that con-
tribute to coagulation. A normal CBC in a patient suspected to
have ongoing bleeding does not rule out active bleeding and
requires serial monitoring if there is a high clinical suspicion.
The same is true for a low hemoglobin, which can suggest occult
internal hemorrhage, chronic anemia resulting from an underlying
disease, or potential bone marrow failure. Platelet counts provide
a crude measurement of coagulation function. There is an
increased risk for bleeding as platelet counts decrease below
100,000. However, it is not until patients reach a critical threshold
of less than 20,000 that they are at risk for spontaneous bleeding.
Also, a normal platelet count does not rule out platelet dysfunc-
tion. Conversely, in certain disease states, such as cirrhosis, an
adaptive response to low platelet counts by the coagulation system
develops, and the patient can be paradoxically hypercoagulable
despite the abnormally low platelet count. It is also important
A
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Chapter 4
BLEEDING
DISORDERS IN
SURGICAL PATIENTS
Jason M. Samuels, MD,
Hunter Burroughs Moore, MD, PhD,
and Ernest E. Moore, MD
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Chapter 4 ◆ Bleeding Disorders in Surgical Patients 10.e1
Abstract
One of the most common indications for and complications of
surgery is bleeding. Patients may be at an elevated risk for bleeding
as a result of inherited abnormalities, chronic medical conditions,
or pharmacologic therapies, and the apt surgeon should be able
to identify and address each of these. Moreover, the tests to
identify abnormalities in coagulopathy, either intrinsic or extrinsic,
continue to advance with newer studies, such as thromboelas-
tography and platelet aggregometry. With advancements in the
assessment of coagulation, therapy for bleeding, in addition to
surgical correction when indicated, has become more goal
directed, with blood products and other medication given based
on laboratory findings. Specifically, when bleeding is worsened
by coagulopathy in trauma, the response is to correct the
abnormalities in the different aspects of clot formation, such as
replacing platelets when the platelet plug strength is diminished.
As a result of the increasing specificity of the management of
bleeding, an algorithm provides a roadmap to addressing underly-
ing factors that may prolong or worsen bleeding before or after
a surgical intervention is undertaken.
Keywords
bleeding
hemorrhage
resuscitation
coagulation
thromboelastography
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Chapter 4 ◆ Bleeding Disorders in Surgical Patients 11
variety of platelet receptors that are common drug targets. These
are most commonly used to assess the response to a variety of
antiplatelet medications, including aspirin and clopidogrel.
Surgical services have begun implementing these studies to assess
the risk for bleeding in a patient on these medications who
requires urgent surgical intervention. A minority of patients are
poor responders to these antiplatelet regimens and thus may
not require a delay before surgery once confirmed by a platelet
mapping study.
For massively bleeding patients, early blood component
therapy is essential. To prevent the development of a
dilutional coagulopathy, red blood cell (RBC) transfusions should
be administered in a ratio of 2 to 1 with fresh frozen plasma
(FFP). FFP not only provides a myriad of clotting proteins but
is also the optimal colloid to reverse shock. Early administration
of platelets and cryoprecipitate is recommended, although the
exact ratio of platelets to other products is of ongoing scientific
debate. The ideal management now appears to be with the
guidance of TEG or ROTEM.
Liver disease is frequently encountered among trauma and
transplant services. This presents most often with an elevated
INR but commonly coexists with other coagulation study
abnormalities. Management of mild bleeding can begin with
the administration of IV vitamin K, which leads to an effect in
8 hours. More rapid correction of the INR can occur with
prothrombin complex concentrate (PCC), although data dem-
onstrating a benefit are lacking in the setting of cirrhosis. In
addition, FFP and cryoprecipitate can replace deficient factors
and fibrinogen in a patient with poor hepatic synthetic function
with ongoing bleeding.
Trauma-induced coagulopathy is often seen in severely
injured patients. This is best managed by a TEG-guided
resuscitation strategy as described previously. Of note, in patients
H
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with an abnormal TEG but without signs of active hemorrhage,
product administration may not be required.
Fibrinolysis historically was managed by fibrinogen replace-
ment with cryoprecipitate administration while treating
the underlying cause. The newer agents tranexamic acid and
aminocaproic acid can shut down fibrinolysis and thus provide
an early treatment strategy when fibrinolysis is ongoing. Identify-
ing which patients require antifibrinolytic therapy can be
accomplished with TEG. If the lysis at 30 minutes is 5% or
greater, antifibrinolytic therapy should be initiated in trauma.
However, during elective surgery, the indications for using
antifibrinolytics are different. Preemptive tranexamic acid (TXA)
has been demonstrated to reduce surgical bleeding in high-risk
obstetric, cardiac, and orthopedic surgery.
The most important management of bleeding in the setting
of consumptive coagulopathies such as disseminated
intravascular coagulation (DIC) begins with treatment of the
underlying cause (e.g., sepsis, pancreatitis, etc.). These patients
often face platelet, fibrinogen, and coagulation factor deficien-
cies and thus should receive transfusions of platelets, FFP, and
cryoprecipitate as indicated by laboratory and clinical studies
(e.g., platelet number, fibrinogen level, TEG studies). Specifically,
patients with platelets < 50k should receive a platelet trans
fusion, and those with fibrinogen level < 100 should receive
cryoprecipitate.
Platelet dysfunction is often a confounder because of the
common use of antiplatelet agents for cardiovascular disease.
Dual antiplatelet therapy (aspirin and clopidogrel) is now routine
for most endovascular stents. Chronic renal and liver disease
impairs platelet function, and there are rare inherited platelet
deficiencies. Heparin-induced thrombocytopenia is another cause
of thrombocytopenia in postoperative patients, presenting with
a decrease in platelet count of 50% or more and a total platelet
K
L
M
History and physical:
Previous surgical bleeding
Easy bruising
Family history
Medications
Chronic liver disease
Chronic renal disease
Hematologic disease
Collagen vascular disease
Recent illnesses
Bleeding
disorders
Labs:
Complete blood count
Prothrombin time (INR )
Activated partial thromboplastin
Time
Fibrinogen
Dimers
Thromboelastography
Platelet aggregometry
Massive
transfusion
Platelet
dysfunction
Liver disease
Renal disease
Consumptive
coagulopathies
Von Willebrand’s
disease
Hemophilias
Trauma induced
coagulopathy
Fibrinolysis
Non-warfarin
anticoagulants
Warfarin
Platelets
Plasma
Cryoprecipitate
DDAVP
Factor VIII
Factor IX
TXA
Dialysis
Anti-Xa
Direct thrombin
Heparin Protamine
Clopidogrel
aspirin
Inherited
Acquired
Praxbind, dialysis
Treat underlying cause
TEG
ROTEM
PCC
FFP
Goal Directed Therapy
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N
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D
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12 Part I ◆ Perioperative Care
Patients with milder forms of Von Willebrand’s disease
(types 1 and 2) with bleeding often respond well to
1-desamino-8-D-arginine-vasopressin (DDAVP) administration.
In patients with a complete absence of Von Willebrand’s factor
(type 3 disease), the first-line treatment in bleeding patients is
Von Willebrand’s factor where available. Alternatively, cryopre-
cipitate provides high levels of FVIII, or FFP may be used for
factor replacement.
Platelet dysfunction secondary to renal failure frequently
responds to DDAVP, although the mechanism behind the
rescue of uremic platelets is unknown. Although infrequently
used, cryoprecipitate is known to improve platelet function in
uremia, presumably via an endothelial mechanism. Dialysis should
be initiated as early as possible in bleeding uremic patients because
this will correct the underlying cause.
REFERENCES
Baraniuk S, Tilley BC, del Junco DJ, et al. Pragmatic randomized optimal
platelet and plasma ratios (PROPPR) trial: design, rationale and
implementation. Injury. 2014;45:1287–1295.
Gonzalez E, Moore EE, Moore HB. Management of trauma-induced
coagulopathy with thrombelastography. Crit Care Clin. 2017;33:119–134.
Gonzalez E, Moore EE, Moore HB, et al. Goal-directed hemostatic
resuscitation of trauma-induced coagulopathy: a pragmatic randomized
clinical trial comparing a viscoelastic assay to conventional coagulation
assays. Ann Surg. 2016;263:1051–1059.
Pollack CV Jr. Managing bleeding in anticoagulated patients in the emergency
care setting. J Emerg Med. 2013;45:467–477.
Trauma ACoSCo. ATLS Advanced Trauma Life Support for Doctors - Student
Course Manual. 9th ed. American College of Surgeons; 2012.
Q
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count < 150k. This typically occurs between 5 and 10 days after
heparin administration.
Warfarin therapy remains common and acts through the
reduction of liver-produced vitamin K–dependent factors
II, VII, IX, and X. Thus vitamin K is used for slow reversal of
warfarin, and FFP provides a more rapid effect. However, active
bleeding warrants direct replacement with four-component PCC.
Newer oral anticoagulants and heparin derivatives present
a challenge in the bleeding surgical patient. Patients receiving
unfractionated heparin may receive protamine if emergent reversal
of anticoagulation is necessary. Protamine is less efficacious with
low-molecular-weight heparin but may still be given for severe
bleeding. Patients receiving direct Xa inhibitors such as apixaban
and rivaroxaban can be reversed with PCC, although this practice
has not been demonstrated to be efficacious is clinical studies.
Moreover, surgeons should use this judiciously because PCC
increases the risk for thrombosis in these patients. Currently
only dabigatran, a direct thrombin inhibitor, has a reversal agent
(idarucizumab). This reversal agent has a prohibitive cost and
infrequent availability, and thus PCC or dialysis may be used to
reverse the anticoagulant effects as well.
Patients with hemophilia A and B should receive factor
concentrates when available. In settings where such agents
are unavailable, FFP may be administered; however, large volumes
are required for the desired effect. Cryoprecipitate may be used
in hemophilia A, but again, a large volume is required.
N
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14
arterial and venous thromboses equally, particularly in vascular
and cardiac surgery populations. The associated thrombotic risk
is highest in patients with higher levels of PF4-heparin antibodies,
drop in platelet count of more than 70%, or both. Although
patients can develop HITT after treatment with low-molecular-
weight heparin, the incidence is much higher in those treated
with unfractionated heparin.
Diagnosis of an inherited thrombophilia is often made after
presentation with an unprovoked VTE, and rarely with
arterial thrombosis. Common inherited hypercoagulable states
include factor V Leiden gene mutation, prothrombin G20210A
mutation, protein C and S deficiency, antithrombin deficiency,
and antiphospholipid syndrome (APS). Factor V Leiden gene
mutation is the most inherited thrombophilia and results in
resistance to activated protein C. It is diagnosed either by genetic
testing to identify the mutation or by functional activated protein
C assays. The second most common inherited thrombophilia,
prothrombin G20210A mutation results in increased circulating
prothrombin levels and is diagnosed by genetic testing (in the
presence or absence of anticoagulation). Proteins C and S are
vitamin K–dependent anticoagulants, and their deficiency is
confirmed by laboratory testing demonstrating decreased levels
(50% or less of normal) and free protein S antigen. A functional
assay is used to test for antithrombin deficiency; however, this
should not be done at the time of initial diagnosis because there
may be a transient reduction of antithrombin levels, leading to
misinterpretation. APS occurs as either a primary condition or
in the setting of another inherited rheumatologic disease, most
commonly systemic lupus erythematosus. Diagnosis is made
with immunoassays testing for antibodies to cardiolipin and
lupus anticoagulant along with dilute Russell viper venom test.
Clinical suspicion for HITT should be raised in patients
with recent exposure to heparin with an absolute platelet
count of ≤150,000 mm
3
or with a relative decrease ≥50% from
baseline. The 4 T’s score can be used to estimate HITT likelihood
and assesses the degree of thrombocytopenia, timing relative to
heparin exposure, presence of a thrombotic event, and other
causes of thrombocytopenia. The diagnosis is confirmed with
laboratory testing for heparin-dependent antibodies utilizing
serologic or functional assays or both.
HITT management should be initiated before laboratory
confirmation in those patients felt to have an intermediate
or high risk based on their 4 T’s score. Treatment includes removal
of all sources of heparin and initiation of anticoagulation with
either direct thrombin inhibitors (bivalirudin or argatroban) or
factor Xa inhibition (fondaparinux). Warfarin therapy should
not be used initially because there is an increased incidence of
warfarin-induced skin necrosis in HITT patients; however, once
appropriate anticoagulation is reached with another agent and
platelet counts have risen above 150,000  mm
3
, patients can
transition to warfarin for continued long-term anticoagulation.
The gold standard therapy for a newly diagnosed VTE is
continuous heparin infusion while transitioning to oral
warfarin therapy, a vitamin K antagonist. Warfarin dosage should
be titrated to obtain an international normalized ratio (INR) of
2.0 to 3.0. More novel oral anticoagulants include dabigatran, a
direct thrombin inhibitor, and direct factor Xa inhibitors such
as rivaroxaban and apixaban.
F
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Although a hypercoagulable patient may present with arterial
bed manifestations, most provoked and inherited causes
of hypercoagulability are diagnosed after venous thromboem-
bolism (VTE). VTE is classically associated with Virchow’s triad:
stasis, endothelial injury, and inherited or acquired hypercoagu-
lable state. In many patients, multiple risk factors are present at
the time of VTE diagnosis. Many pretest probability scoring
systems have been developed; however, the Wells score is the
most commonly used. In the presence of a Wells score ≤1 and
a normal D-dimer level, the pretest probability for VTE is 0.9%.
Common symptoms of acute VTE include swelling, pain,
and warmth of the involved extremity. History should include
questions about potential risk factors, history of previous
thrombosis events, and medications. A physical examination may
reveal calf or thigh tenderness, unilateral edema, erythema, and
in severe cases, loss of pedal pulses.
Further work-up includes laboratory testing and imaging.
Patients should have a complete blood count, including
platelets, and chemistries and liver function tests. Flow cytometry
can also be performed on a complete blood count to evaluate
for myeloproliferative disorders and paroxysmal nocturnal
hemoglobinuria. A coagulation profile should also be obtained
to evaluate prothrombin time and activated partial thromboplastin
time. A D-dimer level can be checked as part of the Wells score.
If there is clinical concern for pulmonary embolus (PE), an
arterial blood gas can evaluate for hypoxemia and/or hypocapnia.
Additionally, electrocardiography (ECG) may demonstrate
right-heart strain with inverted T-waves in the right precordial
and inferior leads. Duplex ultrasound is the gold standard for
diagnosing VTE of the extremities, whereas computed tomography
angiogram (CTA) of the chest is used to evaluate for PE.
Patients with a hypercoagulable state can be stratified into
two cohorts, provoked and inherited. Common causes of
provoked hypercoagulability include recent major surgery,
prolonged immobility (>48 hours), malignancy, major trauma,
and hormone replacement. Malignancies most often associated
with hypercoagulability in order of prevalence are lung (17%),
pancreas (10%), colorectal (8%), renal (8%), and prostate
(7%). Hormone replacement includes the use of oral contracep-
tives, hormonal replacement therapy (HRT), and testosterone
supplementation.
Heparin-induced thrombotic thrombocytopenia (HITT)
is another provoked cause of hypercoagulability in patients
with recent heparin exposure who possess antibodies against
complexes of platelet factor 4 (PF4) and heparin. It may affect
A
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Chapter 5
HYPERCOAGULABLE
PATIENT
Bryan A. Ehlert, MD
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Chapter 5 ◆ Hypercoagulable Patient 14.e1
Abstract
Hypercoagulable patients most commonly present with a new
diagnosis of venous thromboembolism (VTE). Virchow’s triad
of stasis, vascular injury, and hypercoagulability are the classic
risk factors associated with VTE. Patients are further stratified
into provoked and inherited hypercoagulable states, with many
patients overlapping into both cohorts. Venous duplex ultrasound
is the gold standard for VTE diagnosis, and anticoagulation should
be initiated in the absence of any contraindications. For patients
with provoked VTE, treatment should be continued for 3 months,
whereas those with unprovoked DVT or symptomatic pulmonary
embolus should be treated for 6 months. Indefinite anticoagulation
should be considered in patients with provoked DVT where the
underlying risk factor has not been resolved, patients with an
unprovoked symptomatic pulmonary embolus, patients with
active malignancy with low to moderate bleeding risk, and patients
with high-risk inherited thrombophilias. The Vienna Prediction
Model can also be used to estimate recurrence risk when establish-
ing an anticoagulation strategy.
Keywords
hypercoagulable state
venous thromboembolism
pulmonary embolus
thrombophilia
heparin-induced thrombotic thrombocytopenia
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Chapter 5 ◆ Hypercoagulable Patient 15
After diagnosis of acute VTE, anticoagulation should be
maintained for a minimum of 3 months in all patients. In
patients with a provoked VTE in which the prominent risk factor
or factors have been removed, cessation of therapy can occur
after 3 months. Patients with provoked VTE with persistent risk
factors (prolonged immobility, active malignancy, etc.) may benefit
from treatment for 6 months; furthermore, those with unprovoked
VTE should also be treated for 6 months. In any patient undergo-
ing treatment for more than 3 months, the risk for bleeding
versus the risk for recurrence should be considered. Evidence
suggests that a normal D-dimer level after 3 months of antico-
agulation is associated with decreased recurrence risk; however,
it is not recommended to routinely check D-dimer levels to
determine the need for continued anticoagulation because of
its low specificity. Indefinite anticoagulation beyond 6 months
is recommended for patients with unprovoked symptomatic PE,
recurrent unprovoked VTE, active malignancy with low to
moderate bleeding risk, and patients with high-risk inherited
thrombophilias: protein C or S deficiency, antithrombin deficiency,
homozygous factor V Leiden mutation, and homozygous
J
Heparin-induced
thrombotic
Thrombocytopenia
(HITT)
Hypercoagulable
patient
History/physical exam
Risk factors
- Wells score
Symptoms/exam
Imaging/labs
Provoked
Recent major surgery
Inherited
CBC
Chemistries
Coagulation profile
D-dimer
ABG
EKG
Lower extremity duplex U/S
CT angiogram chest
Prolonged immobility
Malignancy
Major trauma
Hormone replacement
Anticoagulation
DiagnosisT reatment
Prothrombin 20210A
Antiphospholipid syndrome
Protein C/S deficiency
Antithrombin deficiency
Factor V Leiden
Anticoagulation
Duration of treatment
- Vienna calculator
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F
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prothrombin gene mutations. Of note, heterozygous factor
V Leiden is not felt to be an indication for indefinite anticoagula-
tion. An additional resource for determining the duration of
anticoagulation after an initial unprovoked VTE is the Vienna
Prediction Model. This model uses a nomogram based on patient
gender, location of the initial VTE, and D-dimer levels. Based
on point values for each component, the risk for recurrence at
1 and 5 years is determined. The clinician can then use this
risk for recurrence to determine the need for continued
anticoagulation.
REFERENCES
Arepally GM, Ortel TL. Heparin-induced thrombocytopenia. N Engl J Med.
2006;355:809–817.
Eichinger S, Heinze G, Jandeck LM, Kyrle PA. Risk assessment of recurrence
in patients with unprovoked deep vein thrombosis or pulmonary
embolism: the Vienna Prediction Model. Circulation. 2010;121:1630–1636.
Kearon C, Akl EA, Ornelas J, et al. Antithrombotic therapy for VTE disease:
CHEST guidelines and expert panel report. Chest. 2016;149(2):315–352.
Stevens SM, Ansell JE. Thrombophilic evaluation in patients with acute
pulmonary embolism. Semin Respir Crit Care Med. 2017;38:107–120.
Downloaded for Adolfo Brea Andrade ([email protected]) at Autonomous University of Guadalajara from ClinicalKey.com by Elsevier on November 09, 2019.
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16
risk for infection given time on the mechanical ventilator, central
venous lines, and indwelling urinary catheters. The frequent use
of antibiotics in the ICU puts these patients at risk for multidrug-
resistant organism infections. The diagnosis of occult sepsis may
require additional radiographic evaluation by abdominal
ultrasound, computed tomography, or hepatobiliary iminodiacetic
acid scan.
The lower genitourinary tract infection is the most common
postoperative infectious cause of fever. Female and obese
patients are at the highest risk. Bacturia is present in 5% of
patients with indwelling catheters and increases at a rate of 3%
to 8%/catheter day. Clinical history has a high predictive value
in uncomplicated cystitis. A urinalysis should be obtained before
a urine culture. A negative result is a strong predictor of a negative
urine culture and excludes a urinary tract infection. A positive
urine culture is defined as >10
5
organisms.
Hospital-acquired pneumonia and ventilator-associated
pneumonia can be diagnosed clinically or by a bacteriological
diagnosis. Quantitative cultures should be drawn before starting
antibiotic therapy and tailored to cover organisms based on the
patient’s risk for carrying multidrug-resistant organisms.
Bacteremia in the postoperative patient is not common,
with a reported incidence of up to 3%. When present, it
carries a 20% to 35% mortality rate and up to 60% mortality
rate for ICU patients. Blood culture is the standard diagnostic
test but can have a low yield in the first 72 hours after surgery.
A temperature exceeding 39.4 °C in the early (hours to first
few days) postoperative period requires immediate evaluation
of the patient. All surgical dressings should be removed to inter-
rogate for evidence of a necrotizing soft tissue infection (NSTI).
The diagnosis is typically clinical and requires prompt surgical
intervention.
REFERENCES
American Thoracic Society; Infectious Diseases Society of America.
Guidelines for the management of adults with hospital-acquired,
ventilator-associated, and healthcare-associated pneumonia. Am J Respir
Crit Care Med. 2005;171:388–416.
Aubuchon JP, Dzik WS. Reports on clinical transfusion medicine in the early
days of transfusion. Transfusion. 2010;50:963–967.
Badillo AT, Sarani B, Evans SR. Optimizing the use of blood cultures in the
febrile postoperative patient. J Am Coll Surg. 2002;194(4):477–487.
Engoren M. Lack of association between atelectasis and fever. Chest.
1995;107:81–84.
Frank SM, Kluger MJ, Kunkel SL. Elevated thermostatic set point in
postoperative patients. Anesthesiology. 2000;93:1426–1431.
Garibaldi RA, Brodine S, Matsumiya S, Coleman M. Evidence for the
non-infectious etiology of early postoperative fever. Infect Control.
1985;6(7):273–277.
Lesnikov VA, Efermov OM, Korneava EA, Van Damme J, Billiau A.
Fever produced by intrahypothalamic injection of interleukin-1 and
interleukin-6. Cytokine. 1991;3:195–198.
Mackowiak PA. Drug fever: mechanisms, maxims and misconceptions. Am J
Med Sci. 1987;294(4):275–286.
Stovall RT, Haenal JB, Jenkins TC, et al. A negative urinalysis rules out
catheter-associated urinary tract infection in trauma patients in the
intensive care unit. J Am Coll Surg. 2013;217(1):162–166.
Ustin JS, Malangoni MA. Necrotizing soft-tissue infections. Crit Care Med.
2011;39(9).
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A careful history and physical examination should direct
the radiographic and laboratory work-up in the postoperative
period. Close attention should be paid to the pulmonary examina-
tion, prosthetic catheters, all surgical wounds, and the extremities.
The surgical wound classification and the time elapsed from
surgery are important determinants in the probability of the
wound being the source of the infectious causes. The incidence
of postoperative fever ranges from 15% to 47%. Two temperatures
greater than 38.5 °C within a 24-hour period constitute a
postoperative fever. Although there are both infectious and
noninfectious causes, the presence of a postop fever may herald
a serious complication.
Additional diagnostic work-up, including laboratory evalu-
ations of blood, urine, and pulmonary and wound fluids
should be guided by the physical examination findings.
Infectious causes in the postoperative period include surgical
site infection, pneumonia, urinary tract infection, and
intravascular catheter–associated infections.
Most fevers in the early postoperative period are caused by
inflammation and resolve spontaneously. Fever is activated
by circulating pyrogens. Exogenous pyrogens can directly cause
fevers (i.e., endotoxin [lipopolysaccharide]) or stimulate the
release of cytokines (TNF alpha, IL-6, IL1beta, INF-alpha, MIP-1)
from mononuclear phagocytes. Systemic levels of IL-6 correlate
with a postoperative increase in body temperature from baseline.
IL-6 is also influenced by the duration and invasiveness of the
procedure. Noninfectious causes in the early postoperative period
include inflammation from the trauma of surgery, nonhemolytic
febrile transfusion reactions (FNHTRs), and drug fevers. FNHTRs
are seen 1 to 6  hr post transfusion, and it is important to rule
out an acute hemolytic reaction. Antibiotics (i.e., beta-lactam
and sulfonamide) account for one-third of drug fevers. Atelectasis
is often cited as a noninfectious cause of fever, but its occurrence
is felt to be coincidental.
Surgical site infections are classified as incisional or organ/
space. Superficial (skin/soft tissue) and deep (soft tissue/
fascia) incisional are diagnosed by appearance on physical
examination. Organ/space surgical site infections are diagnosed
with diagnostic imaging, which is most useful 5 to 7 days
postoperative when most routine postsurgical fluid collections
have resolved.
Critically ill patients in the surgical intensive care unit (ICU)
are at risk for infections and may not mount a febrile
response given comorbidities and therapy. They are at increased
A
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Chapter 6
POSTOPERATIVE
FEVER
David J. Ciesla, MD, and
Thomas J. Herron, MD
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Chapter 6 ◆ Postoperative Fever 16.e1
Abstract
Fever is common after surgery. Although often a normal physi-
ologic response to tissue injury, it can also be a sign of more
serious causes that require prompt treatment. The presence of
a postoperative fever triggers a workup that directed at identifying
a source so that appropriate therapy is selected.
Keywords
Post-operative
Fever
Infection
Surgical site infection
Bacteremia
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Chapter 6 ◆ Postoperative Fever 17
History & physical examination:
                    Postoperative day
                    Wound classification
                    Pulmonary
                    Surgical wound
                    Extremities
                    Intravascular catheters
Temperature > 38.5 °C
Labs & radiographic imaging:
                    CBC
                    Urinaly sis +/− urine culture
                    Blood cultures
                    Ches t X-ray
                    Computed tomography
Noninfectious:
          Inflammatory response from surgery
          Febrile, nonhemolytic transfusion reaction
          Medi cation/drug fever
Infectious
Pneumonia
Urinary tract infection
Surgical site infection
Bacteremia
Surgical critical care:
                CA UTI
                CLABS I
                VA P
                Ac alculous cholecystitis
Necrotizing soft tissue
infection
C
A
B
D
E
F
G
H
I
J
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18
Some targeted studies have yielded results in this area
supporting continuation of AC throughout the procedure.
For example, the BRUISE CONTROL trial demonstrated
that allowing the INR to drift below 3 before pacemaker or
defibrillator placement was associated with fewer bleeding
events than the interruption of warfarin and a heparin bridge.
Usually, violation of a major body cavity, the axial skeleton, or
long bones; peripheral arterial surgery; tissue or organ biopsy;
or procedures lasting >1 hour are considered “major” and risk
for bleeding significantly higher. Ultimately, bleeding risk assess-
ment for a given procedure is best left to the discretion of the
proceduralist.
When discussing a bridge to AC, consideration is usually for
the use of heparin until which time an oral agent (usually a
VKA, given previously noted considerations) becomes therapeutic.
To Err Is Human, published by the Institute of Medicine, under-
scored that medication errors are the most frequent category of
inpatient preventable medical errors, and of those, heparin has
consistently been one of the top offenders. Mortality rates associ-
ated with bleeding events are about 10%, approximately the
same or more than a pulmonary embolism.
In 2015, the BRIDGE trial was published, a noninferiority
trial assessing the use of AC bridging in atrial fibrillation (afib)
patients. With more than 1800 subjects, the study demonstrated
noninferiority of nonbridging compared with bridging in the
perioperative period with respect to thromboembolic (TE) events
(three events in each group), whereas rates of major and minor
bleeding were significantly higher in the bridged group (major:
3.2% vs. 1.3%; minor 20.9% vs. 12%). Retrospective analyses
evaluating perioperative bridging strategies have yielded similar
results in the realms of deep venous thrombosis (DVT) and
mechanical heart valves.
Thromboembolic (TE) risk will vary based on the indication
for AC. Broadly, indications for AC are venous thrombo-
embolic event (VTE), specifically DVT or pulmonary embolism
(PE); nonvalvular afib; or mechanical heart valve (MHV). Risk
stratification should be performed for each indication, as
follows:
• VTE/PE: Patients may be categorized as high, moderate,
or low risk based on time since the initial event, underlying
thrombophilic disorders, and other comorbid conditions.
Recent publications suggest that the risks for low- and
moderate-risk groups are sufficiently similar that they may
be approached in the same fashion and do not necessitate
bridging.
• Nonvalvular afib: Risk stratification is best performed
utilizing the CHA2DS2-VASc score into low-, moderate-,
and high-risk groups for TE events. The acronym encom-
passes variables found to be predictive of stroke risk, and
a score is designated in a weighted fashion: Congestive
heart failure, Hypertension, Age ≥75 (for 2 points), Dia-
betes, prior Stroke or transient ischemic attack (TIA) (for
2 points), Vascular disease, Age 65 to 74, and Sex Category.
The “2017 Expert Consensus Decision Pathway for Peri-
procedural Management of Anticoagulation in Patients
With Nonvalvular Atrial Fibrillation” notes a CHA2DS2-
VASc score of 7 to 9 as high risk.
• MHV: Considerations include valve location (aortic, mitral,
other), type of mechanical valve, and whether other
concomitant risk factors exist. The stakes for mechanical
E
For elective procedures, a full history and physical should
be performed, including ascertaining which anticoagulant
(AC) the patient is taking and the indication for its use.
Until recently, vitamin K antagonists (VKAs) were the mainstay
of maintenance AC agents. Warfarin is the only VKA available
for use in the United States. Direct-acting oral anticoagulants
(DOACs) have been increasing in use and will likely continue
to do so, especially given their preference in recent AC guidelines.
If appropriate to restart the agent based on periprocedural
bleeding risk and stable renal and/or hepatic function (depending
on mode of clearance), they may be restarted without any bridge
given their rapidity of onset. DOACs currently are not recom-
mended for use for mechanical heart valves and should not be
considered as a replacement therapy for this indication for VKA
or heparin.
Current published literature regarding bridging strategies for
those on AC do not address interventions performed in urgent
or emergent circumstances; therefore extrapolation to those
clinical situations should be undertaken with caution, especially
because the need for the use of reversal agents for AC in those
circumstances may alter subsequent thrombotic potential.
Ascertain whether the patient has an ongoing need for AC,
ideally in conjunction with the patient’s primary care
provider. If the patient no longer needs AC, it should be stopped
in a time period sufficient for the patient to have no increased
bleeding risk at the time of the elective procedure.
Relevant labs should be assessed. These include at least
baseline prothrombin time (PT)/international normalized
ratio (INR) for those on a VKA to ascertain the degree of
anticoagulation and duration of time needed for the INR to
drift to the desired level before the procedure. Guidelines are
clear that cessation of AC in a time frame to allow for normaliza-
tion is much preferable to the aggressive use of reversal products
or agents. If bridging is recommended, this should also be
performed with an agent whose duration of action is sufficiently
short so as to be ceased just far enough ahead of the procedure
that the patient has the shortest time possible without AC.
Baseline creatinine is appropriate for those on DOACs that
are renally cleared and to assess the suitability of low-molecular-
weight heparin (LMWH) as a bridge, if indicated.
Assess risk for bleeding associated with the procedure.
For procedures that carry a low risk for bleeding, consid-
eration for the continuation of AC should be done. Low-risk
procedures are generally considered to be dental and dermatologic
procedures and endoscopy and procedures performed via cardiac
catheterization.
A
B
C
D
Chapter 7
BRIDGE
ANTICOAGULATION
Lisa Ferrigno, MD, MPH
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Chapter 7 ◆ Bridge Anticoagulation 18.e1
Abstract
This chapter covers periprocedural anticoagulation bridging.
Keywords
anticoagulation bridging
periprocedural
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Chapter 7 ◆ Bridge Anticoagulation 19
valve thrombosis are sufficiently high that interruptions
in AC have dogmatically been avoided. A recent review
demonstrated high rates of major bleeding episodes for
any bridging strategy (19%). Only two TE events occurred,
both of which were preceded by a bleeding event neces-
sitating reversal of bridging AC.
High risk for TE event: High-risk patients are underrepre-
sented in the available literature on bridging. In a recent
retrospective analysis specifically evaluating bridging in patients
with a history of DVT or PE, there were no thromboembolic
rates in the high-risk category, whether they were bridged or
not; however, the numbers of patients in this high-risk category
were exceedingly low. Ideally, elective procedures would be
deferred until the patient reaches a lower risk threshold with
respect to time from the acute event. For others who will carry
lifelong high risk, a balanced decision weighing risk versus benefit
should be performed, and the patient observed closely for bleeding
events, should bridging be performed.
Those at high risk for TE event should likely be bridged,
including the following:
• VTE
• Acute VTE within past 3 months; or
• Severe thrombophilia (deficiency of protein C, protein S,
or antithrombin; antiphospholipid antibody syndrome;
or multiple abnormalities)
• Afib: Those at high risk for stroke or systemic embolism ( >10%
per year) with
• CHA2DS2-VASc score of 7 to 9; or
• Recent (within 3 months) ischemic stroke, transient ische -
mic attack (TIA), or embolic event
F
• MHV
• Mitral valve replacement (MVR); or
• Aortic valve replacement (AVR) and any TE risk factor:
afib/flutter; left ventricular ejection fraction (LVEF) < 35%;
severe mitral stenosis (MS); hypercoagulable disorder; left
atrial dilation > 50 mm; prior TE; spontaneous contrast
in heart on ECHO; or
• Older-generation AVR
Moderate-risk individuals vary as to whether they should
be bridged or not, as follows:
• VTE/PE: Those with moderate risk do not require bridging.
• Acute VTE within past 3 to 12 months; or
• Nonsevere thrombophilia (heterozygous factor V Leiden,
prothrombin 20210 mutation, increased factor VIII activity);
or
• Recurrent VTE; or
• Active cancer
• Afib
• CHA2DS2-VASc score of 5 to 6; or
• Prior history of embolic ischemic stroke, TIA, or systemic
embolism (>3 months previously):
• High bleed risk: No bridge
• Lower bleed risk: Strategy determined based on whether
there is a history of prior TE event:
• Prior TE event: Likely bridge
• No TE event: Bridging not advised
• MHV: Bridge recommended
• MVR; or
• AVR and any TE risk factor: afib/flutter; LVEF < 35%;
severe multiple sclerosis (MS); hypercoagulable disorder;
G
Is AC
indicated?
High
Yes bridge
H&P:
- Indication
- Agent
Labs:
- PT/INR
- GFR
No longer
indicate d
DC
Yes
Assess peri-
procedural
bleeding
risk
Low
Modera te
Consider no interruption
Assess TE
risk
Low No bridge
Modera te
High
Valve
Ye
s bridge
VTE
Atrial
fibrillation
No bridge
NO prior TE event
Prior TE
event
No bridge
Yes bridge
A
B
C
D
E
F
G
H
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ja konjakkia. Kolmas panos oli tätä tavarata lopuillaan, kun toveri
nousi ja sanoi:
— Nyt on aika lähteä. Istu tässä ja odota se aikaa, korkeintaan
minä viivyn puolituntia, mutta hyvässä lykyssä vaan kymmenen
minuuttia.
Suppo jäi odottamaan. Ensin otti hän ja silmäili päivän sanomia
sen verran kuin silmä kykeni enää seuraamaan. Mutta kun ei niistä
mitään luettavata löytänyt, niin täytyi ne työntää syrjään. Sitten
meni hän toiseen huoneeseen katsomaan biljardinpelaajia. Ei sekään
miellyttänyt pitkälti. Häh kun ei ollut mikään pelaaja, niin ei voinut
tarjoutua mukaan peliin, eikä sitä katseleminenkaan huvittanut.
Niissä hommissa oli kuitenkin kulunut viisitoista minuuttia.
— Varmankaan ei ollut täti vielä kotona, koskapahan ei miestä
kuulu, arveli Suppo ja tilasi konjakkia, kun kahvia vielä oli.
Hän teki uudet kupit ja sytytti uuden sikarin… Tuonlaisissa tiloissa
polttavat herrat sikaritupakkaa. Sitten istui hän pää käden nojassa,
löyhäytteli hyvänhajuisia savuja ilmaan ja maisteli vähin erin
kupistaan. Hyvinvoinnin ja kylläisyyden suloinen tunne hiveli hänen
mieltään, täytti koko hänen olentonsa. Ei mitkään sisäiset soraäänet
häirinneet hänen rauhaansa ja hän tunsi olevansa sovinnollisella ja
suosiollisella mielellä koko maailmaa kohtaan.
Keppien räiske ja pallojen pauke kuului viereisestä huoneesta ja
niitä säistävä iloinen nauru, ihastushuudahtukset ja epätoivoisen
kiroukset sekä markköörin yksitoikkoinen, väsyttävä ääni: Valkonen
pallo!… Punanen pallo!… Valkonen pallo!… Punanen pallo!…

Samassa sekoitti tämän raikas naurunpajakka ja hyvähuudot. Joku
oli "tehnyt onnistuneen pallon".
Tästä säpsähti Suppo ja katsoi kelloa. Hän oli jo odottanut lähes
tunnin eikä miestä vielä kuulunut.
— Kummallista! Kovin merkillistä.
Hän nousi ja alkoi astua kahakäteen huoneessa.
— Kun nuokin ilkiävät kuluttaa aikaansa tuonlaisessa joutavassa
kuin biljardinpeluussa, miehiset miehet!
Ja samassa oli hyvänvoinnin tunne ja suloinen sopusointuisuus
kuin siivellä pyyhkäistyt miehestä ja outo kouristus tuntui
sydänalassa.
— Kukapas tässä rupesi kuivin suin odottamaan! Tottapahan tulee
kun joutuu, lohdutteli Suppo Saikkonen itseään ja tilasi yhä kahvia ja
konjakkia.
Mutta kuohuvata mieltä ei uusi panoskaan viihdyttänyt.
— Millä näistä kaikista selvitään, kun toinen tasku on tyhjä ja
toisessa ei ole mitään, tuskitteli hän itsekseen.
Suppo nousi taas ja alkoi rauhatoinna kulkea huoneessa. Hänen
rintaansa ahdisti ja mieltä ellosteli ytelästi, ja koko elämä tuntui niin
tuskalliselta.
Hän asettui ikkunan eteen istumaan, ett'eikö näkisi jonkun
tuttavan kulkevan ohitse, jolla olisi pelastus taskussa, ja
huvittavaahan oli muutenkin ajankuluksi kulkevia katsella.

— Soh, tuoltahan se tuleekin, äänsi Suppo riemuissaan ja lyödä
poukautti lasiin että ruudut oli säpäleiksi lentää.
Tuttava kuulikin ja katsahti ikkunaan ja kun huomasi Supon, alkoi
ystävällisesti nyökyttää päätään. Suppo viittilöi innokkaasti, että tulla
ja tulla sisään.
— Kahviako saan tarjota ja konjakkia? kysyi Suppo, kun tuttava
sisään astui.
— Ottaisin ennemmin punssia? sanoi tämä.
— Kahvia ja puolisko punssia! käski Suppo.
Tulihan sitä.
— Mitkäs kemut sillä Supolla nyt on? uteli toveri.
— Eihän tässä niin mitkään… tavallistahan tämä on.
Ottivat siitä ja maistelivat ja juttelivat, haastelivat ja nauroivat,
maistelivat ja iloitsivat, niinkuin hyvät tuttavat, veljet ainakin
herkkupöydän ääressä.
Toveri oli alussa hieman hämillään eikä tuntenut oikein
sopeutuvansa Supon tilaan, mutta vähin erin alkoi sydän sulaa ja
sopeutuminen syntyä.
— Yhhyh, kuinka tämä on imelätä ja meltoa, täytynee terästää,
sanoi
Suppo ja tilasi lisää konjakkia.
— Tätä kun lirauttaa sekaan, niin muuttuu se maku sanoi hän
saatuansa tuota haluttua nestettä.

Kun siitä toverinkin sydän alkoi auveta ja hellyys mieltä täyttää,
uskalsi Suppo kertoa asiansa ja selittää surullisen tilansa.
— Sepä on ikävä seikka tämä, eikä minullakaan ole markkaakaan
rahaa, surkutteli ystävä osaaottavasti.
— Otatko sinä nyt ja jäät tänne pantiksi, että minä pääsen rahaa
hankkimaan, vai menetkö sinä toimeen? Muu keino nyt ei auta,
puhui Suppo vakavasti.
— Eihän se sovi, että minä jään tänne… voisivat arvata. Parasta
on, että minä lähden tekemään mynttiä ja sinä istut vielä sen aikaa
täällä, selitti ystävä hartaasti.
Niin sovittiin tuosta tärkeästä seikasta ja toveri lähti ja niin kiireesti
lähtikin, ett'ei ehtinyt edes lasiaan pohjaan panna.
Suppo jäi yksin ja oli taas samassa tilassa, odottavassa asemassa,
kuin äsköinkin.
Odotusaika ei nyt kuitenkaan tullut niin pitkäksi, ja hyvä se olikin,
sillä päivällisvieraita alkoi jo saapua yksi toisensa perästä.
Tuskin oli nimittäin Suppo ehtinyt siemata pari kertaa lasistaan,
kun ovi aukeni ja kaupungin lähetti astui sisään. Niinkuin salamat
syksyistä iltaa, valasivat ilon leimaukset Supon muotoa, kun hän näki
miehen.
— Onko se herra Saikkonen? kysyi lähetti
— On.
Ja Suppo sai kirjeen ja lähetti poistui.

Siihen aikaan ei oltu vielä sähköä telefoonina saatu nujerretuksi
ihmisten palvelukseen, ei ainakaan Suomen pääkaupungissa, vaan
täytyi käyttää vanhoja viestinkuljettajia.
Suppo rapasi kirjeen auki, mutta ei mitään kirjavata paperia
ilmestynyt hänen silmiänsä viehättämään.
Paras Veljyt!
Enhän minä mistä voi hankkia rahaa niin sukkelaan…
koehan itse auttaa itseäsi!
Tuus totus
Poku.
Se oli kirjeen sisällys.
— Hädässä ystävä tutaan, oli ainoa, mitä Suppo sai sanotuksi,
kujeen luettuansa, vaikka monikin olisi luullut hänen kirota
karskauttelevan.
— Auta itseäsi! sen neuvon sitä osaa toiselle antaa mikä nokka
hyvänsä, mutta todellista apua ei kukaan tahdo kellekään tehdä.
Näin puhuen naukki hän juomain tähteet suuhunsa, otti lakkinsa ja
lähti.
Puhvetissa selitti hän aivan luonnollisesti, ett'ei hänellä nyt ole
rahaa, millä maksaa otoksensa, että toverit ovat häntä narrinaan
pitäneet ja jättäneet hänet pulaan, vaan pyysi saada käydä vasta
maksamassa.

Siitäkös mellakka nousi! Tuonlaista puhetta ei puhvettineiti ottanut
kuulevaan korvaansa, vaan alkoi sättiä ja parjata. Hätään joutui
isäntä raivoissaan ja vieraat kiertyivät Supon ympärille. Kuuli hän
siinä nimensä puolelta ja toiselta, nimi otettiin kirjaan ja uhattiin sillä
ja sillä, jos ei hetimiten käy maksamassa.
— Tulla ravintolaan syömään ja juomaan eikä ole rahaa
penniäkään taskussa! Hyi, hemmetti, senlaisia herroja! huusi
puhvettineiti ja sillä hän luuli sanoneensa kaiken pahan, mitä
tuonlaisesta miehestä sanoa saattoi.
Ja rähisten ja meluten saatettiin Suppo Saikkonen ulos.
— Olipa hyvä, ett'eivät lyöneet, arveli hän kadulla, päästyänsä
rähäkästä.
Näin onnistui yritys sinä päivänä, vaikka mies ensimmäisenä
vastaan tuli.
Asioitsija.
— Nyt tuli joku, isä! kuului lapsen ääni.
Isä nousi ja meni "konttoriin" katsomaan.
Siellä seisoi nuori nainen, joka ujosti kysyi palveluspaikkaa.
— Ei täällä ole sellaista nyt, vaan kyllä hankitaan, sanoi asioitsija.
— Jos toimittaisitte minulle.

Asioitsija kirjoitti naisen nimen ja asunnon kirjaansa.
— Sisäänkirjoitus maksaa markan.
— Minulla ei ole, vaan vasta…
— Hm… Eikö ole puoltakaan?
— Tuskin, sanoi nainen hätääntyneenä, kuivaten nousevia vesiä
silmistään.
— Eikö edes viittäkolmatta penniäkään, että saisin pullon olutta?
On niin elämä töhkyräistä, kun illalla tuli juotua, puhui asioitsija.
— Ehkäpä sen verran…
Nainen etsi rahakukkaron hameensa poimuista ja antoi lantit.
— Niin tulkaa sitten ylihuomena kuulemaan. Toivon siksi teille
paikan saavani.
— Kiittäen, kostaen lähti nainen.
— Laura, ehkä Alma joutaisi hakemaan pullon olutta ennenkuin
kouluun menee? kysyi asioitsija.
— Miks'ei, mutta meillä ei ole yhtään suupalaa ruokaa.
Syömättäkö
Alman pitää kouluun mennä? sanoi Laura, asioitsijan vaimo.
— Onhan se niin ennenkin… Etkös olekin? kysyi isä.
— Olen ja menen nytkin. Kyllä siellä joku taas minullekin pullaa
antaa, sanoi Alma reippaasti, vaikka vedet tahtoivat silmään kiertyä.

Lapsi lähti hakemaan isälleen olutta.
— Kuinka sinä voit olla tuollainen? kysyi vaimo, hieman
nuhtelevalla äänellä.
— Minkälainen? ärähti asioitsija tylysti. Minkälainen minä olen?
Miten sinä luulet minun muuten kykenevän toimeeni, jos en saa
lasillista olutta… kädet vapisee ja kaikki. Kyllähän tähän taas joku
tulee, että saamme rahaa ruokaan.
Alma toi olutpullon ja lähti syömättä kouluun. Nuorempi lapsi
nukkui vielä kyökin sängyssä.
Asioitsija avasi pullon ja vetäsi sen sisällyksen nahkaansa. Laura
laitteli rikkinäisen peilin edessä, joka vielä muistutti onnellisempia
aikoja, tukkaansa, sovittaen siihen irtolettiä.
— Minä käyn vähäksi aikaa pitkälleni. Jos joku tulee niin havauta,
sanoi asioitsija, oluen juotuaan.
Tukkansa laitettua, alkoi Laura siistiä konttooria.
Asioitsija oli keskikokoinen, lihava, turpea mies, pyöreämuotoinen,
jossa vaihteli sinervä ja punerva maksankarva. Laura, hänen
vaimonsa, oli pitkä ja joukeamuotoinen. Hänellä oli komonokka,
siniset silmät, hivusmarto selvä ja säännöllisesti kaareva korvallista
kohti — kaikki vanhoja muistoja entisen kaunottaren ajoilta. Niin,
kaunotar oli hän ollut, maankuulu, vedenvalio, jolla oli kosijoita
käynyt läheltä ja kaukaa ja joiden joukosta oli vaali ollut vaikea. Yhtä
hän oli rakastanut, toiselle kuitenkin mennyt. Oli tapahtunut se
tavallinen seikka: köyhä oli hyljätty, rikas oli otettu. Vaatimaton
vallesmanni oli saanut rukkaset ja rikas, ylväs kauppias valittu. Tuo

oli vähän tuskastuttanut, kun vallesmanni, kelpo käytännön mies, ei
ollut mennyt hirteen eikä orteen, vaan tyynesti tyytynyt kohtaloonsa.
Pitäjän rikkain tyttö oli Laura Wahrlin… rikkain, pulskin ja kaunein.
Merikululla ja muilla onnistuneilla yrityksillä oli hänen isänsä koonnut
suuret varat ja parhaaseen aikaan lakannut liikettä käyttämästä. Oli
sitten ostanut suuren maatilan, jota nyt viljeli, viettäen levollista
vanhuutta. Laura oli silloin kihloissa pitäjän vallesmannin kanssa, kun
nuori, verevä ja rikas kauppias, Henrik Jakke, muutti seurakuntaan.
Tämä oli iloinen luonteeltaan, hyvä seuramies. Herrain joukossa
osasi hän juoda ja laulaa ja puhua sukkeluuksia, ja naisseuroissa
pitää sitä hengetöntä lörpötystä, jonka hienohelmain suosioon
pyrkivät katsovat niin välttämättömän tarpeelliseksi. Mikäs konsti
hänen oli vallesmanni laudalta lyödä. Kun tyttö koetti vastustella ja
vakuuttaa rakastavansa vallesmannia, selitti isä että se tuli vaan
miestuttavuuksien puutteesta, että hän, Laura, vallesmanniin oli
ihastunut. Nyt oli asia toinen. Kun hän vaan rikkoisi välinsä
vallesmannin kanssa, niin kyllä se olisi helppo unohtaa ja joutua
uusiin tuttavuuksiin. Laura olisi mielellään neuvotellut jonkun hyvän
naistuttavan kanssa, mutta senlaista ei ollut. Äiti oli kuollut ja
kaikkien muitten mielestä oli hänen liittonsa vallesmannin kanssa
sula tuhmuus. Ja niin sai vallesmanni muitta mutkitta rukkaset ja
Laura joutui uusiin tuttavuuksiin. Ja sehän siitä seurasi, jota oli
tahdottukin: kihlaus, kuuliaiset ja uhkeat, monipäiväiset häät. Kaikki
onnittelivat Lauraa, että hän oli hyvän osan valinnut ja suuren onnen
käsittänyt. Sitä sanoivat miehet ja naiset niin herrasväkeä kuin
talonpoikia…
Tämän rikkaan pariskunnan lapsi se on tuo Alma, joka tänä
aamuna lähti syömättä kouluun iloisessa Helsingissä.

Kuinka se on mahdollista?
Heitä on kohdannut "onnettomuus"… Siksihän sitä ihmiset
tavallisesti nimittävät, kun rakennus hajoo, jolla ei ole ollut
tarpeenmukaista perustusta.
Tällainen tarina on lyhyt, surullinen ja — jokapäiväinen.
Oli eletty ylöllisesti niin kauvan kuin oli varoja riittänyt. Sitten oli
myöty talot ja liiat tavarat ja muutettu kauvas toiseen paikkakuntaan
ja koetettu alkaa uudestaan. Mutta hajoavata rakennusta on paha
pönkitä. Uusi yritys ei ollut onnistunut sielläkään. Vararikko oli ollut
lopullinen turva.
Ikävätä on elämä niillä tienoin, jossa on onnestaan haihtunut, ja
ikävätä sieltä on erokin. Useampi senlainen valitsee kuitenkin
jälkimäisen ja niin teki Henrik Jakkekin. Pitkään mietti hän ja aprikoi,
minne olisi lähdettävä ja mitä tehtävä. Viimein päätti hän lähteä
pääkaupunkiin "onneansa koettamaan". Yksin lähti hän ensin ja
kutsui joukkonsa perästä. Yhtä ja toista oli hän ensin puuhannut
kunnes pani asioimiskonttoorin "ylös"…
— Henrik, täällä on vieras, herätti rouva miestään.
Asioitsija meni "konttooriin", joka oli isohko, matala kivijalkahuone,
johon kaksi pientä, katonrajassa olevata ikkunaa vaivoin sai
kuljetetuksi päivän valoa. Kivinen oli permanto, joka melkein aina
kylmänä aikana oli kostea. Kapea porras kadulta johti matalasta
oviaukosta tähän manalaan. Konttoorin vieressä oli vesijohdolla
varustettu kyökki, jonka ikkuna oli pihalle käsin. Tämä oli perheen
tavallinen asunto. Huonekaluja oli konttoorissa ainoastaan iso,
puiseva pöytä, pari natisevaa tuolia ja seinämällä sohvantapanen;

kyökissä oli kaksi leveätä sänkyä vierekkäin, piironki, kaksi tuolia,
halkoloota ja kaappipöytä ikkunan alla.
— Minulla olisi pari kolme haastetta tehtävänä, sanoi vieras.
Asioitsija kuulusteli asian ja alkoi kirjoittaa.
— Etteköhän haettaisi pari pulloa olutta, on tässä vähän niinkuin
kohmelo, virkkoi asioitsija vieraalle muutaman rivin kirjoitettuaan.
— Miks'ei…
Haettihan se.
Kun työ oli tehty, sai asiamies paperit ja hyvät neuvot, kuinka oli
niiden kanssa meneteltävä, että asianomaiset tulisivat laillisesti
haastetuiksi, ja asioitsija sai 6 markkaa vaivoistaan, 2 markkaa
kappaleelta.
— Näet sen nyt, että onhan meillä rahaa, sanoi hän vaimolleen.
Tässä on sinulle viisi ja puoli markkaa, osta niillä ruokaa ja kolme
pulloa olutta minulle. Itselleni pidätän vaan 50 penniä.
Eukon olisi tehnyt mieli kahvia ja hän oli sanomaisillaan, ett'eikö
saisi ostaa sitäkin, vaan hän ei uskaltanut. Siitähän se oli aina
ennenkin riita syntynyt, jos hän oli jotakin tarvinnut. Hän oli tosin jo
tottunut, että täytyi tyytyä siihen, mitä miehensä määräsi ja käski ja
syödä, mitä milloinkin sai, mutta välistä kuitenkin tahtoi tehdä mieli
kahvia ja jotakin parempata ruokaa. Kurjuuskaan ei voi tykkönään
mielitekoa eikä muistoa kuolettaa.
Hän leuhautti saalin hartioilleen, otti korin käteensä ja lähti.

Asioitsija lähti itse myöskin ulos ja pyysi pienen poikansa
sanomaan, että pappa tulee kohta, jos joku sattuisi tulemaan. Hän
osti ensin puodista puolen punttia "kaukaasia"-paperosseja ja hiipi
sitten anniskeluyhtiön ravintolaan, jossa otti kolme viinaryyppyä….
— Pitäähän ihmisen saada ruokaryyppy, onhan tässä jo sen verran
tienattu, arveli hän itsekseen.
Kun hän saapui kotia, tuli Almakin samassa koulusta.
— Onko sinulla paha nälkä, Alma? Elä ole milläsikään, kohta saat
ruokaa. Pappa sai rahaa ja mamma meni ostamaan, puhui asioitsija
niin lempeästi kuin voi.
— Eipä tuosta tiedä mitään, vastasi Alma, vaikka mieltä tahtoi
itkuun vääntää.
— Mistä? kysyi isä, jolta kysymys oli jo unhottunut.
— Nälästäpä.
Kohta saapui mammakin kotia. Hyräillen hän tuli niinkuin hyvällä
mielellä oleva ainakin.
Kohta oli ruoka pöydällä ja käytiin aterioimaan.
— Syö sinäkin Henrik, kerrankaan. Tässä on hyvää lihaa ja
juustoa…
Illaksi laitan lämmintä ruokaa, nyt ei ole aikaa, puhui rouva Jakke.
Henrik otti hätäisesti leipäpalasen ja lihaa ja kävi kohta oluen
kimppuun. Hän ei malttanut ruveta pulloa korkkiruuvilla avaamaan,
vaan työnsi korkin lyijykynällä sisään.

Pikku Kallu vetäysi verkkaan pöytään. Vaikka hän ei ollut koko
päivänä mitään syönyt, ei hän ollut valittanut eikä mitään virkkanut.
Hän oli sellaiseen tottunut. Sanaakaan puhumatta otti hän voileivän,
vetäysi sohvanpäähän paperilappujensa luokse, joilla oli aamusta asti
leikkinyt ja alkoi jatkaa tointaan.
Alma sitä vastoin söi hyvällä halulla ja oli iloinen ja tyytyväinen.
Hän kertoi, kuinka hyvin hän oli taas läksynsä osannut ja kuinka
opettajatar oli kiittänyt ja kuinka hyviä muut tytöt olivat hänelle:
Anna Sjövall oli antanut kaksi konfektia, joista hän toisen oli
säästänyt Kallulle, ja Maria Oksanen ison piparkakun, josta siitäkin
oli Kallu puolet saanut.
Äidit, varsinkin köyhät, joutavat harvoin säännöllisesti syömään.
Niin kävi nytkin. Palasen hän otti ja meni sitten kyökkiin sänkyä
kokoomaan ja siivoamaan.
Isä istua murjotti ja joi olutta… näpisti palasta ja taas joi. Ja kun
yksi pullo loppui, alkoi toisen.
— Laura, tuoss' on lasi sullekin, tule ja ota. Tarvitsethan sinäkin
jotakin, sanoi hän.
Nöyrästi tuli äiti ja otti.
Se oli viimeinen tilkka, jonka vaimo sai.
Sitten pisti asioitsija tupakan ja kävi sohvalle pitkälleen. Siinä
poltteli, nikotteli ja röhki mies vähän aikaa, nukkui sitten ja alkoi
kuorsata.
Illan suussa saapui mies. Hän ei ollut mikään asiamies, vaan
asioitsijan hyvä tuttava, ystävä ja veli.

— Taitaapa mies olla siukkana, sanoi vieras.
— Liekö tuo niin vaarallista, naurahti Laura. Vaivoin saatiin
asioitsija valveelle.
— Terve! Olipa hyvä, että tulit… peijakkaan hyvä. Tuntuu pääni
kipeältä… sinä kait pistouvaat lasin olutta, sinullahan sitä on rahaa.
— Mitäpäs sitä köyhällä on muuta kuin rahaa. Jos Laura on hyvä
ja hakee olutta, sanoi vieras, heittäen 2-markkasen pöydälle.
— Ei! Kyllä minä menen, ehätti Alma sanomaan, ottaen korin
kyökistä.
— Paljoko tuodaan?
— Koko rahan edestä, mutta sineprykohvia, sanoi vieras.
Kun Alma oli oluet tuonut ja Laura lasit toimittanut, alkoi tavallinen
meno.
— Missäs rouvan lasi on? kysyi vieras.
— Kiitos! En välitä.
Mutta eihän siinä mikään auttanut. Rouvankin täytyi ottaa itselleen
lasi. Hän ei istuutunut herrain seuraan, vaan otti olutlasin ja meni
kyökkiin, jossa sen vähin erin ryypiskeli. Miehet vetivät sitä
uhemmin. Kun entiset olivat lopussa, sai Alma noutaa lisää.
Rouvallekin tarjottiin vielä, vaan hän ei mitenkään voinut ottaa
enempätä.
— No, kosk'ei olut kelpaa, niin ottakaa sitten kahvia ja pullaa,
sanoi vieras antaen rouvalle pari markkaa.

Sill'aikaa kun Alma oli ostamassa tarpeita, teki äiti tulen kyökin
hellaan. Alman tultua vetäysi hän lapsineen kyökkiin, puuhasi kahvin
valmiiksi ja alkoi nauttia pienten tovereinsa kera. Siinä tahtoi vanhat
muistot johtua mieleen ja vedet kiertyä silmään.
Miehet eivät huolineet kahvista.
Sitten alkoi äiti puuhata illallista tulelle.
Miehet istuivat konttoorissa ja nauttivat nauttimistaan olutta.
— Tämä oli onnellinen päivä tämä, mutta mitäs huomenna… sanoi
rouva tultuansa konttooriin.
— Huomenna?! Kullakin päivällä on suru itsellään, puhui asioitsija,
jonka kieli jo alkoi käydä kerkiäksi.
— Vieläkö ostamme olutta? kysyi vieras.
— Vielä, vielä! vastasi isäntä.
Olutta haettiin lisää.
— Mull'on huomenna raastupapäivä… kova päivä. Tule sinä,
veikkonen, aamulla tänne, että saan kohmeloryypyn, puhui asioitsija,
kompuroiden sohvan luo, rötkähti siihen ja syvästi nikotellen nukkui
kohta. Vieraskin lähti ja pääsi kuin paasikin jyrkänlaisia portaita
ponnistellen kadulle.
Rouva sulki konttoorin ja meni lapsineen kyökkiin, jossa illasteli,
laittoi lapset maata ja kävi sitten itsekin levolle, saatuaan astiat
puhtaiksi ja paikoilleen.

Vuoteellaan arveli hän jonkun aikaa tämän maailman menoa. Hän
tunsi itsensä onnelliseksi muistoissaan, siunasi hartaasti ja nukkui
kohta, herätäkseen uuden päivän uusiin vaivoihin.
Marivainaja.
En muista, kuinka hän meille tuli, vaan äitini kertoi usein siitä.
Köysissä oli hänet tuotu köyhäin huutokauppaan, kuin
pahantekijä, kädet selän taakse sidottuina.
Tämä oli sitä aikaa tämä, — joka on vielä monen muistissa —
jolloin köyhiä myytiin huutokaupalla, kun ei tunnettu parempata
niiden sijoittamistapaa eikä tietty mielivaivasia sopivammin hoitaa
kuin erityisissä karsinoissa taikka köysissä.
Ja Marivainaja oli mielipuolen kirjoissa.
Niinkuin elukkata oli häntä kuljetettu. Mies oli, taluttanut nuorasta,
toinen ohjaillut takaa köydestä, ett'ei pääsisi pahasti rimpuilemaan.
Perille tultuansa oli hän päästänyt kimakan volinan, huutaen kaiken
maailman "joukkoja" avukseen, pelastamaan "petojen kynsistä".
Tämän nähtyänsä oli isäni käskenyt päästää hänet heti vapaaksi.
Vastenmielisesti olivat miehet totelleet, päästäneet köydet ja
lähteneet samassa pakkulaan… niin oli pelko heidät käsittänyt.
Vaikutus oli kuitenkin ollut vastoin heidän luuloansa. Ensin oli Mari
seisonut kuin puulla päähän lyöty, sitten heltynyt itkuun, heittäytynyt
isäni eteen ja syleillyt hänen polviansa, voimatta lausua sanaakaan.
Itkuansa oli hän jatkanut porstuan kynnyksellä kunnekka oli väsynyt.

Sitten oli kiivennyt tuvan uunille, nukkunut sinne ja maannut kuivilla
päreillä koko toimituksen ajan. — Kotonaan hän ei ollut moniin
aikoihin levollisesti maannut. Herättyänsä oli arasti udellut, mihin oli
joutunut tulevaksi vuodeksi. Kun oli saanut tietää päässeensä
pappilaan, oli hän pyörähtänyt tielle ja juosta viilettänyt yhtä kyytiä
sinne… Vuoden päähän oli vielä kuukauden ajat.
Näin se oli Marivainaja meille tullut.
Hän oli pitkä ja laiha, ijältään nelikymmenissä. Alkuperäisiä
piirteitä ei voinut enää tarkoin erottaa hänen muodossaan, niin oli
tuska ja mielikarvaus ne pitkällisessä vankeudessa väännellyt. Otsa
hänen oli matala, nokka pysty ja hivusmarto epäselvä, tukkansa oli
vaalea, harva ja takkuinen. Muulta ruumiiltaan oli hän solakka ja
muuten säännöllinen paitse kädet, jotka olivat luonnottoman pitkät
ja olkapäät, joiden tavaton jyrkkyys oudostutti äkikseltä. Hänen
haaleansinisissä, vetisissä silmissään oli arka, surullinen katse, joka
toisinaan jähmettyi jäiseksi tuijotukseksi, toisinaan kiihtyi
liekehtiväksi pyörteeksi, mutta mielipuolen mitään sanomatonta
levottomuutta ei niissä milloinkaan huomannut.
Uusi elämä alkoi Marille meillä. Hän sai olla niinkuin tahtoi ja tehdä
mitä halutti. Ei kukaan saanut häntä härnätä, ei loukata eikä
muutenkaan häiritä. Tämä näytti aluksi oudoksuttavan Maria,
niinkuin muut oudoksuivat häntä, mutta viikon, parin perästä oli Mari
jo perehtynyt uuteen oloonsa ja toiset opastaneet häneen, että hän
oli niin talon väkeä kuin muutkin. Hän sai tehdä töitä niitä, joihin
kykeni, tahi olla tekemättä. Ja ahkera hänestä tulikin. Hän askaroitsi
päivin kaikenlaisissa pienissä töissä, joita taloisessa talossa on
yllimmän kyllin, toisin taas joutiloi ja pistäytyi naapurin eukkoja
haastattamassa. Mielipuoleksi, vielä vähemmin raivohulluksi, häntä ei

voinut huomata. Vasta kevätpuoleen alkoi hänessä ilmestyä
nöyrämielisen viitteitä. Hän alkoi tulla levottomaksi ja tähystellä
jäille, ett'eikö rupeaisi näkymään sulia tahi rantaporeita, että pääsisi
uimaan, niinkuin hän sanoi. Kun sitten ensimmäiset poreet
ilmestyivät, paiskautui hän vaatteineen päivineen niihin. Jos ei niissä
vielä sopinut uimaan, niin hän edes pulikoi hetkisen ja juoksi sitten
tupaan ja kuivasi vaatteensa uunilla. Sitä hän sitten uudisti aina
jonkun päivän perästä pitkin kevättä siksi, kun viimeinen jäänsirpale
oli sulanut. Silloin hän jätti uimisen, kun muut alottivat,
uudistaaksensa sen taas seuraavana keväänä. Ja merkillisintä tässä
oli, että hän aina uiskenteli täysissä tamineissa, parhaassa
puvussaan.
Toinen hänen omituisia oireitaan tuli näkyviin kesän päälle.
Hänellä oli kummallinen tapa pitää terveydestään ja
kauneudestaan huolta. Itse hän tiesi keittää ja valmistaa rohtonsa ja
hankkia niihin aineet. Kun nurmennukka alkoi maasta nostaa
vihantaa päätänsä, niin silloin tuli Marille kiirettä hommaa ja touhua.
Hän alkoi kuoria pajahtimia ja kerätä kukkasia, kuljeskellen halki
niittyjen, pitkin pellon pientaria, törmiä ja mäkilöitä, iloisesti laulellen
ja hyppien kuin lapsi. Pajahtimen kuorista keitti hän vettä, rohtoa,
jota nautti halukkaasti pitkin päivää, kun vahvasti uskoi sen lisäävän
terveyttä ja ikää — sekä pesi usein kukista keitetyllä vedellä silmänsä
ja kätensä, että hipiä pysyisi nuorteana ja kauniina.
Omasta itsestään ei ottanut mitään puhuaksensa, kun oli
muutenkin vähäpuheinen, ett'ei hänen menneisyydestään saatu
suurin tietää eikäpä taittu suurin tiedustellakaan. Itse kutsui hän
itseään Marivainajaksi, johon muutkin pian tottuivat.

Näin oli Marivainaja asunut meillä muutamia vuosia hiljaisesti ja
huomiota herättämättä, kun hän alkoi eräänä talvena puhua häistä,
jotka sitten samana keväänä viettikin.
Oli muutama Maaliskuun ilta. Äitini istui rukin takana hyräillen ja
Mari kuori perunoita uunin edessä. Hetken päästä alkoi tämä:
— Marivainaja tarvitsee uudet vaatteet.
— Mitäs se Mari nyt niillä?
— Tarvitsee.
— Mitä vasten?
— Tässä tulee häät…
— Häät?!
— Niin!
— Oikeinko oikeat häät?
— Jo tok'… ihan oikeat.
— Kenenkä häät? Enhän minä ole mitään kuullut.
— Marivainajan.
— Marin häät? — Kaiken varmaan.
— Onkos sulhasta?
— Kuinkas muuten.

Äitini vähän hymähti ja katseli Maria, jonka muoto oli käynyt
hehkuvan punaseksi ja silmät liekehtivät oudosti.
— Missä se Marin sulhanen on?
— Järvessä.
— Järvessä?!
— Järvessä! Niin, niin järvessä, mutta hän on luvannut tulla minua
hakemaan tänä keväänä ja hän tulee, tulee, tulee! puhui Mari
innokkaasti, hyppäsi pystyyn ja alkoi tuohuksissa astua edes takaisin
huoneessa.
Hymy katosi äitini huulilta. Hän katseli Maria pelokkaasti, mutta
antoi rukkinsa pyöriä kahta kiivaammin, olevinaan huomaamatta
mitään.
Hetken päästä viihtyi Mari ja istuutui työlleen.
— Järvessähän se on… järvessä, huokasi Mari raskaasti.
— Milloinka hän on järveen joutunut.
— Siitä on jo kauvan, niin, niin, niin kauvan.
Ja kauvanhan siitä oli…
Mari oli silloin elämänsä keväässä, nuori ja verevä,
kahdeksantoista vuotias impi, varakkaan mökin, Suonsaaren, ainoa
tytär, Kirkonkylän reunamalta. Hän oli kylän suosikki ja
vanhempainsa ilo ja onni. Monta kävi hänellä kosijata, monta
pulskaa ja rikasta, mutta hän ei tahtonut mielistyä miehiin hyvihin,
sanoi tahtovansa olla vanhempainsa "oma ainoa" lapsi. Niin kului

aikaa, mutta viimeinhän se tuli hänenkin vuoronsa… tuli mielitietty.
Se oli nuori torpan poika Korpisilta, joka kirkkomatkoillaan oli
Suonsaaren Marin tuttavuutta tehnyt ja armon hänen edessään
löytänyt. Hän oli pitkä, solakka, reipas nuorukainen, vaalahtava
tukaltaan. Iloinen ja leikillinen oli hän luonteeltaan, jonka
miellyttäviä kokkapuheita tuttavat tytöt mielissään kirkkomäellä
kuuntelivat ja jota oudotkin neitoset suosiollisesti loitompata
katselivat. Tämä oli päässyt Suonsaaren Marin hellään suosioon,
johon moni oli niin innokkaasti pyrkinyt. Eikä Kortteisten
Paavollakaan ollut muuta palavampaa halua, kuin saada Mari kotinsa
katsojaksi, mitä pikemmin sitä parempi. Häät päätettiin viettää
Juhannuksena, kesäisen ilon ja valon juhlana ja sen vuoksi oli
kiiruhdettava kuuliaisia. Ne päätettiin ensi pyhäksi ja lauvantaina
aiottiin käydä "pappiloissa."
Odotettu lauvantai tuli… tuli kaunis, mutta hieman kolea, niinkuin
keväinen ilma usein on, ja iltapuoleen alkoi huokua jäistä usmaa
järveltä kylään.
Suonsaarelaiset kokoutuivat tuttavineen Kalliolle, odottamaan
sulhasta seuroineen. Siinä oli päätetty yhtyä, ottaa lämpöset kupit ja
mennä pappilaan.
Levottomina odotettiin sulhasta.
Oli, näet, jo täydellinen kelirikko, ett'ei jäitä tahtonut päästä
mitenkään, josta syystä sulhasen piti tulla Pankasalon kautta.
Venheellä oli hänen ensin kuljettava Hiekkasalmen ylitse
Pankasaloon ja siitä suksella Kirkkosaareen.
Haihtuivat siinä odotellessa ruusut morsiamen miellyttäviltä
kasvoilta.

Odotettiin yhä…
Jopa vihdoin alkoi Talassaaren päästä näkyä joukko hiihtäjiä. Siinä
ne tulivat, viisi miestä ja kolme naista jotensakin etäällä toisistaan.
Etumaisena ensin yksi mies, sitten toiset parittain, naiset viimeisinä.
Levottomuus alkaa hälvetä odottavista.
Etumainen näyttää haastelevan ja viittovan toisille. Ne kääntyvät
hieman Koirasaareen päin.
Ovat jo puolisalmessa.
Nyt tunnetaan, että etumaisena hiihtää sulhanen — hänkin
kääntyy
Koirasaarta kohti.
Sulhanen tervehtii kohottamalla lakkiaan, kun näkee väkeä
rannalla.
Vaaleana seisoo morsian portailla, pidellen kovasti kaiteesta kiinni.
Sulhanen kiiruhtaa kulkuansa, potkaltaen varomattomasti
eteenkäsin.
Hetki vielä ja — hän on jään alla.
Morsian kaatuu tuskan huudolla portaille.
Riennetään sinne… hän on tainnuksissa.
— Kääntykää enemmän Koirasaarta kohti, kuuluu sulasta sulhasen
iloinen, reipas ääni.

Lähimmäiset rientävät avuksi, mutta ovat kohta samassa
avannossa.
Keväinen jää on haprasta.
— Enemmän Koirasaarta kohti, siell' on jää kovempata, huutaa
sulhanen tavallisella äänellään.
Apua ei huudeta: ei huuto hädästä päästä.
Hetkessä on riski miesjoukko temmannut rannalta talviteloillaan
olevan veneen ja rientää avuksi. Se näyttää saapuvan parhaaseen
aikaan. Kaksi miestä on kohta jäällä, mutta kolmatta ei näy enää,
vaikka se vast'ikään rohkasi toisia hätäilemästä. Suksen kantaa
näkyy jään alta, siihen tartutaan ja, kun se tuntuu raskaalta,
vedetään hiljaksiin, että jalka pysyy varpaallisessa ja sulhanen
saadaan ylös, mutta millään tavalla ei voida häntä enää henkiin
saada, vaikka hätään ovat rientäneet papit ja lukkarit. Elävä henki oli
hänet jo ijäksi jättänyt.
Tuskaa ja valitusta oli sinä iltana Kirkonkylässä.
Liikuttavan puheen tapauksen johdosta piti rovasti kirkossa
seuraavana päivänä, mutta murheellinen morsian ei ollut sitä
kuulemassa. Hänet oli kamala tapaus kokonaan murtanut.
Toinnuttuansa oli hän Marivainaja.
Mari eleli tämän jälkeen hiljaisesti surullisessa kodissaan, johon tuli
vielä uusia surun syitä. Hänen äitinsä saattoivat nämä surulliset
tapahtumat ennenaikaiseen hautaan. Isänsä kuoltua hoidettiin Maria
perinnöillään niin kauvan kuin niitä riitti. Sitten joutui hän mieron
kovalle tielle, jonka kärsimykset ja kivuttamiset saattoivat hänet

usein raivoksi ja köysiin taikka karsinaan. Niissä sammui hänestä
viimeinenkin kipinä järjen valoa.
Hän ei ollut ensimmäinen eikä, Jumala paratkoon, viimeinen, joka
on mieron tietä saanut köysissä kulkea…
Lupaamalla uudet vaatteet sai äitini Marin rauhoittumaan, eikä
häistä ollut sen enempätä puhetta.
Kun kevätpuoleen tuli pitkät suojailmat, jotka kestivät viikkomääriä
ja veivät kaiken lumen maasta, niin tuli Mari levottomaksi. Hän
kuljeskeli pitkin rantoja ja tarkasteli jäitä sekä muistutti joka päivä
äitiäni uusista vaatteistaan. Mutta kun ilma taas jäähtyi ja sataa
tupruutti uutta lunta maan Valkoseksi, niin tyyntyi Marikin ennalleen
ja askaroitsi pienissä toimissaan.
Toukokuu tuli ja rupesi todella kesän tekoon.
Mari sai uudet vaatteet.
Ne olivat sinistä puolivillasta, tehdyt herrastyyliin, kapea, valkonen
rimpsu kaulan ympäri. Äitini olisi antanut mustat vaatteet, mutta
Mari ei niistä pitänyt, vaan sanoi olevansa liian nuori käymään
mustissa. Sinisiin hän sitä vastaan mielistyi suuresti.
Toukokuun puolivälissä alkoi taas Marin levottomuus lisäytyä. Hän
juoksi usein rantaan, ja istuskeli Kallion portailla, katsellen hartaasti
järvelle. Tätä ei saatettu ottaa mihinkään huomioon, kun joka kevät
oli käynyt melkein samalla tapaa.
Eräänä aamuna varhain ilmestyi Mari äitini luokse uusissa
vaatteissaan, sievästi puettuna ja siistittynä. Hän syleili äitiäni

innokkaasti kyynelsilmin, lausuen hätäisesti: häät, häät. Äitini heltyi
eikä voinut aavistaa, mitä tuonlainen käytös merkitsi.
Oli kaunis aamu. Tuuli ei ollut vielä valveella. Aurinko loisti
keväisesti siniseltä taivaalta ja leivo liverteli aamulauluaan ilmassa.
Sulava järvi huokui hiljaisena hienoa usmaa ilmaan…
— Apuun! Apuun! kuului äkkiä huuto, Marivainaja on pudonnut
sulaan!
Erottuansa äidistäni oli hän kiiruhtanut Kalliolle, istunut siellä
portailla ja katsellut järvelle. Äkkiä oli hän sitten hypännyt ylös,
siepannut sukset seinämältä, hiihtänyt jäälle ja paiskautunut sulaan.
Moni oli nähnyt hänen menevän, mutta luullut sitä Marin tavalliseksi
uimamatkaksi.
Tämä tapahtui melkein samoilla paikoin, missä sulhanen oli
hukkunut vuosikymmeniä ennen.
Hänet saatiin kyllä aivan heti ylös, mutta ei enää henkiin tämän
maailman valossa.
Häät oli pidetty…
Talon piruja.
— Talatta! Talatta! kuului toverini huutavan, joka kulki jonkun
matkaa edellä.
Ponnistaen viimeiset voimani riensin minäkin paikalle.

Talo kuin linna oli edessämme mäen notkelmassa.
— Tuossa pätii meidän yötä olla, tuossa, sanoi toverini.
Me istuimme veräjän sulkupuulla ja katselimme laskevan auringon
punervassa valossa päilyvätä seutua.
Olimme tieteellisellä tutkimusmatkalla… On sitä oltu senlaisillakin.
Aamusta ani varhain olimme olleet liikkeellä, eksyneet tieltä,
emmekä koko pitkänä päivänä maistaneet murua muuta kuin
mustikoita metsästä. Meidät oli neuvottu Kivelän mökiltä oikotietä
Pihlajamäkeen ja sanottu olevan montakin mökkiä taipaleella, joissa
voisi levätä ja ruokaa saada. Me emme tavanneet yhtään mökkiä,
emmekä muutakaan ihmisasuntoa koko päivänä. Olimme siis
eksyneet oikealta suunnalta, harhailleet missä lienemmekään ja
menettäneet aikaa paljon enemmän, kuin tavallista tietä tullessa olisi
tarvittu. "Parempi virsta väärää, kuin vaaksa vaaraa" — tuo hyvä
neuvo oli unhottunut meillä kokonaan. Taival oli ollut koko lailla
vaivaloinen. Toisinaan niitä oli polkuja enemmän kuin tarpeeksi,
toisinaan ei ollenkaan. Olimme saaneet rämpiä suosilmäkkeitä,
kavuta kallioita ja tunkeutaa tiheäin metsikköjen läpi. Päivä oli
polttavan kuuma, senlainen, jonkalaisia vaan heinäkuussa voipi olla.
Tuntui kuin päiväkulta olisi tehnyt liiton Pihlajamäen kanssa,
tehdäksensä matkamme niin vaivaloiseksi kuin mahdollista. Päivä
tuntui yhä lisäävän poltinainetta tuliseen uuniinsa ja Pihlajamäki
nostavan yhä pystympään leveätä rintaansa meidän eteemme.
Tuulta ei tuntunut, ei edes henkäystä, joka hiemankaan olisi
viilentänyt kiehuvata kuumetta ja kiehuttavaa hellettä. Siihen vielä
kaikenlaiset kuuman päivän seuralaiset liehuivat ympärillämme,
koetellen ihomme kovuutta, ja jos eivät saaneet purra eivätkä pistää,
niin koettivat tunkeutua suuhun ja sieramiin. Oli kuin hiiden

hörhiläiset olisivat saaneet meidät valtaansa, löylyttääkseen. Siinä oli
polttiaista, siinä hyttystä, siinä mäkärätä ja surviaista, siinä itikkata ja
muuta pientä lentiäistä. Liikkeessä ollessaan noilta hieman rauhaa
sai, mutta herkesipä levolle, yhteen kohti pitkälleen, niin kohta olivat
nuo ystävät kiinni joka kohdassa, missä vaan lomaa puremiseen oli.
Toverini, joka astui edellä, pitäen suuntaa silmällä, oli reipas mies,
joka ei vähistä välittänyt. Hänellä oli keppi oikeassa ja leheksiä
vasemmassa kädessä, joilla hän, hosui ympärilleen kuin riivattu ja
astui vaan ja lauleli. Minä tallustelin perässä väsyneenä,
näännyksissä ja huohottaen kuin hyvätkin palkeet, heittäytyen
pitkälleni jokaiseen varjoon ja katvepaikkaan, josta kuitenkin oli asia
hetimiten taas taipaleelle, kun tuo elävitten joukko syöksi niskaani.
Kun päivä alkoi mailleen kääntyä, niin kävi kuumuus vähin erin
kärsittävämmäksi, mutta siipiniekat tulivat sitä kiukkuisemmiksi…
Nyt olivat kuitenkin päivän vaivat unhotetut, kun talo oli
edessämme… talo kuin linna.
Läksimme taloon kesantopellon piennarta, jota myöten polku veti.
Pelto oli hyvässä muokassa, odottaen kylväjätä. Ojat olivat vasta
pohjatut ja siivotut, piertamet kuokitut ja ojamullat hajotetut. Näitä
minä en olisi huomannut enkä pitänyt niillä väliä, jos ei toverini, joka
oli virkku ja reipas kuin kosken kala, olisi huomannut ja minulle
huomauttanut. Muutamakseen huomasi hän miehen, joka makasi
vasta pohjatussa ojassa… näytti sikeästi nukkuvan.
— Siinä kaite lienee viileä maata, sanoi toverini.
Pääsimme pihaan.

Ei yhtään elävätä sielua näkynyt, ei kuulunut talossa.
Astuimme tupaan.
Se oli heiniä täynnä… heiniä kuivamassa. Niitä oli lattialla, niitä
penkillä ja uunilla, niitä kaikki orret täpösen täynnä.
Muuan akkanen ihminen istui karsinpenkillä ja ruopotteli päätään.
Minä nakkausin heti heinille pitkälleni.
— Hyvää iltaa! alkoi toverini.
— Pankaahan siihen, vastasi nainen karsinpenkiltä. Toverini vähän
ällistyi naisen oudosta tervehdyksestä ja tarkasteli ihmistä.
— Missäs isäntäväki on? kysyi hän sitten.
— Ettäkö sinne menisitte, ärähti nainen.
— Eipähän niin sinne, eikä tänne, vaan että saisimme kysyä
yösijaa, ehätin minä sanomaan, ett'ei toverini, joka oli kiivas
luonteeltaan, ehtisi pikastua.
— Näyttääkös tässä sijaa puuttuvan? kysäsi akka jotenkin äreästi.
— Eipä silti, eikä sen tähden, vaan onhan tavallista ja tarpeellista
matkamiehen sitä kysyä, selitin minä niin sävyisästi kuin voin.
— No, nyt sen tiedätte, ärähti nainen.
— Onkos talossa ruokaa? kysäsi tylysti toverini, joka alkoi ärtyä
akan viisastelusta.

— Ei täss' ole koskaan ruuatta eletty, sanoi nainen heti ja
hörymättä.
— Niinpä kanna sitten pöytään ja sukkelaan! käski toverini äänellä,
joka osotti, että käskyä oli siekailematta toteltava.
Nainen lähti ja nopeaan lähtikin.
Ensi panos oli kolme kokonaista, paksua leipää, joita monikin
vertaisi myllyn kiviin.
— Mitä se mies tuolla ojassa makaa? kysyin minä, saadakseni
tietää, millä mielellä arvoisa emäntämme nyt oli.
— Mikä makaa missäkin, vastasi hän samassa ja meni ulos
hakemaan lisää monttumia pöytään.
Toverini otti muistikirjansa ja minä aloin tarkastella toimeliasta
emäntäämme, joka höntäsi ovessa edestakaisin, tuoden aina yhden
kappaleen kerralla pöytään. Hän näytti tarkoin seuraavan
sananlaskua: "laiska kerralla katkaseksen, viidesti vireä käypi".
Tarkastettuaan aina hieman pöytää, pyörähti hän jotakin puuttuvata
noutamaan… milloin se oli veitsi, milloin lautanen, milloin mikin.
Hän oli punakka, vaaleatukkainen, varmaankin vanhempi kuin
näytti. Hänen otsansa oli oudon matala ja hivusmarto epäselvä,
posket lihavat, hyllyvät, paljon otsaa leveämmät, nokka kevelä ja
leveä, sieramien väliseinä paksu ja lihakas, joten itse reijät
supistuivat jotenkin pieniksi, suu leveä… korvallisille asti, huulet
paksut, pyöreät ja mehevät, joiden välistä loisti kaksi riviä valkeita,
säännöllisiä hampaita, korvat olivat suuret ja pörhällään. Leuka vielä
puuttuu tästä kuvasta, mutta puuttui se alkuperäisestäkin. Sitä ei

ollut muuta kuin pieni nystyrä noiden pullevain poskien välissä.
Tämän seikan mainitsen viimeiseksi, vaikka ensiksi sen katsoja
huomasi.
Hänen puvustaan ei ollut paljon puhettakaan… mikäpäs sitä
senlaisessa värissä. Päällään oli vaan lyhythihainen, avopäänteinen
paita, polveen asti ulottuva hameenrepale… Ei muuta mitään ja
tuskinpa tarvitsikaan.
— So, vieraat, päin pöytään, selin seinään! sanoi hän, kun
mielestään oli saanut ruuan laitetuksi.
Kahta käskyä ei tarvittu.
Olipa siinä "ruokakultaa ja monttumia"! Komppania sotaväkeä olisi
huoleti voinut pöytään käydä.
Siinä oli, paitse noita kolmea leipäkyörää, sievonen punkka voita,
pytty suolasta, suurta lahnaa, kaukalo muikkuja, iso, savustettu
sianlape, paistetut vasikan nivuset, kaksi viilipyttyä, iso tuoppi nuorta
maitoa — kaikki maukasta ja hyvää. Tavallinen pärepuukko oli liha-
astian vieressä, edessämme lautaset, linkkuveitsi kummallakin
lautasella, linkkuveitsi, senlainen, tasakärkinen, joita laukkuryssät
entiseen aikaan kauppailivat.
Ruoka-ajaksi pistäytyi emäntämme ulos.
Kun olimme lopettaneet kelpo ateriamme ja emäntämme alkanut
kantaa hössytellä ruokia pöydältä, ilmestyi mies tuvan ovesta.
Se vasta oli näkemys!

Jos arvoisa emäntämme oli tanakka, lihava, punakka, hyllyvä, niin
oli tämä hontelo, laiha, luinen, ihan luuranko, kaikin puolin
emäntämme vastakohta. Hän oli tavan pitkä, polvet hieman
koukussa, tukka takkuinen, kaiken karvanen, muoto joukea, pitkä,
otsansa oli onteva, huomattavasti kovertunut sisäänpäin, silmät
pienet ja tiirottavat, nokka kippura ja pieni, huulet ohuet ja tiivisti
kiinni, leuka pitkä ja vahva, josta huoleti olisi puolet riittänyt
emäntämme leuvan jatkoksi ja sittenkin olisi miehelle jäänyt
tavallinen leuka. Muotonsa oli iholtaan väritön, likasen harmaa.
Tämän muotoinen oli mies, joka ilmestyi tuvan ovesta ja tuli
suoraan meidän luoksemme.
— Terve! sanoi hän ja pisti kättä meille kummallekin ja istuutui
rahille.
— Kuulkaapas, hyvät vieraat, kun teitä pirut pelkäävät, jatkoi hän
siitä. Kun minä makasin tuolla ojassa ja odottelin piruja, niin ei niitä
tänä iltana tullutkaan. Minä aattelin, että mikähän niillä nyt on, kun
eivät tulekaan, vaikka muina iltoina hypätä luikkivat ylitseni, että
parta viuhkaa… Sitten tulitte te, ja minä arvelin, että noita, noita
kaite ne pelkäävät.
— Kyllä ne meitä ainakin pikkupirut pakenevat, sanoi toverini.
— Ne, näet, vainoovat minua, ett'en saa niiltä rauhaa näin illan
kuhjussa muualla kuin ojassa, sinne eivät, näet, huomaa tulla. Öillä
en saa niiltä maata muualla kuin pöydällä. Siihen eivät osaa, vaikka
niitä tuvan täydeltä tulla pakkaa tupaan, selitti ukko hätäisesti, ikään
kuin vavahdellen pelosta.
— Mitä piruja ne senlaiset ovat? kysyi toverini.

— Talon piruja, vastasi emäntämme karsinpenkiltä, johon hän taas
oli asettunut, saatuaan ruuat korjuuseen.
— Tottapa ne lienevät talon piruja, arveli ukkikin.
Huolimatta piruista taikka muista, heitin minä kengät jalastani ja
aloin kokoilla heiniä vuoteekseni.
Kun nainen karsinpenkiltä tämän huomasi, nousi hän sanaakaan
puhumatta ja meni ja toi suuren syleyksen makuuvaatteita ja laittoi
kaksi tilaa lattialle. Kokosi ensin heiniä kasaan, levitti niille karkean
alusvaatteen, pani lakanan sen päälle, asetti päänalaset ja leväytti
somasti koristellun peitteen molemmille vuoteille.
— Maatkaa tuossa, vieraat, jos piruilta saatte, sanoi hän sitten,
meni ja asettui entiselle paikalleen karsinpenkille.
Ukki istua noljotti rahilla ja katseli naisen toimia.
— Ei, vieraat! Ei, hyvät vieraat, se sovi. Ette siinä rauhaa saa,
sanoi hän, kun emäntämme oli tilat tehnyt, ja nousi katsomaan
soveliaampaa paikkaa.
— Kyllä me siinä saatamme nukkua hyvinkin… Ei tänne pirut tule,
ei ikinä enää, sanoi toverini vakavasti.
Minä heitin päältäni ja kävin tilalleni.
— Ettäkö pirujen kanssa liitossa nämät vieraat, arveli ukki,
enemmän kuitenkin itsekseen.
— Emme liitossa, emmekä missään, sanoi toverini päättävästi,
vaan pirut pelkäävät meitä… pelkäävät eivätkä uskalla tulla

likimaillekaan.
— Pelkäävät eivätkäkö uskalla?
— Aivan niin. Ja ne pelkäävät jokaista kelpo työmiestä.
Ukki istui ja tirkisteli toverini vakaita kasvoja.
— Pelkäävätkö työm…? kysäsi hän.
— Pelkäävät! Työmiestä ne pelkäävät, ahkerata, mutta joutilasta,
laiskaa vetelystä ne vainoovat ja pyytävät pauloihinsa, puhui toverini
varmasti.
Ukki jäi sanattomaksi ja katseli naista, joka istui karsinpenkillä.
— Tuokaapa minulle raamattu tahi uusi testamentti, pyysi toverini.
Nainen lähti ja toi tanakan kirjan.
— Tämä on pyhä kirja, sanoi toverini, ottaen kirjan. Sitä, joka tätä
kirjaa lukee, tekee ahkerasti työtä ja käypi kirkossa, sitä eivät pirut
koskaan kiusaa, eivätkä vainoo, puhui toverini vakavasti hartaalla
äänellä, asettaen raamatun pöydän nenälle.
Se oli tuonlainen vanha, vahva, puukantinen raamattu, vahvoilla
messinkiheloilla varustetuilla hakasilla, jonkalaisia nähdään vielä
siellä täällä maaseuduilla maassamme. Se oli "Turusa, Prändätty
j.n.e., 1758", niinkuin ensi lehden alareunassa oli luettavana.
Ukki hieman hymähti toverini puhuessa ja näytti epäilevältä ja
katseli karsinpenkillä istuvata naista, johon puhe näytti tehneen
vaikutuksen.

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Surgical Decision Making 6th Edition Edition Robert C. Mcintyre

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Surgical Decision Making 6th Edition Edition Robert C. Mcintyre

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