Complications in Equine Surgery [1 ed.] 2020025496, 2020025497, 9781119190073, 9781119190080, 9781119190158

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COMPLICATIONS IN EQUINE SURGERY

COMPLICATIONS IN EQUINE SURGERY Edited by

Luis M. Rubio-Martinez and Dean A. Hendrickson

This edition first published 2021 © 2021 by John Wiley & Sons, Inc Blackwell Publishing was acquired by John Wiley & Sons in February 2007. Blackwell’s publishing program has been merged with Wiley’s global Scientific, Technical and Medical business to form Wiley-Blackwell. The right of Luis M. Rubio-Martinez and Dean A. Hendrickson to be identified as the authors of the editorial material in this work has been asserted in accordance with law. Registered Office John Wiley & Sons, Inc., 111 River Street, Hoboken, NJ 07030, USA Editorial Office 111 River Street, Hoboken, NJ 07030, USA For details of our global editorial offices, customer services, and more information about Wiley products visit us at www.wiley.com. Wiley also publishes its books in a variety of electronic formats and by print-on-demand. Some content that appears in standard print versions of this book may not be available in other formats. Limit of Liability/Disclaimer of Warranty The contents of this work are intended to further general scientific research, understanding, and discussion only and are not intended and should not be relied upon as recommending or promoting scientific method, diagnosis, or treatment by physicians for any particular patient. In view of ongoing research, equipment modifications, changes in governmental regulations, and the constant flow of information relating to the use of medicines, equipment, and devices, the reader is urged to review and evaluate the information provided in the package insert or instructions for each medicine, equipment, or device for, among other things, any changes in the instructions or indication of usage and for added warnings and precautions. While the publisher and authors have used their best efforts in preparing this work, they make no representations or warranties with respect to the accuracy or completeness of the contents of this work and specifically disclaim all warranties, including without limitation any implied warranties of merchantability or fitness for a particular purpose. No warranty may be created or extended by sales representatives, written sales materials, or promotional statements for this work. The fact that an organization, website, or product is referred to in this work as a citation and/or potential source of further information does not mean that the publisher and authors endorse the information or services the organization, website, or product may provide or recommendations it may make. This work is sold with the understanding that the publisher is not engaged in rendering professional services. The advice and strategies contained herein may not be suitable for your situation. You should consult with a specialist where appropriate. Further, readers should be aware that websites listed in this work may have changed or disappeared between when this work was written and when it is read. Neither the publisher nor authors shall be liable for any loss of profit or any other commercial damages, including but not limited to special, incidental, consequential, or other damages. Library of Congress Cataloging-in-Publication Data [Names: Rubio Martinez, Luis M., editor. | Hendrickson, Dean A., editor. Title: Complications in equine surgery / edited by Luis M. Rubio Martinez, Dean A. Hendrickson. Description: Hoboken, NJ : Wiley-Blackwell, 2021. | Includes bibliographical references and index. Identifiers: LCCN 2020025496 (print) | LCCN 2020025497 (ebook) | ISBN 9781119190073 (hardback) | ISBN 9781119190080 (adobe pdf) | ISBN 9781119190158 (epub) Subjects: MESH: Horse Diseases–surgery | Intraoperative Complications–veterinary | Postoperative Complications–veterinary | Horses–surgery | Surgery, Veterinary–methods Classification: LCC SF951 (print) | LCC SF951 (ebook) | NLM SF 951 | DDC 636.1/089–dc23 LC record available at https://lccn.loc.gov/2020025496 LC ebook record available at https://lccn.loc.gov/2020025497] Cover Design: Wiley Cover Images: courtesy of Sussex Equine Hospital, Tanya Bricker, Dean Hendrickson Set ­in ­9.5/12.5pt ­STIXTwoText ­by­SPi Global, ­Pondicherry, ­India 10  9  8  7  6  5  4  3  2  1

Dedicated to Eva, Marcos, and Olivia, for their love, patience, and support. Luis M. Rubio-Martinez Dedicated to Amy for her love, patience, and continued support of my crazy endeavors. Dean A. Hendrickson

vii



Contents



Foreword  xi

Preface  xiii Acknowledgements  xv

List of Contributors  xvi

1

Surgical Complications  1 Luis M. Rubio-Martinez and Dean A. Hendrickson

2

Complications of Parenteral Administration of Drugs  10 Julie E. Dechant

3

Complications of Intravascular Injection and Catheterization  16 Julie E. Dechant

4

Complications of Endoscopy  25 Julie E. Dechant

5

Complications of Nasogastric Intubation  29 Julie E. Dechant

6

Complications of Fluid Therapy  36 Angelika Schoster and Henry Stämpfli

7

Complications Associated with Hemorrhage  57 Margaret C. Mudge

8

Complications of Blood Transfusion  64 Margaret C. Mudge

9

Complications Associated with Sutures  70 Ian F. Devick and Dean A. Hendrickson

10

Complications of Bone Graft Harvesting, Handling, and Implantation  79 Lynn Pezzanite and Laurie R. Goodrich

11

Complications of Cryosurgery  87 Ann Martens

12

Complications of Laser Surgery  95 Kenneth E. Sullins

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Contents

13

Complications of Systemic Analgesic Drugs  109 Maria Amengual-Vila and Eva Rioja Garcia

14

Complications of Loco-Regional Anesthesia  118 Eva Rioja Garcia

15

Complications of Sedative and Anesthesia Medications  135 Rachel C. Hector and Khursheed Mama

16

Complications During Recovery from General Anesthesia  154 Alexander Valverde

17

Complications Associated with Surgical Site Infections  168 Denis Verwilghen and J. Scott Weese

18

Complications of Reconstructive Surgery  196 Jacintha M. Wilmink and Debra C. Archer

19

Complications of Excessive Granulation Tissue  204 Jacintha M. Wilmink and Debra C. Archer

20

Complications of Skin Neoplasia  212 Debra Archer and Jacintha M. Wilmink

21

Complications of Skin Grafting  222 Debra C. Archer and Jacintha M. Wilmink

22

Complications of Oral and Salivary Gland Surgery  233 Patrick Martin Dixon and Richard J.M. Reardon

23

Complications of Esophageal Surgery  254 Louise L. Southwood

24

Complications of Stomach Surgery  265 Louise L. Southwood

25

Complications of Splenic Surgery  272 Eileen Sullivan Hackett

26

Complications of Abdominal Approaches  279 Shauna P. Lawless and Eileen Sullivan Hackett

27

Complications of the Intraoperative Colic Patient  291 Anje G. Bauck and David E. Freeman

28

Complications of the Postoperative Colic Patient  310 Louise L. Southwood

29

Complications of Surgery of the Rectum and Anus  374 Michael A. Spirito

Contents

30

Complications of Abdominal Surgery: Incisional Hernia  378 John P. Caron

31

Complications of Equine Laparoscopy  391 Donna L. Shettko and Dean A. Hendrickson

32

Complications of Endoscopic Laser Surgery  404 Jan F. Hawkins

33

Complications Following Surgery of the Equine Nasal Passages and Paranasal Sinuses  413 Lynn Pezzanite and Jeremiah T. Easley

34

Complications of Pharynx Surgery  427 Norm G. Ducharme and Fabrice Rossignol

35

Complications of Larynx Surgery  438 Fabrice Rossignol and Norm G. Ducharme

36

Complications of Surgery for Diseases of the Guttural Pouch  468 Anje G. Bauck and David E. Freeman

37

Complications of Equine Tracheal Surgery  488 John Peroni

38

Complications of Equine Thoracic Surgery  491 John Peroni

39

Complications of Testicular Surgery  498 James Schumacher and Thomas O’Brien

40

Complications of Penile and Preputial Surgery  522 James Schumacher and Thomas O’Brien

41

Complications of Ovarian and Uterine Surgery  532 James Schumacher and Thomas O’Brien

42

Complications of Vulvar, Vestibular, Vaginal, and Cervical Surgery  550 James Schumacher and Thomas O’Brien

43

Complications of Urinary Surgery  571 Sara K.T. Steward and Luis M. Rubio-Martinez

44

Complications of Diagnostic Tests for Lameness  583 Ellen R. Singer

45

Complications of Synovial Endoscopic Surgery (Arthroscopy, Tenoscopy, Bursoscopy)  601 Troy N. Trumble and Michael C. Maher

46

Complications of Equine Orthopedic Surgery  629 Kyla F. Ortved and Dean W. Richardson

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47

Complications of Surgery of the Equine Foot  667 Britta S. Leise

48

Complications of Surgical Correction of Angular Limb Deformities  683 Robert Hunt and Amy M. Buck

49

Complications of Surgical Correction of Flexural Limb Deformities  694 Belinda Black and James R. Vasey

50

Complications of Splint Bone Fractures  718 Timothy Lescun

51

Complications of Craniomaxillary and Mandible Fractures  730 Timothy Lescun

52

Complications of Tendon Surgery  739 Roger K.W. Smith

53

Complications of Muscle Surgery  757 Brad Nelson

54

Complications of Regenerative Medicine  769 Ashlee E. Watts

55

Complications of Osseous Cyst-Like Lesions  774 Ashlee E. Watts

56

Complications of Equine Ophthalmic Surgery  779 Kate S. Freeman and Dennis E. Brooks

57

Complications of Diagnostic Procedures of the Nervous System  815 Laura Johnstone

58

Complications of Anterior Cervical Fusion  826 Barrie DonLeo Grant

59

Complications of Surgery for Impingement of Dorsal Spinous Processes  833 Luis M. Rubio-Martinez

60

Complications of Peripheral Nerve Surgery  843 Yvonne A. Elce

Index  855

xi

Foreword When I was invited to write this foreword to the book Complications in Equine Surgery, Dr. J.D. Wheat’s (R.I.P.) wise insight at the outset of my equine surgery residency immediately came to mind. He was then an internationally renowned equine surgeon at the University of California, Davis, and a man of few, but often “powerful” words! I had a case that developed a wound infection after the placement of an implant following an eye enucleation. A colleague passed by and encouragingly piped up that it never happened to their cases! Dr Wheat’s retort was: “If it didn’t happen, it is because you never did enough!” The editors, Luis Rubio-Martinez and Dean Henrickson, are to be commended for tackling this challenging, important surgical topic. They are experienced and internationally renowned equine surgeons and appropriate leaders for this tome. They have lined up an impressive team of knowledgeable equine surgeons from all over the world, with pertinent expertise to address the plethora of complications that may arise following equine surgical interventions. Complications are, unfortunately, part and parcel of our surgical discipline. Indeed, they are perhaps one of the most challenging parts of our working lives. Paradoxically, a lack of exposure during residency training can leave less experienced surgeons feeling ill-equipped to deal with them. A variety of emotional responses are triggered when surgical complications arise. Depending on experience, these may include feelings of failure, guilt, shame, anxiety, or embarrassment. For some, a natural instinct is “fight or flight,” while others choose to “bury their head in the sand,” or worst of all – blame others. Although the equine surgical patient may be harmed and the first victim of a surgical technical error, the surgeon may also be the second victim in emotional terms  [1], particularly when serious complications arise. It is usually a humbling experience that we should learn from. The ideal approach when complications arise is to accurately diagnose the nature of the problem, analyze the cause, treat it to the best of our ability using an evidencebased approach, and learn from it. Rapid disclosure of adverse events to the horse owner with good professional

communication and thorough documentation will help avoid litigation or, at the very least, prepare for it. The art of communication will help the experienced surgeon navigate these knotty situations, and junior surgeons and residents should listen well and consult and learn from more experienced colleagues. Talking to a colleague about the surgical error  [1] may also help to reduce the emotional burden incurred by the surgeon implicated. The word complication is derived from the Latin word complicare for a fold, the opposite to smooth – the desired outcome following a surgical intervention. F.D. Roosevelt’s statement “A smooth sea never made a skilled sailor” is fitting for surgery and surgeons! The words complication and adverse event, although they have different meanings, are often used interchangeably. Adverse events have been defined as “an unintended injury or complication resulting in prolonged length of hospital stay, disability at the time of discharge, or death caused by healthcare management and not by the patients’ underlying disease” [2]. Adverse events may cause preventable equine patient harm, prolong hospitalization, and increase costs. It is interesting that most adverse events in human hospitals are associated with surgery  [3]. Furthermore, surgeons should note that nonoperative management errors were more frequent than errors in surgical techniques and included monitoring, incorrect or delayed treatment, diagnostic error. or delay [4]. Complications may be a consequence of an adverse event, but an adverse event may occur without complication. Careful surgical planning (patient, surgical theatre, and equipment) and communication with the surgical team, intraoperative technique, and perhaps most important, non-operative management, should keep complications to a minimum. Unfortunately, evidence-based information on complications in equine surgery is not always available, as some of the equine surgical complications are extremely rare and treatment depends on the creativity and experience of the attending surgeon at the time. This is often the real-life situation!

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Foreword

Future efforts to improve patient safety should target research on the leading causes of potentially preventable equine patient surgical harm, identified from collected data on the frequency, severity, and preventability of adverse events. The Clavien-Dindo classification of surgical complications, now widely employed in human surgery, or variations thereof, would be a useful tool for grading complications in future equine studies [5]. A text book addressing this subject is timely, unique, and fills an important niche and will be an invaluable and comforting “go-to” resource, particularly for less experienced

junior surgeons, to provide guidance on decision-making in challenging cases. It will provide access to the experience of many expert surgeons. Niels Bohr stated that “an expert is a person who has made all possible mistakes in a small field!” Hopefully, this body of work will inspire and pave the way for new research studies on this topic to move this important surgical field forward. Professor Sheila Laverty MVB DACVS DECVS. Faculty of Veterinary Medicine, University of Montreal, St. Hyacinthe, Canada

R ­ eferences 1 Wu, A. (2000). Medical error: the second victim. The doctor who makes mistakes needs help too. B.M.J. 320 (7237): 726–727. 2 Brennan, T.A., Leape, L.L., Laird, N.M., et al. (1991). Incidence of adverse events and negligence in hospitalized patients. Results of the Harvard Medical Practice Study I. N. Engl. J. Med. 324: 370–376. 3 Baker, G.R., Norton, P.G., Flintoft, V., et al. (2004). The Canadian adverse events study: the incidence of adverse

events among hospital patients in Canada. J.A.M.C. 170: 1678–1686. 4 Anderson, O., Davis, R., Hanna, G.B., et al. (2013). Surgical adverse events: A systematic review. Am. J. Surg. 206 (2): 253–262. 5 Dindo, D., Demartines, N., and Clavien, P.A. (2004). Classification of surgical complications: a new proposal with evaluation in a cohort of 6,336 patients and results of a survey. Ann. Surg. 240 (2): 205–213.

xiii

Preface As surgeons we read and learn with enthusiasm about surgical treatments and techniques and enjoy performing those on our patients aiming to achieve a successful outcome for them. That successful outcome is the result of many factors including good knowledge and technique, mentorship, interaction with peers, experience and, of course, the availability of evidence-based literature and resources. Publications in the form of textbooks and journals play a central role in our individual training and progression, and will remain as key in the further evolvement of equine surgery and formation of new equine surgeons. As residents we feel thrilled and enormously satisfied when we observe how application of those surgical treatments translates into survival of our patients. It is with great satisfaction when as surgeons we remove gloves, gown and mask at the end of a surgical procedure that has been completed effectively. The satisfaction is bigger when the patient gets discharged from the hospital and increases further when we learn from owners, trainers or referring veterinarians that the patient has successfully returned to their previous or intended use. However, as surgeons we all learn that many hurdles are to be cleared in the pre-, intra-, and postoperative periods to reach that successful outcome. On occasions, there are unforeseen circumstances or factors that we may not be able to control or that escape our individual experience. We all have experienced surgeries that do not go according to plan, despite having cautiously read and memorized all steps of the surgical procedures. Not uncommonly, we encounter individual variations, intraoperative incidents or situations that may escape the standard descriptions in the literature. Surgical steps may be carefully followed without guarantee that they will translate into results as described in textbooks or papers. In the postoperative period, we are vigilant of our patients hoping for a steady recovery to hospital discharge and successful return to previous use. We monitor our patients closely with special attention to detect early signs that may alert us to occurrence of complications or deviation from the uneventful recovery path. This represents a source of stress for the responsible clinician and especially

for residents when they are questioned by their mentors about unexpected signs, possible complications, reasons, and how those could have been prevented and be treated at the time. The stress also extends to client communication, as the effect of those complications on the outcome of that particular patient may not be readily described in the scientific literature. All these bumps along the way can be referred to as complications that jeopardize the well-desired successful outcome for our patients. Although we will not be able to save all patients, the science to accurately predict, diagnose, and manage complications, in addition to training and experience, hopefully give the surgeon the ability to adapt to those less-than-ideal situations while providing the means to achieve the best successful outcome for that patient. The editors are delighted to present this new textbook Complications in Equine Surgery. The original idea of this project came from one of the editors (LRM) during his early years as a surgery resident and young equine surgeon. In 2014, LRM and DAH started with the design of the project and in 2015 Wiley Blackwell came on board. After another 6 years we are finally seeing the project completed. The aim of this project was to gather relevant and important information to increase awareness, literacy, and evidence on the prevention, identification, and management of complications commonly associated with diagnostic and surgical procedures performed on equine patients. Literature resources of this kind are common and abundant in human medicine but limited in equine surgery, and veterinary medicine in general. The editors present this textbook in a format that markedly differs from other equine and veterinary textbooks. Complications are the mainstay of the chapters, which are divided into a number of sections including definition, risk factors, diagnosis, prevention, and treatment. This textbook is not only aimed at equine surgery residents and surgeons, but also to all those equine clinicians that very often and carefully take care of the patients in their pre- and postoperative times. We trust that all of you will find this textbook useful.

xiv

Preface

This project has only been possible thanks to the excellent editorial team at Wiley, and the invaluable, hard work of many authors who have contributed chapters to this textbook. We have endeavored to include a long list of worldwide experts in different areas of equine surgery. An emphasis has been made to include references, even though these may sometimes be limited to single case

reports, small case series, or limited notes in publications. We trust this textbook will strive for the further development and building-up of evidence-based information in the field of complications in equine surgery, aiming to contribute to the equine surgeons’ education and success, as well as the welfare of our equine patients. Luis M. Rubio-Martinez Dean A. Hendrickson

xv

Acknowledgements The editors of this textbook would like to thank: ●●

●●

All the staff at Wiley, especially Skye Loyd and Melissa Hammer, for believing in the project initially and for all their invaluable hard work during the journey and making this project a reality. Thank you for your priceless guidance, dedication, and patience. All our colleagues who have contributed to this textbook and made this project happen. Thank you for your time, effort, and patience in this long endeavor that finally has reached its destination.

●●

●●

To all our colleagues in our careers (colleagues, mentors, peer clinicians, residents, and interns), as well as all those equine patients that during the years have gifted us with our experiences, successes, and under-successes. All those experiences have improved our knowledge and skills and hopefully made us better surgeons. And finally, special thanks to our families for their understanding and unconditional support, despite the many evenings and holidays when they did not get our attention.

xvi

­List of Contributors Maria Amengual-Vila, DVM, DECVAA, MRCVS Clinical Anesthetist Highcroft Veterinary Referrals Witchurch, Bristol United Kingdom Debra C. Archer, BVMS, PhD CertES(soft tissue), DECVS, FRCVS, FHEA Professor in Equine Surgery Institute of Veterinary Clinical Studies University of Liverpool Liverpool United Kingdom Anje G. Bauck, DVM, DACVS-LA Clinical Assistant Professor Department of Large Animal Clinical Sciences College of Veterinary Medicine University of Florida Gainesville, FL Belinda Black, BSc, BVMS, DVSc DACVS-LA Equine Surgeon Murray Veterinary Services West Coolup Western Australia Dennis E. Brooks, DVM, PhD, DACVO Professor Emeritus University of Florida Gainesville, FL Amy M. Buck, MS, DVM Hagyard Equine Medical Institute Lexington, KY John P. Caron MVSc, DVM, DACVS Professor Equine Surgery Department of Large Animal Clinical Sciences Michigan State University East Lansing, MI

Julie E. Dechant, DVM, MS, DACVS, DACVECC Professor of Clinical Equine Surgical Emergency and Critical Care Department of Surgical and Radiological Sciences School of Veterinary Medicine University of California–Davis Davis, CA Ian F. Devick, DVM, MS, DACVS-LA Associate Veterinarian Weatherford Equine Medical Center Weatherford, TX Padraic Martin Dixon, MVB, PhD, FRCVS, DEVDC(Equine) Professor of Equine Surgery Division of Veterinary Clinical Studies The Royal (Dick) School of Veterinary Studies Midlothian Scotland Norm G. Ducharme, DVM, MSc, DACVS James Law Professor of Surgery Cornell University Hospital for Animals (CUHA) College of Veterinary Medicine Cornell University, Ithaca NY Jeremiah T. Easley, DVM, DACVS Assistant Professor Department of Clinical Sciences College of Veterinary Medicine and Biomedical Sciences Colorado State University Fort Collins, CO Yvonne A. Elce, DVM, DACVS Lead of the Equine Hospital Langford Vets Equine Hospital Langford, Bristol United Kingdom

List of Contributors xvii

David E. Freeman, MVB, PhD, DACVS Appleton Professor in Equine Surgery Large Animal Clinical Sciences College of Veterinary Medicine University of Florida Gainesville, FL Kate S. Freeman, MEM, DVM, DACVO Affiliate Faculty of Ophthalmology Colorado State University Fort Collins, CO Laurie R. Goodrich, DVM, PhD, DACVS Professor of Orthopedics Department of Clinical Sciences Colorado State University Fort Collins, CO Barrie DonLeo Grant, DVM, MS, DACVS, MRCVS Equine Consultant Bonsall, CA Eileen Sullivan Hackett, DVM, PhD, DACVS, DACVECC ACVS Associate Professor Equine Surgery and Critical Care Department of Clinical Sciences Colorado State University Fort Collins, CO Jan F. Hawkins, DVM, DACVS Professor of Large Animal Surgery Department of Veterinary Clinical Sciences Purdue University West Lafayette, IN Rachel C. Hector, DVM, MS, DACVAA Department of Clinical Sciences Clinical Instructor, Anesthesia Colorado State University Fort Collins, CO Dean A. Hendrickson, DVM, MS, DACVS Professor of Surgery Department of Clinical Sciences College of Veterinary Medicine and Biomedical Sciences Colorado State University Fort Collins, CO Robert J. Hunt, DVM, MS, DACVS Hagyard Equine Medical Institute Lexington, KY

Laura Johnstone, BVSc, MVSc, DACVIM (LAIM) Cromwell New Zealand Shauna P. Lawless, MVB Resident – Equine Surgery and Lameness Department of Clinical Sciences Colorado State University Fort Collins, CO Britta S. Leise, DVM, PhD, DACVS-LA Associate Professor of Equine Surgery Department of Veterinary Clinical Sciences Louisiana State University, School of Veterinary Medicine Baton Rouge, LA Timothy B. Lescun, BVSc (Hons), MS, PhD, DACVS Associate Professor of Large Animal Surgery Department of Veterinary Clinical Sciences, Purdue University College of Veterinary Medicine West Lafayette, IN Michael C. Maher, DVM, DACVS-LA Staff Surgeon Brandon Equine Medical Center Brandon, FL Khursheed Mama, DVM, DACVAA Professor, Anesthesiology Department of Clinical Sciences Colorado State University Fort Collins, CO Ann Martens, DVM, PhD, DECVS Professor of Large Animal Surgery Department of Surgery and Anesthesiology of Domestic Animals Faculty of Veterinary Medicine Ghent University Merelbeke, Belgium Margaret C. Mudge, VMD, DACVS, DACVECC Department of Veterinary Clinical Sciences The Ohio State University Columbus, OH

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List of Contributors

Brad Nelson, DVM, MS, PhD, DACVS-LA Assistant Professor, Equine Surgery Principal Investigator, Preclinical Surgical Research Laboratory Department of Clinical Sciences College of Veterinary Medicine and Biomedical Sciences Colorado State University Fort Collins, CO Thomas O’Brien, MVB, DACVS-LA Fethard Equine Hospital, Kilknockin County Tipperary Ireland Kyla F. Ortved, DVM, PhD, DACVS, DACVSMR Assistant Professor of Large Animal Surgery Department of Clinical Studies New Bolton Center, School of Veterinary Medicine, University of Pennsylvania Kennett Square, PA Lynn Pezzanite, DVM, MS, DACVS Post-doctoral Fellow/PhD Student Department of Clinical Sciences and Translational Medicine Institute College of Veterinary Medicine and Biomedical Sciences Colorado State University Fort Collins, CO John Peroni, DVM, MS, DACVS Professor of Surgery Department of Large Animal Medicine Veterinary Medical Center University of Georgia Athens, GA

Eva Rioja Garcia, DVM, DVSc, PhD, DACVAA, DECVAA, MRCVS Clinical Director of Anaesthesia and Analgesia Optivet Referrals Havant, Hampshire United Kingdom Fabrice Rossignol, DVM, DECVS Equine Clinic Grosbois Boissy Saint Leger France Luis M. Rubio-Martínez, DVM, DVSc, PhD, DACVS, DECVS, DACVSMR, MRCVS Sussex Equine Hospital, Ashington, West Sussex, United Kingdom CVet Ltd. Equine Surgery and Orthopedics, United Kingdom Angelika Schoster, Dr.med.vet, DVSc, PhD, DVSc, DACVIM, DECEIM Clinic for Equine Internal Medicine University of Zurich Switzerland James Schumacher, DVM, MS, DACVS, MRCVS Department of Large Animal Clinical Sciences College of Veterinary Medicine University of Tennessee Knoxville, Tennessee Donna L. Shettko, DVM, MSN, DACVS Western University of Health Sciences Pomona, CA Ellen R. Singer, BA, DVM, DVSc, DACVS, DECVS, FRCVS Director, E Singer Equine Orthopaedics and Surgery Ltd. Neston, Cheshire United Kingdom

Richard J.M. Reardon, BVetMed (hons), MVM, PhD, FHEA, CertES(orth.), DECVS, DEVDC(equine), MRCVS Senior Lecturer in Equine Surgery The Royal (Dick) School of Veterinary Studies University of Edinburgh Easter Bush, Midlothian Scotland

Roger K. W. Smith, MA, VetMB, PhD, DEO, FHEA, ECVDI LAassoc, DECVSMR, DECVS, FRCVS Professor of Equine Orthopedics Department of Clinical Sciences and Services The Royal Veterinary College Hatfield, Hertfordshire United Kingdom

Dean W. Richardson, DVM, DACVS Charles W. Raker Professor of Equine Surgery Chief, Large Animal Surgery New Bolton Center, School of Veterinary Medicine, University of Pennsylvania Kennett Square, PA

Louise L. Southwood, BVSc, PhD, DACVS, DACVECC Professor, Large Animal Emergency & Critical Care Department of Clinical Studies New Bolton Center School of Veterinary Medicine University of Pennsylvania Philadelphia, PA

List of Contributors xix

Michael A. Spirito, DVM Davidson Surgery Center Hagyard Equine Institute Lexington, KY

James R. Vasey, BVSc, FANZCVSc Goulburn Valley Equine Hospital Congupna, Victoria Australia

Henry Stämpfli, DVM, Dr.Med.Vet., DACVIM Professor Retired Large Animal Medicine, Clinical Studies Ontario Veterinary College University of Guelph Guelph, Ontario Canada

Denis Verwilghen, DVM, MSc, PhD, DES, DECVS Associate Professor in Equine Surgery Head of the Camden Equine Centre School of Veterinary Science – Faculty of Science University of Sydney Australia

Sara K.T. Steward, DVM Equine Surgery Resident Veterinary Teaching Hospital Department of Clinical Sciences Colorado State University Fort Collins, CO Kenneth E. Sullins, DVM, MS, DACVS Professor of Equine Surgery College of Veterinary Medicine Midwestern University Glendale, AZ Troy N. Trumble, DVM, PhD Associate Professor Veterinary Population Medicine Department University of Minnesota College of Veterinary Medicine St. Paul, MN Alexander Valverde, DVM, DVSc, DACVAA Associate Professor Department of Clinical Studies Ontario Veterinary College University of Guelph Guelph, Ontario Canada

Ashlee E. Watts, DVM, PhD, DACVS Associate Professor Department of Large Animal Clinical Sciences Texas A&M University College Station, TX J. Scott Weese, DVM, DVSc, DACVIM Department of Pathobiology Ontario Veterinary College University of Guelph Guelph, Ontario Canada Jacintha M. Wilmink, DVM, PhD, DRNVA WOUMAREC (Wound Management and Reconstruction in Horses) Wageningen The Netherlands

1

1 Surgical Complications

Luis M. Rubio-Martinez DVM, DVSc, PhD, DACVS, DECVS, DACVSMR, MRCVS1 and Dean A. Hendrickson DVM, MS, DACVS2 1

Sussex Equine Hospital, Ashington, West Sussex, United Kingdom and CVet Ltd. Equine Surgery and Orthopedics, United Kingdom College of Veterinary Medicine and Biomedical Sciences, Colorado State University, Fort Collins, Colorado

2

­Overview The term “surgical complication” is frequently used in the medical profession, but its definition in the medical literature has been inconsistent over the years. The World Journal of Surgery defines “surgical complication” as “any undesirable, unintended, and direct results of an operation affecting the patient that would not have occurred had the operation gone as well as could reasonably be hoped” [1]. This definition suggests that a surgical complication is dependent on the surgical skill of the surgeon, the facilities and equipment available and the condition of the patient.

­ ist of Complications Associated L with Surgery: ●● ●● ●● ●● ●● ●● ●● ●●

Morbidity and mortality Surgical checklists Perioperative consequences of surgical trauma Metabolic and nutritional effects Neuroendocrine Systemic inflammatory response Pain Impact of host factors and comorbid conditions

“Surgical complications,” otherwise referred to as “operative complications,” are not restricted to the time window of the surgical procedure itself but comprise both intraand postoperative complications [2]. The duration of surgery defines the time window for intraoperative complications; meanwhile, postoperative complications are not restricted to those occurring during hospitalization

but are defined according to a time period. A 30-day period after the surgical procedure, either during or after hospitalization, has been used in human medicine [2]. All surgical procedures are associated with a degree of risk and the benefits of any procedure need to be weighed against any potential complications so that the clinician and the patient or animal owner can make a balanced and informed decision. This discussion should also cover complementary techniques that augment results to optimize physical, occupational and societal goals [3]. In veterinary medicine, owners’ expectations, engagement and commitment, animal welfare and economics need also to be balanced. Surgical complications can be classified into patientrelated complications (related to patient-specific characteristics, rather than to a procedural error), and practitioner-related complications (arising from errors that directly lead to undesirable and unintended results affecting the patient, but also as a result of a faulty technique) [3]. Although surgical errors may be frequently linked to complications, some errors may not result in complications. Recognition of errors and complications provide unique instances to learn from and to work toward avoiding or preventing their re-occurrence [4]. To maximize this process the following practitioner’s goals have been defined in human medicine [3, 5]: 1) Minimize errors by applying an appropriate surgical technique. 2) Identify and manage errors in a timely manner and in a way that would prevent ensuing complications. 3) Identify and manage complications in a timely manner and appropriately.

Complications in Equine Surgery, First Edition. Edited by Luis M. Rubio-Martinez and Dean A. Hendrickson. © 2021 John Wiley & Sons, Inc. Published 2021 by John Wiley & Sons, Inc.

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Surgical Complications

4) Identify and consider patient-related complications in the decision-making process, so that they can be anticipated, prevented or managed correctly. It is not uncommon for clinicians to adopt routines that prevent and manage complications on the basis of personal experience. However, in some cases this may be associated with “making the same mistakes with increasing confidence over an impressive number of years” [6]. In human medicine, standards of expected outcomes for groups of patients require evidence-based practice, making seniority and individual experience less important [7]. ­Evidence-based literature in this area has quickly developed over the last decades, and several textbooks and journals dedicated to surgical complications are available in the human field. The application of an evidence-based approach for prevention, identification and management of surgical complications should result in a reduction in mistakes in the clinical decision-making process. In addition, it will also identify areas on which further research is warranted.

­Morbidity and Mortality Morbidity (from Latin morbidus, meaning sick, unhealthy) is a diseased state, disability, or poor health due to any cause [8]. Surgical morbidity relates to those morbid states that are related to a surgical procedure performed on a patient. Although traditionally defined by the presence or absence of specific postoperative complications, surgical morbidity represents any clinically significant, non-fatal, adverse outcome associated with a surgical procedure [9]. Morbidity can be divided into local (associated with operation site, e.g. wound dehiscence) or general (related to any operation, e.g. acute renal failure). It can also be subdivided based on timely occurrence as intraoperative or postoperative; the latter being further considered as immediate, early, late or long-term, although these are based on arbitrary time thresholds [9]. These categories overlap and are closely interconnected, as for example a specific, local complication such as surgical site infection may have general or systemic effects such as pyrexia, inappetence and motor dysfunction, which are not procedure specific [9]. Surgical mortality is any death regardless of cause, occurring: (1) within 30 days after surgery in or out of the hospital; or (2) after 30 days during the same hospitalization period subsequent to the operation  [10, 11]. In patients undergoing more than one surgical procedure during a single hospitalization, mortality is assigned to the first operation during hospitalization [10]. In human medicine, postoperative morbidity has been shown to have a significant effect on mortality in patients

undergoing major surgery;  [12] however, the association between general postoperative morbidity and long-term outcome or functionality is not well established [9]. This stems from the inconsistent reporting of morbidity in relation to definition, type and criteria, which leads to a lack of reliability in the recording of complications data [9]. Surgical mortality is a concrete universal outcome measure, but unlike morbidity, mortality recording has traditionally been inconsistent as a result of variable duration of hospitalization, follow-up information, and number of surgical procedures performed during the same hospitalization period or different hospitalization periods [10]. Evidence-based knowledge on complications has rapidly evolved and continues to do so in human medicine. The Morbidity and Mortality Conferences (MMCs) were established in the beginning of the 20th century at the Massachusetts General Hospital in Boston  [13], with the aim to improve the quality and safety of human healthcare  [14]. The MMCs have become a requirement for all human medicine surgical training programs in high-risk specialties such as surgery, anesthesia, intensive care and oncology, being a key factor in the accreditation of human hospitals  [15]. These conferences are associated with improvements in healthcare quality and patient safety through analysis of failures  [15]. To further improve the effectiveness of these MMCs, additional structured frameworks such as the Physician Peer Review have been implemented, enabling surgeons to review and evaluate peer surgeons’ results and take corrective actions [16, 17]. These systems aim to improve competencies, protect patients from harm and assist institutions in their evaluations of surgical outcomes, with the ultimate goal of improvement of patient outcome through implementation of measures to identify and prevent operative complications. In 1991, Copeland et  al. developed the “Physiological and Operative Severity Score for the numeration of Mortality and morbidity (POSSUM)” as a representative method for evaluating the result of surgery in patients [18]. This system includes a physiological score and an operation severity score to calculate individual risk for morbidity and mortality. Classification systems for perioperative complications (such as the Clavien–Dindo classification) have been developed [19] and application of these systems has confirmed their prediction of morbidity and mortality rates in humans [20]. Over the last few years, equine studies have focused on identification of prognostic factors, mainly associated with mortality, in patients suffering from certain conditions or undergoing specific surgical procedures. From those studies, risks factors have been identified which provide useful information during the decision-making process between veterinarian and horse owner. However, inconsistent definitions, limited

­Metabolic and Nutritional Effect  3

­ opulations and diverse management regimes often limit p universal conclusions. Adaptations of POSSUM-like strategies to the equine surgical field warrant consideration.

­Surgical Checklists The Safety Checklist was developed by Dr. Atul Gawande with the intention of improving outcomes, team dynamics and patient safety in an intensive care unit of a human hospital  [21]. Based on their successful implementation, in 2008 the World Health Organization (WHO) instituted the Surgical Safety Checklist (SSC) as a global initiative to improve surgical safety of human patients. Since then, SSCs have become standard practice in human hospitals and are slowly being implemented in veterinary hospitals. These checklists cover introduction of surgical and anesthetic teams, identification of patient, consent, procedure to be performed, anatomical location, estimated duration of surgery, availability of equipment, and potential complications among others. Use of SSCs has assisted in prevention of potential safety hazards and errors in the operating room, and improved safety and communication among operating staff  [22–24]. Their implementation has been associated with reduced morbidity, length of in-hospital stay and mortality [25]. Sustained use of SSCs seems to be discipline-specific and is more successful when physicians are actively engaged and leading implementation [26]. In addition, implementation of SSCs did not negatively impact the operating room efficiency, whilst reducing overall disposable costs, in a large multispecialty tertiary care human hospital [27].

­Perioperative Consequences to Surgical Trauma Any surgical procedure is associated with some degree of tissue trauma, which results in a stress response by the patient’s body. This stress response follows the same pathways as that after accidental trauma or disease; however, the magnitude of the stress response will vary with the severity of the stimulus. The patient’s condition, severity of disease, anesthesia and surgical procedure will all contribute to the stimulus of a stress response. Healthy patients undergoing elective minor surgery may not sustain any significant effects, but patients with severe trauma or critical illness can enter prolonged catabolic states with notable consequences to morbidity and mortality. The stress response is multifactorial and governed by inflammatory, metabolic, neurohormonal and immunologic pathways. As a consequence, it is difficult to ­categorize

the degree of stress response as there is no single variable or combination thereof that define stress in a consistent manner. A combination of variables encompassing all involved pathways, and even variables related to other body systems susceptible to stress-related consequences such as the reproductive system, should be included to define the short- and long-term effects of stress [28]. The pathways involved are totally interrelated and difficult to separate, but for the purpose of this review the stress response in the surgical patient will be divided into four sections: metabolic/nutritional effects, neuroendocrine consequences, inflammatory response, and pain.

­Metabolic and Nutritional Effects In the 1930s, Cuthbertson described the body’s post-traumatic response as an immediate “ebb” or shock phase followed by the flow phase [29]. The short-lived (24–48 h) ebb phase is characterized by reductions in blood pressure, cardiac output, body temperature and oxygen consumption, and when associated with hemorrhage, hypoperfusion and lactic acidosis, depending on the severity. The latter flow phase is characterized by hypermetabolism, increased cardiac outputs, increased urinary nitrogen losses, altered glucose metabolism and accelerated tissue catabolism. The nutritional status of the human surgical patient is well recognized as a factor associated with morbidity and mortality [30, 31]. Malnourished patients show a reduction in survival, immune function, wound healing and gastrointestinal functions, and associated prolonged hospitalization and increased infection [32, 33]. Preoperative fasting, anesthesia, surgery and disease all contribute to the stress hypermetabolic response. Stimulation of the sympathetic nervous system causes release of catecholamines, an increase in oxygen delivery and consumption at the tissue level, and a rise in body temperature. As a consequence, the resting energy expenditure increases. Individual assessment of resting energy expenditure has become an integral part of the management of the human surgical patient. Providing adequate perioperative nutritional support is standard of care in humans, as malnutrition or overfeeding are associated with poorer outcome [34]. Horses undergoing surgery are subject to variable preoperative fasting times, and colic patients may undergo prolonged food and even water restriction perioperatively. However, standard assessment of the nutritional status of the equine patient is not common, and nutritional support is often limited to intravenous and/or oral fluids with electrolytes. Other nutrients such as glucose, aminoacids and lipids are less frequently incorporated in the form of either enteral or parenteral nutrition. [35].

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The healthy adult horse can tolerate food deprivation, commonly referred to as simple starvation or pure protein or calorie malnutrition (PPCM), for 24–72 hours with minimal systemic consequences [36]. In this situation, healthy humans sustain neuroendocrine changes leading to a lower metabolic rate and resting energy expenditure. This is associated with decreased blood glucose, insulin, increased glucagon and down-regulation of catecholamines. Initial hepatic glycogenolysis and gluconeogenesis followed by use of fat stores maintain normal blood glucose values and survival, while lean tissue (protein) is spared. Energy demands are increased in patients with a prior history of malnutrition, increased metabolic rate (i.e. young growing animals), underlying metabolic abnormalities, sepsis, severe trauma, or underweight animals at higher risk of stress response. The effect of fasting on stressed catabolic patients is a hypermetabolic state with increased resting energy expenditure. This is the result of the catecholamine release by the stimulated sympathetic nervous system and the inflammatory cytokines released at the site of injury, inflammation, disease or surgery [37, 38]. The magnitude of this hypermetabolic state relates to the severity of the disease or trauma. Stimulation and/or release of corticotrophin, cortisol, epinephrine, growth hormone and glucagon result in an increased resting metabolic rate characterized by insulin resistance, increased glucocorticoid secretion, gluconeogenesis, dysregulation of glycemia, lipolysis, proteolysis, nitrogen loss and rapid malnutrition  [39]. Blood triglycerides should be monitored, and appropriate nutritional support instituted in horses at risk of developing hyperlipemia such as obese animals (especially miniature horses and donkeys), lactating mares, and horses suffering from Cushing’s syndrome or equine metabolic syndrome. The response to an elective surgical procedure will be more limited in a healthy than in a critically ill patient or a patient with severe trauma. However, an increase in metabolic rate occurs postoperatively in humans after simple elective surgery  [40]. Anesthesia and midline abdominal exploratory laparotomy increased the postoperative caloric demand in healthy horses by 10% in experimental conditions  [41]. Increased demands in critically ill equine patients are expected to be higher but have not been quantified to the editors’ knowledge. Due to the patient’s size and weight, local changes in muscle metabolism can also be substantial in the recumbent horse under general anesthesia. Physical compression of muscle groups is associated with restricted local blood perfusion and an increased demand for energy through anaerobic metabolism in the muscle  [42]. This

can lead to use of adenosine triphosphate and creatinine phosphate as energy sources and production of lactate, which can extend into the recovery period  [43, 44]. Because of decreased venous drainage from the muscle, increased muscle lactate is not paralleled by the lower plasma lactate during anesthesia and increases in plasma lactate and potassium extend into the recovery period [42, 44–46]. These metabolic changes can be apparent in healthy horses, especially in the heavy patient and prolonged anesthesia, but changes are more pronounced and commonly recognized in prolonged anesthetics and ill horses such as colic cases [43, 46]. Nutritional supplementation will reverse catabolic processes during simple starvation; however, it will not completely reverse those during metabolic stress, which will remain as long as tissue injury persists. Nutritional support of the critically ill patient aims to minimize the severity of protein loss and morbidity associated with the disease. The goal should be to re-institute food intake as soon as possible and if that is not possible, consider nutritional support. Nutritional support can be provided in the form of enteral or parenteral nutrition. The enteral route is always preferred as it provides a trophic stimulus for the gastrointestinal tract and has a protective effect against bacterial translocation across the intestinal wall [47]. Early enteral nutrition (initiated within 48 h after surgery) significantly decreased morbidity and length in critically ill human patients  [48], and lessened the hypermetabolic and catabolic responses to injury in human and animals [49]. When the enteral route is not available, parenteral nutrition can be used in the form of partial (most commonly) or total parenteral nutrition. Although there is a paucity of published studies, there are some reports of clinical application of enteral and parenteral nutrition in foals and adult horses, from which some guidelines can be obtained [35, 47, 48, 50–55]. Parenteral nutrition is not exempt of complications and, therefore, close monitoring of patients receiving it is required  [52, 55, 56]. A clinical nutrition counselling service has recently been pioneered at a referral equine hospital [57].

­Neuroendocrine Surgical patients undergo a sympathetic nervous system response with activation of adrenocortical axis and release of catecholamines, cortisol and glucagon. The degree of surgical trauma will determine the magnitude of this endocrine response, with redistribution of blood flow to preserve important organs, splenic contraction to increase blood volume, mobilization of resources to provide sub-

­Systemic Inflammatory Respons 

strates such as glucose and fatty acids, and activation of the immune system in more severe cases [58, 59]. General anesthesia itself is associated with a stress response characterized by sympathetic output in healthy horses  [45]. Inhalation anesthesia increased adrenocorticotropic hormone and cortisol release in healthy horses [60, 61], and even in glycerol and non-esterified fatty acids in prolonged anesthesia in healthy horses  [45]. On the contrary, total intravenous anesthesia seemed to cause a lesser stress response than gas anesthesia, although duration of anesthesia and other factors have important effects  [62]. Fasting, re-feeding and anesthetic drugs (i.e. α2-agonists) affect insulin regulation and therefore different drug combinations, and induction and anesthetic protocols contribute to large variability of the hyperglycemic response and circulating levels of these stress markers in the equine patient [63‑65]. Laparoscopic surgery under standing sedation and local anesthesia produced increased cortisol and non-esterified fatty acids plasma levels in horses [66]. Minor elective surgery under general anesthesia (skin sarcoid removal or laryngeal surgery) produced minor changes in blood glucose, lactate or plasma non-esterified fatty acid (NEFA) values, beyond those caused by anesthesia  [63]. Equine patients undergoing elective arthroscopic surgery showed transient hyperglycemia and increased beta-endorphin and cortisol [67]. Cortisol response in people undergoing surgery correlates with surgical trauma and is higher in abdominal than other minor surgeries [68, 69]. Similarly, a 1.6-fold [67] versus a 10-fold [70] increase in plasma cortisol was observed in horses undergoing arthroscopy or abdominal surgery, respectively. Horses with acute colic showed only a mild increase in plasma cortisol intraoperatively, but already had much higher preoperative cortisol levels, which indicates that the stress response in these patients may be already nearing or at maximum level before undergoing surgery  [71]. Postoperative return to baseline of cortisol levels correlates with surgical trauma, being faster after elective arthroscopy than elective abdominal surgery  [64]. This return was longest in colic cases (~60 h) compared with 24 hours in the non-colic group [71]. Sustained increased levels of cortisol in the postoperative period may also reflect response to pain or further trauma in this time period [70]. Surveillance of metabolic and endocrine changes in perioperative equine patients is limited. A recent report investigating the metabolic and hepatic changes in 32 surgical adult colic patients, revealed that hepatic dysfunction, hepatobiliary disease and alterations in metabolism are common in equine colic patients  [72]. Surgical colic patients showed increased levels of bile acids, bilirubin, tri-

glyceride and glucose concentrations and activities of liver enzymes such as GGT, AST, AP and SDH, whereas plasma ammonia was expected to remain within normal ­limits [72–74]. This may indicate hepatocellular injury in equine colic patients but could otherwise be associated with underlying diseases, transient bile duct obstruction, vascular compromise of the liver, or ascending infection from intestinal contents into the liver [72, 74, 75]. Increased TG values have the potential to progress organ damage  [76], and were in fact negatively associated with survival  [72]; however, a return of TG to normal values was observed at the time of re-feeding in most horses  [72]. Elevated bile acid concentrations at admission were associated with decreased survival in colic patients, although increased bile acid can also be the result of prolonged fasting (>3 days) [72]. Hypothermia is another factor that occurs during surgery, which in humans has been associated with an adrenergic response  [77]. A decrease in the mean core body temperature occurs in horses during standing laparoscopy and horses under general anesthesia with or without surgery  [45, 78, 79], but the effects of hypothermia on the stress response in horses are unknown. In conclusion, the stress response to anesthesia and surgery is multifactorial, with pain, tissue perfusion and energy availability being important determinants of stress. Differences in fasting period, anesthetic protocol, length of anesthesia, anesthetic protocol, surgical procedure, surgical trauma, and systemic condition of the patient will have definite effects on the type and magnitude of stress markers such as glycaemia, and plasma insulin, cortisol and NEFA in horses [67], as has been shown in humans.

­Systemic Inflammatory Response All surgery leads to systemic inflammatory response syndrome (SIRS). The majority of information is found in the human literature. It is assumed that similar effects can be found in the equine patient. The inflammatory response consists of hormonal, metabolic and immunological components. The more severe the surgical insult, the more severe the inflammatory response  [80]. The hormonal response is characterized by various stress hormones. In people, adrenaline and cortisol levels are increased in the face of surgery, as are glucagon, growth hormone, aldosterone and antidiuretic hormone. The extent of surgical trauma correlates well with the levels of ACTH and cortisol  [81]. If patients develop postoperative complications, other abnormalities can occur. In people, critically ill patients can have a cortisol deficiency. High dose therapy

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with glucocorticosteroids has been associated with increased mortality, while low doses may have beneficial effects by increasing their response to noradrenaline [82]. The metabolism is decreased in the first few hours after surgery. However, this is soon followed by a catabolic and hypermetabolic phase. This phase is characterized by break down of skeletal muscle and fat  [83]. Oxygen delivery to the tissues is important during this hypermetabolic phase. The body reacts by vasodilating, increasing the heart rate, increasing cardiac output, and increasing the respiratory rate [84]. A leukocytosis occurs in the peripheral blood and granulocytes and macrophages accumulate in the damaged tissues  [85]. Many pro-inflammatory cytokines are released leading to inflammation. The amount of cytokine release is well correlated with both the magnitude and duration of surgery and the risk of postoperative complications. If the initial pro-inflammatory response is exaggerated, sever systemic inflammatory response syndrome may occur.

­Pain Surgical procedures will lead to a pain response. It is well supported that the more invasive a procedure is, the more pain the patient will experience. Horses are typically stoic animals when it comes to exhibiting pain. It is thought that they mask signs of pain from predators, including humans, to minimize possible predation  [86]. In one study, it was determined that horses undergoing surgery paid decreased attention toward novel objects and decreased responsiveness to auditory signals  [87]. The relationship between pain, behavioral distress and physiological stress is com-

plex and difficult to determine. Consequently, endocrine measures may not be accurate indicators of pain alone. It is also difficult to separate the inflammatory process ­associated with surgery and surgical complications from the pain response associated with surgery and surgical complications. The measurement of equine pain is probably best accomplished with multidimensional pain scales  [88]. The Horse Grimace Scale has been recently described and is easy to use and has a high reliability between observers [89].

I­ mpact of Host Factors and Comorbid Conditions Blood loss impairs the body’s ability to deliver oxygen to the tissues and oxygen delivery to the tissues is important during injury [84]. Lack of oxygen impairs the body’s ability to heal. Diagnosing blood loss in the horse can be challenging due to the large reservoir of red blood cells stored in the spleen. Splenic contraction can maintain packed cell volume and total protein in the acute stages of hemorrhage [90]. Fluid volume expansion can actually reduce the effectiveness of oxygen delivery, making blood transfusions an important aspect of improving oxygen delivery. Pituitary pars intermedia dysfunction is thought to impair corneal wound healing in horses  [91]. There also appears to be an association between PPID and degenerative suspensory ligament desmitis [92]. It seems reasonable then that horses with PPID may have difficulty in healing. This should be considered when operating on horses with PPID.

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36 Carr, E.A. and Holcombe, S.J. (2009). Nutrition of critically ill horses. Vet. Clin. N. Am. Equine Pract. 25 (1): 93–108, vii. 37 Lewis, L.D. (1995). Feeding and care of horses with health problems. In: Equine Clinical Nutrition and Feeding and Care, 2e (ed. L.D. Lewis), 289–299. Baltimore (MD): Williams & Wilkins. 38 Campbell, I.T. (1999). Limitations of nutrient intake. The effect of stressors: trauma, sepsis and multiple organ failure. Eur. J. Clin. Nutr. 53 Suppl 1: S143–147. 39 Bessey, P.Q., Watters, J.M., Aoki, T.T. et al. (1984). Combined hormonal infusion simulates the metabolic response to injury. Ann. Surg. 200 (3): 264–281. 40 Carli, F., Webster, J., Ramachandra, V. et al. (1990). Aspects of protein metabolism after elective surgery in patients receiving constant nutritional support. Clin. Sci. (Lond). 78 (6): 621–628. 41 Cruz, A.M., Cote, N., McDonell, W.N. et al. (2006). Postoperative effects of anesthesia and surgery on resting energy expenditure in horses as measured by indirect calorimetry. Can. J. Vet. Res. 70 (4): 257–262. 42 Serteyn, D., Pincemail, J., Deby, C. et al. (1991). Equine postanesthetic myositis: an ischaemic reperfusion phenomenon. J. Vet. Anaesth. 18 (Supp 1): 319–322. 43 Edner, A., Essen-Gustavsson, B., and Nyman, G. (2005). Muscle metabolic changes associated with long-term inhalation anaesthesia in the horse analysed by muscle biopsy and microdialysis techniques. J. Vet. Med. A. 52 (2): 99–107. 44 Edner, A., Nyman, G., and Essen-Gustavsson, B. (2002). The relationship of muscle perfusion and metabolism with cardiovascular variables before and after detomidine injection during propofol-ketamine anaesthesia in horses. Vet. Anaesth. Analg. 29 (4): 182–199. 45 Edner, A.H., Nyman, G.C., and Essen-Gustavsson, B. (2007). Metabolism before, during and after anaesthesia in colic and healthy horses. Acta Vet. Scand. 49: 34. 46 Edner, A.H., Essen-Gustavsson, B., and Nyman, G.C. (2009). Metabolism during anaesthesia and recovery in colic and healthy horses: a microdialysis study. Acta Vet. Scand. 51: 10. 47 Carr, E.A. (2012). Metabolism and nutritional support of the surgical patient. In: Equine Surgery, 4e (ed. J.A. Auer and J.A. Stick), 62–67. St. Louis, Missouri: Saunders Elsevier. 48 Rokyuta, R., Jr., Matekovic,M., Krouzecky, A. et al. (2003). Enteral nutrition and hepatosplanchnic region in critically ill patients – friends or foes? Physio. Res. 52 (1): 31–37. 49 Robert, P.R. and Zaloga, G.P. (2000). Enteral nutrition. In: Textbook of Critical Care, 4e (ed. W. C. Shoemaker, S.M. Ayres, and A. Grenvick), 875–882. Philadelphia: Saunders Elsevier.

50 Jose-Cunilleras, E., Viu, J., Corradini, I. et al. (2012). Energy expenditure of critically ill neonatal foals. Equine. Vet. J. Suppl. (41): 48–51. 51 McKenzie, H.C. 3rd, and Geor, R.J. (2009). Feeding management of sick neonatal foals. Vet. Clin. N. Am. Equine Pract. 25 (1): 109–119, vii. 52 Myers, C.J., Magdesian, K.G., Kass, P.H. et al. (2009). Parenteral nutrition in neonatal foals: clinical description, complications and outcome in 53 foals (1995–2005). Vet. J. 181 (2): 137–144. 53 Krause, J.B. and McKenzie, H.C. 3rd. (2007). Parenteral nutrition in foals: a retrospective study of 45 cases (2000–2004). Equine Vet. J. 39 (1): 74–78. 54 Durham, A.E. (2006). Clinical application of parenteral nutrition in the treatment of five ponies and one donkey with hyperlipaemia. Vet. Rec. 158 (5): 159–164. 55 Lopes, M.A. and White, N.A. 2nd. (2002). Parenteral nutrition for horses with gastrointestinal disease: a retrospective study of 79 cases. Equine Vet. J. 34 (3): 250–257. 56 Jeejeebhoy, K.N. (2001). Total parenteral nutrition: potion or poison? Am. J. Clin. Nutr. 74 (2): 160–163. 57 Vergnano, D., Bergero, D., and Valle, E. (2017). Clinical nutrition counselling service in the veterinary hospital: retrospective analysis of equine patients and nutritional considerations. J. Anim. Physiol. Anim. Nutr. (Berlin). 101 (Suppl 1): 59–68. 58 Clarke, R.S. (1973). Anaesthesia and carbohydrate metabolism. Br. J. Anaesth. 45 (3): 237–243. 59 Oyama, T. (1973). Endocrine responses to anaesthetic agents. Br. J. Anaesth. 45 (3): 276–281. 60 Luna, S.P., Taylor, P.M., and Wheeler, M.J. (1996). Cardiorespiratory, endocrine and metabolic changes in ponies undergoing intravenous or inhalation anaesthesia. J. Vet. Pharm. Ther. 19 (4): 251–258. 61 Taylor, P.M. (1991). Stress responses in ponies during halothane or isoflurane anaesthesa after induction with thiopentone or xyulaxine/ketamine. J. Assoc. Vet. Anaesth. 18: 8–14. 62 Wagner, A.E. (2009). Stress associated with anesthesia and surgery. In: Equine Anesthesia Monitoring and Emergency Therapy, 2e (ed. W.W. Muir and J.A.E. Hubbell), 101–108. St. Louis, Missouri: Saunders Elsevier. 63 Robertson, S.A. (1987). Some metabolic and hormonal changes associated with general anaesthesia and surgery in the horse. Equine Vet. J. 19 (4): 288–294. 64 Robertson, S.A., Steele, C.J., and Chen, C.L. (1990). Metabolic and hormonal changes associated with arthroscopic surgery in the horse. Equine Vet. J. 22 (5): 313–316.

 ­Reference

65 Taylor, P.M. (1989). Equine stress responses to anaesthesia. Br. J. Anaesth. 63 (6): 702–709. 66 van Dijk, P., Lankveld, D.P., Rijkenhuizen, A.B. et al. (2003). Hormonal, metabolic and physiological effects of laparoscopic surgery using a detomidine-buprenorphine combination in standing horses. Vet. Anaesth. Analg. 30 (2): 72–80. 67 Robertson, S.A., Malark, J.A., Steele, C.J. et al. (1996). Metabolic, hormonal, and hemodynamic changes during dopamine infusions in halothane anesthetized horses. Vet. Surg. 25 (1): 88–97. 68 Cooper, G.M., Paterson, J.L., Ward, I.D. et al. (1981). Fentanyl and the metabolic response to gastric surgery. Anaesthesia. 36 (7): 667–671. 69 Elliott, M. and Alberti, K.G.M.M. (1983). The hormonal and metabolic response to surgery by narcotics and general anaesthesia. Clin. Anaesth. 3: 247–270. 70 Taylor, P.M. (1985). Changes in plasma cortisol concentration in response to anaesthesia in the horse. In: 2nd International Congress of Veterinary Anaesthesiology: 1985; Sacramento, 165–166. 71 Stegmann, G.F. and Jones, R.S. (1998). Perioperative plasma cortisol concentration in the horse. J. S. Afr. Vet. Assoc. 69( 4): 137–142. 72 Underwood, C., Southwood, L.L., Walton, R.M. et al. (2010). Hepatic and metabolic changes in surgical colic patients: a pilot study. J. Vet. Emerg. Crit. Care (San Antonio). 20 (6): 578–586. 73 Gardner, R.B., Nydam, D.V., Mohammed, H.O. et al. (2005). Serum gamma glutamyl transferase activity in horses with right or left dorsal displacements of the large colon. J. Vet. Intern. Med. 19 (5): 761–764. 74 Davis, J.L., Blikslager, A.T., Catto, K. et al. (2003). A retrospective analysis of hepatic injury in horses with proximal enteritis (1984–2002). J. Vet. Intern. Med. 17 (6): 896–901. 75 Cotovio, M., Monreal, L., Navarro, M. et al. (2007). Detection of fibrin deposits in horse tissues by immunohistochemistry. J. Vet. Intern. Med. 21 (5): 1083–1089. 76 Dunkel, B. and McKenzie, H.C. 3rd. (2003). Severe hypertriglyceridaemia in clinically ill horses: diagnosis, treatment and outcome. Equine Vet. J. 35 (6): 590–595. 77 Frank, S.M., Higgins, M.S., Fleisher, L.A. et al. (1997). Adrenergic, respiratory, and cardiovascular effects of core cooling in humans. Am. J. Physiol. 272 (Pt 2): R557–562. 78 Tomasic, M. (1999). Temporal changes in core body temperature in anesthetized adult horses. Am. J. Vet. Res. 60 (5): 556–562.

79 Cruz, A.M., Kerr, C.L., Boure, L.P. et al. (2004). Cardiovascular effects of insufflation of the abdomen with carbon dioxide in standing horses sedated with detomidine. Am. J. Vet. Res. 65 (3): 357–362. 80 Toft, P. and Tønnesen, E. (2008). The systemic inflammatory response to anaesthesia and surgery. Curr. Anaesth. Crit. Care. 19 (5): 349–353. 81 Choileain, N.N. and Redmond, H.P. (2006). Cell response to surgery. Arch. Surg. 141 (11): 1132–1140. 82 Annane, D., Sébille, V., Charpentier, C. et al. (2002). Effect of treatment with low doses of hydrocortisone and fludrocortisone on mortality in patients with septic shock. J.A.M.A. 288 (7): 862–861. 83 Bessey, P.Q., Jiang, Z.M., Johnson, D.J. et al. (1989). Posttraumatic skeletal muscle proteolysis: the role of the hormonal environment. World J. Surg. 13 (4): 465–470. 84 Russell, J.A., Ronco, D., Lockhat, A. et al. (1990). Oxygen delivery and consumption and ventricular preload are greater in survivors than in non-survivors of the adult respiratory distress syndrome. Am. Rev. Respir. Dis. 141 (3): 659–665. 85 Toft, P., Tønnesen, E., Helbo-Hansen, H.S. et al. (1994). Redistribution of granulocytes in patients after major surgical stress. A.P.M.I.S. 102 (1): 43–48. 86 Ashley, F.H., Waterman-Pearson, A.E., Whay, H.R. (2005). Behavioural assessment of pain in horses and donkeys; application to clinical practice and future studies. Equine Vet. J. 37 (6): 565–575. 87 Dodds, L., Knight, L., Allen, K. et al. (2017). The effect of postsurgical pain on attentional processing in horses. Vet. Anaesth. Analg. 44 (4): 933–942. 88 de Grauw, J.C. and van Loon, J.P.A.M. (2016), Systematic pain assessment in horses. Vet. J. 209: 14–22. 89 Dalla Costa, E., Minero, M., Lebelt, D. et al. (2014). Development of the horse grimace scale (HGS) as a pain assessment tool in horses undergoing routine castration. PLoS ONE. 9: e92281 90 Mudge, M.C. (2014). Acute hemorrhage and blood transfusions in horses. Vet. Clin. N. Am. Equine Pract. 30 (2): 427–436. 91 Hart, K.A., Kitchings, K.M., Kimura, S. et al. (2016). Measurement of cortisol concentration in the tears of horses and ponies with pituitary pars intermedia dysfunction. Am. J. Vet. Res. 77 (11): 1236–1244. 92 Hofberger, S.C., Gauff, F., Thaller, D. et al. (2018). Assessment of tissue-specific cortisol activity with regard to degeneration of the suspensory ligaments in horses with pituitary pars intermedia dysfunction. Am. J. Vet. Res. 79 (2): 199–210.

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2 Complications of Parenteral Administration of Drugs Julie E. Dechant DVM, MS, DACVS, DACVECC School of Veterinary Medicine, University of California–Davis, Davis, California

O ­ verview Parenteral administration refers to the administration of drugs by a route other than the oral route. This would include intravascular, intramuscular, subcutaneous, intradermal, intra-synovial, and epidural routes of administration. Intravascular and epidural injections will be discussed in subsequent chapters. Subcutaneous and intra-dermal routes of administration have a low risk of complications and will not be reviewed in this chapter. This chapter will focus on complications of intramuscular and intra-synovial injections.

­ ist of Complications Associated with L the Parenteral Administration of Drugs: ●● ●● ●●

●● ●● ●● ●●

Intramuscular administration Anatomical and procedural considerations Local muscle reaction: from mild inflammation to abscess formation Clostridial myonecrosis Intra-synovial administration Post-injection synovitis and lameness Medication errors

­Intramuscular Administration Anatomical and Procedural Considerations The most common muscle groups used for intramuscular injection are the cervical (trapezius), pectoral, gluteal, and caudal thigh (semimembranosus, semitendinosus) muscles  [1, 2]. Most veterinarians do not advocate use of the gluteal muscles, because this site provides poor drainage if any septic complications develop after injection  [2]. Injection technique requires identification of local anatomy and recognition of topical landmarks.

The skin overlying the proposed injection site should be clean; however, there is no consensus if topical disinfection with alcohol reduces the risk of bacterial inoculation [1, 2]. For a full-sized horse, a 1.5” needle should be used to allow for deep penetration into the muscle and it is prudent to use a larger-sized needle (18–19 gauge), because smaller needles can break off in the muscle if the patient resists the injection. In most circumstances, it is best to place the needle in the muscle without the syringe and then attach the syringe to the hub of the needle. The syringe should be aspirated to ensure no contamination of the site with blood before injecting the medication, because many intramuscularly administered medications are not compatible with intravenous injection (e.g. procaine penicillin) or would have a different dosage if administered by the intravenous route (e.g. sedatives) [1, 2]. Ideally, no more than 10 ml should be injected at one site; the needle is redirected if larger volumes are administered [1, 2].

­ ocal Muscle Reaction: From Mild L Inflammation to Abscess Formation Definition  Local muscle inflammatory reactions are

characterized by swelling and soreness after intramuscular injection of a substance. Severe local inflammations with infection show local accumulation of purulent material (abscess). Risk Factors ●●

●● ●●

The cervical and pectoral muscles appear to be more predisposed to muscle soreness, likely because these are smaller muscle groups compared to the gluteal or semimembranosus/semitendinosus muscles. Repeated injection into the same location. Some types of vaccines are anecdotally associated with a higher risk of injection site abscesses. Certain medications, typically acidic formulations or those with

Complications in Equine Surgery, First Edition. Edited by Luis M. Rubio-Martinez and Dean A. Hendrickson. © 2021 John Wiley & Sons, Inc. Published 2021 by John Wiley & Sons, Inc.

­Clostridial Myonecrosi 

­ on-aqueous carriers (gentamicin, tetracyclines, enron floxacin, flunixin, phenylbutazone, etc.) are associated with increased tissue reactivity.

referred to as clostridial myositis, malignant edema, or clostridial cellulitis [4].

Pathogenesis  Local swelling and soreness are common

intramuscular injection, and has been reported after flunixin meglumine (most commonly), dipyrone, Vitamin B with or without iron, tripellennamine, dexamethasone, furosemide, vaccines, among others [4–6].

complications, especially after repeated or large volume administrations or administration of irritating medications [2]. Abscess formation is a less common complication following intramuscular injection  [1, 2] but may occur if the local inflammatory response is severe or if the injection site has been contaminated with bacteria. Abscesses may form even after intramuscular antimicrobial administration. Prevention  Maximize aseptic technique for intramuscular injection or use alternate routes of administration for medication, if available. Rotation of injection sites is desired when frequent dosing is required and may delay development of muscle soreness by allowing time for the inflammation to resolve  [2]. If a site becomes swollen or sore, it should no longer be used for injection  [2]. Some practitioners advocate to avoid the gluteal muscles as this  location is very difficult to drain if abscessation develops [2]. Diagnosis  Inflammation

and/or soreness can be appreciated as raised, hardened and/or painful areas during normal clinical examination of the area. Abscess formation should be considered if the local muscle swelling appears severe or if the horse develops a fever.

Treatment  Avoid use of that location for further injections

and apply warm compresses for analgesia. Warm compresses can also be used to help mature the abscess prior to establishing external drainage. In severe cases of muscle soreness, systemic non-steroidal anti-inflammatory treatment may be necessary. Drain abscess at a dependent location. The gluteal muscles are particularly difficult to drain if abscessation develops.

Expected Outcome  Although most localized muscle soreness or abscessation resolves without long-term consequence, fibrotic myopathy may develop after intramuscular injection  [3]. This may be an additional consideration when administering intramuscular medications to performance horses.

C ­ lostridial Myonecrosis Definition  Clostridial myonecrosis is a rapidly progressing, necrotizing infection of muscle that is characterized by severe local and systemic clinical signs [4–6]. It may also be

Risk Factors  Clostridial myonecrosis can develop after any

Pathogenesis  All of these syndromes are referencing

necrotizing soft tissue infections with Clostridium perfringens, Clostridium septicum, Clostridium chauvoei, and Clostridial sporogenes that develop after intramuscular injections or muscular trauma [5]. It is not known if these infections result from inoculation of clostridial spores at the time of injection or injury, or if these spores are quiescent within the tissue and they germinate after a muscle injury creates a suitable anaerobic environment  [5,  6]. Proliferation of clostridial organisms results in the production of extracellular enzymes and exotoxins, which propagate the local tissue injury and progress to signs of systemic toxemia.

Prevention  Due to the variety of medications associated with clostridial myonecrosis, it is difficult to eliminate the risk; however, flunixin meglumine, B vitamins, and tripellennamine appear higher risk and should be avoided. It would seem advisable to maximize aseptic techniques for intramuscular injection and use alternate routes of administration for medication, if available. Diagnosis  Clinical signs of clostridial myonecrosis (colic, lethargy, inappetence, pyrexia, progressive localized painful, emphysematous swelling) develop within 48–72 hours of intramuscular injection  [4–6]. Palpable subcutaneous emphysema in the affected muscle was present in 34 out of 37 cases  [4]. The emphysema is often rapidly progressive along muscle planes and is associated with systemic signs of fever, obtundation, and shock  [4–6]. A presumptive diagnosis can be based on a history of recent intramuscular injection and local swelling, pain, and emphysema. Ultrasound is helpful in identifying emphysema within the deeper tissues. Treatment should not be delayed until there is a confirmed diagnosis, but presence of Gram-positive rods on Gram stain provides further support and anaerobic culture of Clostridia is confirmatory [5, 6]. Treatment  Aggressive treatment is necessary once clostridial myonecrosis is suspected or confirmed. Aggressive antimicrobial therapy should be instituted promptly and continued for 10–14 days  [5]. High-dose intravenous penicillin should be started to treat the clostridial infection [5, 6]. Other antimicrobial agents have been suggested but lack the same spectrum against

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Complications of Parenteral Administration of Drugs

Clostridia (ampicillin, cephalosporins, tetracyclines) or will not attain high tissue concentrations (metronidazole)  [6]. Intravenous fluid therapy is started to support the cardiovascular system. Non-steroidal anti-inflammatory medication and other analgesic agents are administered, and other treatments (fresh frozen plasma, platelet transfusion, etc.) may be given as needed  [5]. Another mainstay of treatment is surgical fenestration of the area to allow drainage of the accumulated fluid and gas, debridement of necrotic tissue, and oxygenation of the affected area  [4–6]. Fenestration and debridement may need to be extended into previously unaffected areas on subsequent days. If clostridial myonecrosis involves the cervical muscles, it may be necessary to place a tracheostomy tube to secure the airway or a feeding tube for enteral nutrition, because edema may progress cranially to cause dyspnea and dysphagia. Expected Outcome  Prognosis for clostridial myonecrosis is

guarded to poor  [4–6]. Horses may not survive despite aggressive medical and surgical treatment. Owners should be warned that the recovery period may be protracted and there will be extensive tissue loss in the affected area.

­Intra-Synovial Administration Intra-synovial medication may be used for diagnostic purposes (local anesthetic agents) or for therapeutic purposes (anti-inflammatory medications, chrondroprotective agents, or antimicrobial therapy).

­ ost-Injection Synovitis P and Lameness Definition  A post-injection flare is an acute, non-septic inflammatory response to the medication [7, 8]. Aside from the discomfort of the patient and the anxiety of the owner, the biggest concern related to a post-injection flare is differentiating it from septic synovitis. Septic synovitis is an inflammatory response of the synovial cavity associated with infection. Risk Factors ●● ●●

●●

Substandard aseptic technique Post-injection flares: ○○ Injected substance: corticosteroids, local anesthetics, hyaluronate, and polysulfated glycosaminoglycans Post-injection synovial sepsis: ○○ In humans: failure of aseptic technique, experience of practitioner, use of multi-dose vials, injection through

○○

infected tissue, concurrent systemic infection, and use of immunosuppressive drugs [9, 10] In horses: ◼ Corticosteroids [11–13] ◼ Polysulfated glycosaminoglycan or hyaluronic acid [11] ◼ Combination of corticosteroid-polysulfated glycosaminoglycan [13] ◼ Dexamethasone had higher risk than betamethasone [12] ◼ Treating veterinarian [12, 13], >20 years in practice by the treating veterinarian [14] ◼ Technical factors: 2 minutes were recommended [19]; however, a survey

­Medication Error 

of equine veterinarians suggested that not clipping and >7-minute preparation time was associated with reduced risk of infection  [14]. Clipping may be beneficial if the area is soiled. The injection should be performed in a clean, dry, non-dusty environment that is protected from wind [12]. Concurrent administration of antibiotics with the intrasynovial medication is used by some veterinarians. Routine use of antibiotics concurrent with intra-synovial medication has not been shown to statistically alter the risk of infection, likely because the incidence of infection in these studies is low [12, 13]. Concurrent administration of antibiotics is recommended any time polysulfated glycosaminoglycans are injected intra-synovially  [15]. Inclusion of antimicrobial agents should not replace strict aseptic technique, and has the potential to interfere with the efficacy of the primary medication. Diagnosis  Non-septic inflammation or joint flare occurs

within several hours of the intra-synovial administration and is characterized by synovial effusion and pain [7, 8]. In general, a post-injection flare will occur acutely (within hours), will respond rapidly to anti-inflammatory medication, and does not persist beyond 1–2 days [7, 8]. Signs of septic synovitis include localization of pain, heat, and effusion in the injected synovial structure. Clinical signs of septic synovitis typically occur within 2.5–4 days of injection, but may occur 1–19 days after injection [12, 20]. Intra-synovial corticosteroid injections may delay recognition of the problem, because the anti-inflammatory effect of the medication may suppress clinical signs. Diagnosis should be supported by synoviocentesis with cytology and culture of the synovial fluid. Traditionally, cytological findings of >30,000 total nucleated cells/μl, >80% neutrophils, and >4.0 g/dl total protein is supportive of the diagnosis  [21, 22]. If intra-synovial corticosteroids have been administered, infection may be associated with silicone rubber > nylon > polyvinyl chloride > polyurethane > silastic [1, 2, 4, 12]. Catheter size: Longer and larger diameter catheters are more inflammatory than short, narrow catheters [8, 12]. Catheter site handling: Catheter sites should be kept clean from environmental contamination, secured, and maintained with aseptic technique.

Pathogenesis  Development of thrombophlebitis is related to the inflammatory and pro-coagulant environment present within the catheterized vessel  [11]. Catheterrelated factors (type, duration, contamination, instability), patient-related factors (concurrent disease, hypoproteinemia, endotoxemia, infection), and infusate characteristics (hyperosmolar, acidic, microparticulate) contribute to the degree of inflammation and coagulable state within the vessel. Bacterial colonization is not always associated with vascular changes [12, 13]; however, septic thrombophlebitis is a serious complication. Prevention  Catheters should be placed and managed aseptically, adequately stabilized, and kept clean and protected from soiling or external trauma, with the caveat that daily inspection should continue despite protective wraps. Some clinicians advocate removal of all catheters after 48–72 hours and replacement in an alternate site if continued use is needed [12]; however, signs of thrombophlebitis can occur within 24 hours and repeated catheterization increases the risk of thrombophlebitis. Administration of lowmolecular weight heparin (dalteparin) in colic patients was associated with less subclinical (ultrasonographic) changes of thrombophlebitis than unfractionated heparin [14]. Nonsteroidal anti-inflammatory treatment was found to be protective in another study [15]. Reduction in catheter flow may be caused by early development of a thrombus at the catheter tip.

venous drainage, associated veins may become dilated and tissues may become edematous (i.e. facial and nasal edema associated with jugular venous thrombosis) [1, 4, 16]. Monitoring  Ultrasound examination of the catheter site and associated vein is most sensitive to detect early signs of thrombophlebitis, such as thickening of the vein and development of a thrombus on the catheter (Figure 3.2) [1, 2, 4, 15]. The entire length of the catheter should be ultrasounded, because thrombi are often initiated at the distal tip. Ultrasonographic evidence of thickening of the vein is evident in at least 27% of catheterized veins maintained for at least 24 hours  [15], although external clinical changes are seen in approximately 8–18% of colic patients [17, 18].

Figure 3.1  Photograph of a left jugular catheter insertion site associated with nodular thickening and suppurative exudate. Source: Courtesy of Pablo Espinosa.

Diagnosis  Catheter sites should be closely monitored on at

least a daily basis for evidence of thickening or pain at the insertion site or along the catheter [1, 2, 4, 8]. Clinical signs of thrombophlebitis can occur within 24 hours and include thickening at the insertion sites, local swelling, heat, cordlike thickening of the vein, suppurative exudate (Figure 3.1), pain on palpation, and if septic, may progress to fever, obtundation, and systemic signs associated with septic embolization to distant sites  [1, 2, 4, 11]. Thrombophlebitis may also result in perivascular nerve injury, such as Horner’s syndrome and left laryngeal hemiplegia. If thrombophlebitis results in occlusion of

Figure 3.2  Transverse ultrasound image of the jugular vein shown in Figure 3.1. Hyperechoic material was identified superficial to the jugular vein (arrowhead). There was localized thickening (arrows) of the jugular vein wall (perivasculitis). The jugular vein remained patent. Source: Courtesy of Pablo Espinosa.

­Intravascular Foreign Bodie

Treatment  If there are any signs of thrombophlebitis,

the  catheter should be removed immediately and the catheter should be cultured or saved for culture if any concerns. Treatment should be instituted if there is local swelling, pain, or inflammation, and includes warm compresses and topical anti-inflammatory treatment (dimethylsulfoxide or diclofenac). If signs of fever, suppurative discharge, or cellulitis are present, then systemic antimicrobial treatment is indicated and should be guided by culture and sensitivity results. If re-catheterization is necessary, the affected vein must not be used and it is recommended to use another anatomic site (i.e. do not use contralateral jugular vein, if possible, because thrombophlebitis of both jugular veins can impede venous drainage from the head). If thrombophlebitis results in abscess formation or complete occlusion of the vein (Figure 3.3), it may be necessary to surgically drain, resect, or reconstruct the vein [16, 19].

Expected Outcome  Most cases of thrombophlebitis will resolve uneventfully, but may require prolonged antimicrobial therapy. Sequellae may include cosmetic blemish, permanent occlusion of the affected vein, residual edema or varicosities in the area drained by the affected vein, and laryngeal hemiplegia. Septic embolization and dissemination of infection to internal locations may occur and may be associated with additional morbidity and mortality.

­Intravascular Foreign Bodies Definition  Needle emboli, catheter fragmentation, and loss of the guidewire are causes of intravascular foreign bodies during catheter placement and/or management of indwelling catheters [1, 5, 8, 20]. Risk Factors ●●

●●

Use of small gauge (20 gauge or smaller) needles, inadequate restraint of a fractious patient, or manufacturer defect. Risk factors for loss of guidewires identified in human medicine and relevant to veterinary medicine are inexperience in the technique or equipment, lack of adequate supervision, distractions during catheter placement, and high workload  [21]. Patient restraint and resistant during the procedure would be important in equine settings. Catheter kinking and breakage should be considered for any catheter type, especially as duration of catheterization increases, and clinicians should be most alert to ­failure in catheters made of stiffer materials (poly­ tetrafluoroethylene, polyethylene, polypropylene) and over-the-needle stylet catheters, because they have to be stiffer to allow insertion.

Figure 3.3  Local abscessation of a jugular thrombophlebitis with complete thrombosis of the right jugular vein at the level of the abscess and 10 cm caudally. Source: Courtesy of Pablo Espinosa.

Pathogenesis  Catheter fragmentation may occur during placement of over-the needle stylet catheters if the catheter is advanced and then retracted back over the stylet and the stylet pierces the side of the catheter  [1]. Loss of the guidewire during placement of an over-the-wire catheter using a Seldinger technique is not uncommon in human or veterinary medicine [21, 22]. The most common reason for loss of the guidewire is not holding onto the guidewire at all times that the wire is in the vein [22]. Catheters may be accidentally transected when the sutures are being cut during catheter removal. Indwelling catheters may bend and break (Figure  3.4), particularly if they are made of more rigid material [1, 2, 20, 23]. In an experimental study evaluating long-term jugular vein catheterization, 67% of

Figure 3.4  Polyurethane catheter removed from a jugular vein 48 hours after being placed. The catheter is seen to have multiple areas of bending and kinking. Source: Julie E. Dechant.

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Complications of Intravascular Injection and Catheterization

polytetrafluoroethylene catheters kinked, cracked or broke within 14 days, and 100% of polytetrafluoroethylene catheters kinked and broke within 30 days  [12]. In the same study, none of the silicone rubber or polyurethane catheters broke, even after 30 days of catheterization [12]. Re-use of needles is a risk factor in breaking and causing needle emboli in human intravenous drug abuse [24], but re-use of hypodermic needles is ill-advised in veterinary practice. Diagnosis  Needle emboli can occur when the needle

breaks off the hub during placement (Figure 3.5). This will be recognized immediately because the hub and syringe will be free from the needle. Catheter fragmentation will not be recognized until the catheter is removed and found to be incomplete. Loss of the guidewire is typically recognized immediately in veterinary medicine  [22]; however, delayed recognition is common in human medicine [21]. Catheter breakage is immediately evident if it occurs at the time of catheter removal; however, if the failure occurs in an indwelling catheter, it may not be recognized. During aspiration or injection of the catheter, any evidence that air bubbles are being aspirated or bubbling under the skin during injection is strongly suggestive that

there is a defect in the catheter at or near the insertion site. Intravascular foreign bodies should be localized by radiographs starting at the site of penetration and proceeding along the vein toward the thorax (Figure 3.5) [1, 20]. Ultrasound may be needed to evaluate the site of insertion (although manipulation of the tissues makes ultrasound less desirable than radiographs) or to evaluate if the intravascular foreign body is in the heart [1, 20]. Treatment  For any intravascular foreign bodies, immediate steps to be taken would be occlusion of the vein on the cardiac side of the insertion point to try to prevent migration into the heart and pulmonary vasculature  [5]. Defective catheters should be removed immediately. During removal, the vein should be occluded on the cardiac side of the vein so that any catheter fragments can be trapped at the site and prevented from embolization [5]. If the intravascular foreign body is accessible, it should be removed to prevent complications, assuming the risks of removal do not outweigh the benefits [8, 20, 25]. Direct approaches can be made to the jugular vein, but this should be done under general anesthesia with radiographic control to guide dissection. Endovascular retrieval is preferred in humans  [25]; however, horse size will be limiting to this technique unless the patient is a foal or pony-sized or the intravascular foreign body is located in the jugular vein or cranial vena cava [20, 22]. In an experimental study, 5 out of 6 horses with experimental catheter transection had the transected catheter located in the proximal or distal pulmonary arteries at necropsy 30 hours later [26]. Outcome  In general, it is believed that intravascular foreign bodies located within the pulmonary vasculature carry a low risk of complications [1, 8].

Expected

V ­ ascular Air Embolism/Bleeding Definition ●●

●●

Vascular air embolism is the aspiration of a significant amount of air from the environment into the vasculature and the resulting systemic effects. Blood loss from a disconnected catheter port.

Risk Factors ●●

Figure 3.5  Lateral radiograph of the cranial cervical region (cranial to the left of the image) in a horse that was referred for treatment and removal of a needle fragment that broke off during attempted venipuncture of the left jugular vein. An intravenous catheter was placed in the contralateral (right) jugular vein. The needle fragment was located medial to the jugular vein in the cranial cervical region. Source: Courtesy of the University of California, Davis Veterinary Medical Teaching Hospital Diagnostic Imaging Service.

●●

Large gauge, jugular vein catheters Catheters placed above heart level (for air embolism)

Pathogenesis  Vascular air embolism may occur during catheter placement before the injection cap is attached to the catheter or it may occur after placement if the injection cap or extension set becomes dislodged from the catheter. Air may be passively aspirated into the catheter because of the negative pressure within the jugular vein when the

  ­Reference

horse’s head is elevated. The total volume and rate of air aspiration are related to the development and severity of clinical signs. Reportedly, up to 0.25 ml/kg body weight of air may be aspired in horses before clinical signs develop [6, 27] Pulmonary edema results from the inflammatory response and vascular resistance induced by air in the pulmonary microvasculature. Cardiac dysrhythmias or neurological signs occur when the pulmonary vasculature is saturated and air enters the systemic circulation and embolizes to the coronary or cerebral microvasculature or if air moves retrograde (cranially) in the jugular vein  [1, 27–31]. Cardiovascular collapse can occur if a large air embolus creates an air-lock in the right ventricle, reducing cardiac output [29]. Passive aspiration of air is not a significant concern with catheters that are placed below heart level or in horses with lowered head positions (hemorrhage would be a complication of dislodgement of injection caps or ports from these catheters). Blood loss from a disconnected catheter port is rare, because most horses will clot before life-threatening amounts of blood are lost [1, 2]. Prevention  Risk of vascular air embolism or blood loss following disconnection of catheter attachment can be minimized by securing injection caps or extension sets with luer lock ports. Regular monitoring of horses with indwelling catheters will minimize the length of time that a catheter is disconnected. Theoretically, placement of catheters in the vein against the direction of blood flow (i.e. up the jugular vein) would prevent air embolism, but would create additional problems (increased catheter thrombosis, resistance to injection, and potential for exsanguination if catheter is disconnected) [31]. Diagnosis  Clinical signs of vascular air embolism are

tachycardia, tachypnea, muscle fasciculations, agitation, respiratory distress and pulmonary edema and may include neurological signs and cardiovascular collapse [1, 27–31]. The signs may be attributed to vascular air embolism if they occur in association with disconnection of the

injection cap or extension set from the catheter. The diagnosis may be supported by arterial blood gas analysis and auscultation of a mill-wheel murmur  [27–29]. Echocardiography can also be used to confirm the diagnosis, but most cases are diagnosed presumptively [27– 29]. Diagnosis of exsanguination from the catheter is obvious due to the external blood loss. Treatment  Treatment of vascular air embolism starts with immediate replacement of the injection cap or extension set to prevent further aspiration of air. Nasal insufflation of oxygen can help treat respiratory distress and can speed resorption of air emboli by changing pressure gradients to help diffusion of nitrogen out of the air bubbles and reducing their size  [1, 29]. Pulmonary edema can be managed with furosemide, corticosteroids, and nonsteroidal anti-inflammatory drugs. Similarly, neurological signs can be managed with anti-inflammatory (dimethyl sulfoxide, corticosteroids, non-steroidal anti-inflammatory drugs), neuroprotective (thiamine, Vitamin E) and anticonvulsant (benzodiazepines, barbiturates) treatments, as necessary [1, 30, 31]. Intravenous fluids should be administered if cardiovascular compromise is evident, but they may exacerbate pulmonary or cerebral edema. The volume of blood loss may be significant in hypocoagulable patients or small-sized patients  [1, 2]. Treatment includes replacement of the injection port and administration of intravenous fluids or whole blood, if signs of hypovolemia are present or severe [1]. Expected Outcome  If recognized promptly and vascular air

aspiration is limited, clinical signs can improve and horses can return to normal after vascular air emboli. In one study, 19% of horses were euthanized or died subsequent to vascular air embolism [27–31]. Similarly, blood loss from a disconnected catheter was unlikely to be significant or affect prognosis, unless the hemorrhage was not recognized or treated.

­References 1 Higgins, J. (2015). Preparation, supplies, and catheterization. In: Equine Fluid Therapy (ed. C.L. Fielding and K.G. Magdesian), 127–141. Ames: John Wiley & Sons. 2 Tan, R.H.H., Dart, A.J., and Dowling, B.A. (2003). Catheters: a review of the selection, utilization and complications of catheters for peripheral venous access. Aust. Vet. 81: 136–139.

3 Spriet, M., Trela, J.M., and Galuppo, L.D. (2015). Ultrasound-guided injection of the median artery in the standing sedated horse. Equine Vet. J. 47: 245–248. 4 Barakzai, S. and Chandler, K. (2003). Use of indwelling intravenous catheters in the horse. In. Pract. 25: 264–271.

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Complications of Intravascular Injection and Catheterization

5 Hardy, J. (2009). Venous and arterial catheterization and fluid therapy. In: Equine Anesthesia: induction, maintenance and recovery phases of anesthesia. In: Equine Anesthesia: Monitoring and Emergency Therapy, 2e (ed. W.W. Muir and J.A.E. Hubbell), 131–148. St. Louis: Elsevier Saunders. 6 Muir, W.W. (1991). Complication: induction, maintenance and recovery phases of anesthesia. In: Equine Anesthesia: Monitoring and Emergency Therapy, 1e (ed. W.W. Muir and J.A.E. Hubbell), 419–443. St. Louis: Mosby Year Book, 7 Sweeney, R.W. and Sweeney, C.R. (1984). Transient Horner’s syndrome following routine intravenous injection in two horses. J. Am. Vet. Med. Assoc. 185: 802–803. 8 Lorello, O. and Orsini, J.A. (2014). Intravenous catheter placement. In: Equine Emergencies: Procedures and Treatments, 4e (ed. J.A. Orsini and T.J. Divers), 9–11. St. Louis: Elsevier Saunders. 9 Gabel, A.A. and Koestner, A. (1963). The effects of intracarotid artery injection of drugs in domestic animals. J. Am. Vet. Med. Assoc. 142: 1397–1403. 10 Divers, T.J. (2014). Appendix 4 – Adverse drug reactions, air emboli, and lightning strike. In: Equine Emergencies: Procedures and Treatments, 4e (ed. J.A. Orsini and T.J. Divers), 812–816. St. Louis: Elsevier Saunders 11 Dolente, B.A., Beech, J., Lindborg, S. et al. (2005). Evaluation of risk factors for developments of catheterassociated jugular thrombophlebitis in horses: 50 cases. J. Am. Vet. Med. Assoc. 227: 113–1141. 12 Spurlock, S.L., Spurlock, G.H., Parker, G. et al. (1990). Long-term jugular vein catheterization in horses. J. Am. Vet. Med. Assoc. 196: 425–430. 13 Ettlinger, J.J., Palmer, J.E., and Benson, C. (1992). Bacteria found on intravenous catheters removed from horses. Vet. Rec. 130: 248–249. 14 Fiege, K., Schwarzwald, C.C., and Bombeli, T. (2003). Comparison of unfractioned and low molecular weight heparin for prophylaxis of coagulopathies in 52 horses with colic: a randomized double-blind clinical trial. Equine Vet. J. 35: 506–513. 15 Geraghty, T.E., Love, S., Taylor, D.J. et al. (2009). Assessment of subclinical venous catheter-related diseases in horses and associated risk factors. Vet. Rec. 164: 227–231. 16 Russell, T.M., Kearney, C., and Pollock, P.J. (2010). Surgical treatment of septic jugular thrombophlebitis in nine horses. Vet. Surg. 39: 627–630. 17 Mair, T.S. and Smith, L.J. (2005). Survival and complication rates in 399 horses undergoing surgical treatment of colic. Part 2: short-term complications. Equine Vet. J. 37: 303–309.

18 Lankveld, D.P.K., Ensink, J.M., Dijk, P.V. et al. (2001). Factors influencing the occurrence of thrombophlebitis after post-surgical long-term intravenous catheterization of colic horses: a study of 38 cases. J. Vet. Med. A. 48: 545–552. 19 Rikjenhuizen, A.B. and van Swieten, H.A. (1998). Reconstruction of the jugular vein in horses with post thrombophlebitis stenosis using saphenous vein graft. Equine Vet. J. 30: 236–239. 20 Culp, W.T.N., Weisse, C., Berent, A.C. et al. (2008). Percutaneous endovascular retrieval of an intravascular foreign body in five dogs, a goat, and a horse. J. Am. Vet. Med. Assoc. 232: 1850–1856. 21 Pokharel, K., Biswas, B.K., Tripathi, M. et al. (2015). Missed central venous guide wires: a systematic analysis of published case reports. Crit. Care Med. 42: 1745–1756. 22 Nannarone, S., Falchero, V., Gialletti, R. et al. (2013). Successful removal of a guidewire from the jugular vein of a mature horse. Equine Vet. Educ. 25: 173–176. 23 Hoskinson, J.J., Wooten, P., and Evans, R. (1991). Nonsurgical removal of a catheter embolus from the heart of a foal. J. Am. Vet. Med. Assoc. 199: 233–235. 24 Kulaylat, M.N., Barakat, N., Stephan, R.N. et al. (1993). Embolization of illicit needle fragments. J. Emerg. Med. 11: 403–408. 25 Schechter, M.A., O’Brien, P.J., and Cox, M.W. (2013). Retrieval of iatrogenic intravascular foreign bodies. J. Vasc. Surg. 57: 276–281. 26 Scarratt, W.K., Pyle, R.L., Buechner-Maxwell, V. et al. (1998). Transection of an intravenous catheter in six horses: effects and location of the catheter fragment. In: Proc. Am. Assoc. Equine Pract. 44: 294–295. 27 Parkinson, N.J., McKenzie, H.C., Barton, M.H. et al. (2018). Catheter-associated venous air embolism in hospitalized horses: 32 cases. J. Vet. Intern. Med. 32: 805–814. 28 Caporelli, F., McGowan, C.M., and Tulamo, R.M. (2009). Suspected venous air embolism in a Finnhorse. Equine Vet. Educ. 21: 85–88. 29 Pellegrini-Masini, A., Rodriguez Hurtado, I., Stewart, A.J., et al. (2009). Suspected venous air embolism in three horses. Equine Vet. Educ. 21: 79–84. 30 Holbrook, T.C., Dechant, J.E., and Crowson, C.L. (2007), Suspected air embolism associated with post-anesthetic pulmonary edema and neurologic sequelae in a horse. Vet. Anesth. Anal. 34: 217–222. 31 Bradbury, L.A., Archer, D.C., Dugdale, A.H.A. et al. (2005). Suspected venous air embolism in a horse. Vet. Rec. 156: 109–111.

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4 Complications of Endoscopy Julie E. Dechant DVM, MS, DACVS, DACVECC School of Veterinary Medicine, University of California–Davis, Davis, California

O ­ verview

Risk Factors ●●

Endoscopy is performed using a flexible video-endoscope, although rigid endoscopes may be used for certain surgical applications. The upper respiratory tract, larger airways of the lower respiratory tract, proximal gastrointestinal tract (esophagus, stomach and proximal duodenum), caudal intestinal tract (rectum and distal small colon), lower urinary tract (urethra, bladder and occasionally ureters), and uterus are commonly examined using endoscopy. This chapter will review complications associated with endoscopic examination procedures, whereas surgical endoscopic procedures will be discussed separately. Similarly, complications associated with arthroscopy, tenoscopy, laparoscopy and thoracoscopy will be reviewed in their respective chapters. Complications can occur related to equipment damage, patient injury from the endoscope, and sequellae from insufflation.

­ ist of Complications Associated L with Endoscopy ●● ●● ●● ●●

Epistaxis/mucosal trauma Equipment damage Insufflation-related complications Air embolism

­Epistaxis/Mucosal Trauma Definition  Epistaxis is the presence of hemorrhage exiting the nares. Mucosal trauma includes bruising, abrasions, and lacerations which can occur during passage of the endoscopy into any hollow organ.

●● ●● ●●

Small-sized horses or foals Insufficient restraint Unsedated patients Restriction of the passageway to be scoped by luminal masses or extraluminal swelling

Pathogenesis  Similar to passage of a nasogastric tube, there is the potential risk of epistaxis or other mucosal trauma. The severity of this injury is typically much less than for nasogastric intubation, because passage of the endoscope is visually guided and directed and the endoscopes are generally narrower in diameter and more pliable than most nasogastric tubes. Sources of epistaxis would most likely include the nasal mucosa during endoscope advancement, because visualization would reduce the risk of traumatizing the nasal turbintate and ethmoid turbinates. However, further advancement of the endoscope into a more restricted space (guttural pouches, esophagus) could result in inadvertent flexing of the scope into the turbinates. Advancement of the endoscope into the urethra, ureters, uterus, or caudal intestinal tract could cause direct mucosal trauma in some cases. Prevention  Use of intranasal phenylephrine, which causes vasoconstriction of mucosal vessels, and application of carbomethylcellulose lubricant, which reduces friction between the endoscope and the passageways, may reduce mucosal trauma and irritation in small patients or patients with restricted nasal passages. Treatment and  Expected Outcome  Most epistaxis and

mucosal trauma complications associated with endoscopy are self-limiting and do not need specific treatment. If severe epistaxis occurred, treatment could be applied

Complications in Equine Surgery, First Edition. Edited by Luis M. Rubio-Martinez and Dean A. Hendrickson. © 2021 John Wiley & Sons, Inc. Published 2021 by John Wiley & Sons, Inc.

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similar to that described for epistaxis associated with nasogastric intubation (see Chapter  5: Complications of Nasogastric Intubation).

­Equipment Damage Definition  Crushing damage to the endoscope by mastication Risk Factors ●●

●● ●●

Upper airway endoscopy or gastroscopy without endoscope protector Inexperience Oral endoscopy without a mouth speculum

Pathogenesis  The most common damage is associated with endoscopy of the nasopharynx due to retroflexion of the endoscope into the oral cavity. Damage can occur at the end of the endoscope if the leading edge retroflexes into the oral cavity or it may occur in the body of the endoscope if the scope does not advance through the cranial esophageal sphincter and a loop of the endoscope retroflexes into the oral cavity (Figure 4.1). This would be most common when performing esophagoscopy and gastroscopy, because of the intentional induction of a swallowing reflex to enter the esophagus and the long length of the endoscope used for gastroscopy. Upper airway endoscopy is not immune to oral retroflexion, although the risk is much lower because the esophagus is not intentionally entered. Use of the endoscope to evaluate the oral cavity directly exposes the endoscopy to risk of damage by the teeth. The damage is caused by the horse chewing on the scope and the scope will be immediately non-functional.

Definition  Insufflation is the directed administration of air through the endoscope to provide distension and visualization of collapsible hollow organs and can result in small intestinal volvulus or rupture of a hollow viscus.

Prevention  This complication can be minimized by

Risk factors

awareness of the risk of it occurring during gastroscopy and upper airway endoscopy. The person passing the endoscopy controls the forward motion. This person should be careful when advancing the endoscope until confident in its location. Once seated in the esophagus, the person advancing the scope should make sure that there is aboral advancement of the scope synchronous with advancement of the endoscope into the nasal cavity. Alternatively, a larger diameter hollow tube can be positioned through the nasal cavity and into the esophagus [1]. The gastroscope is then passed through this tube, which prevents any resistance to passage and retroflexion of the endoscope in the nasopharynx [1]. Oral speculums must be used for any oral endoscopy procedures and the scope should be protected by a rigid sheath when in the mouth, if possible.

Figure 4.1  Photograph showing large segment (spanning the 160 cm to 205 cm gradations) of crushing and damage to a 3-meter gastroscope after a segment of the midbody of the endoscope retroflexed into the oral cavity, where it was chewed by the patient. Source: Julie E. Dechant.

­Insufflation-related Complications

●● ●●

None identified Inattention during procedure

Pathogenesis  These complications are likely the result of the effective creation of a one-way valve when performing endoscopy in long, narrow, tubular organs, whereby there is no means for the insufflated air to escape and depressurize the system. Segmental jejunal volvulus has been described as a complication after gastroscopy [2]. The incidence of jejunal volvulus is low, with only 1–2 cases per year per institution included in their study (0.3–3.2%/year) [2]. All of the horses had gas distension of the affected small intestine, which was presumed to be related to the gas insufflation associated with gastroscopy. In the report of jejunal volvulus, there was no apparent association with duration

­Air Embolis 

of gastroscopy, duration of feed withholding, or use of duodenoscopy. Although bladder rupture has not been directly described as a complication of cystoscopy in the literature, this author has observed a case in which prolonged urethroscopy and insufflation was used in an attempt to endoscopically remove a urethrolith [3]. The procedure resulted in retropulsion of the urethrolith into the bladder. Subsequently, a perineal urethrotomy was performed to ensure patency of the urinary tract, but bladder rupture and uroperitoneum was diagnosed 12 hours later. It cannot be proven that the urethroscopy caused the bladder rupture, but this was seen as a potential cause for the complication. Gastric rupture has not been described in the equine literature as a sequella of gastroscopy; however, gastric rupture has been described in a human patient during diagnostic upper gastrointestinal endoscopy  [4]. While this complication would be unlikely in most normal-sized horses, it may be a potential complication in small patients. Prevention  The authors of the jejunal volvulus case series concluded that it is advisable to minimize the duration and amount of air insufflated into the duodenum, reduce the amount of sedatives administered, and to use suction to decompress the stomach after gastroscopy is completed [2]. Bladder rupture and hypothetical gastric rupture are presumed to be exceptionally rare occurrences. Therefore, it is difficult to identify preventative measures. It may be prudent to avoid prolonged cystoscopy, especially if the urethra is partially obstructed. Diagnosis  Jejunal volvulus was diagnosed as the presence

of severe colic signs requiring colic surgery within a few hours of the gastroscopy procedure. Gastric rupture (hypothetical) or bladder rupture could be identified as the loss of distension at the time of the endoscopic examination. In the proposed clinical case, bladder rupture was identified as signs of uroperitoneum several hours later.

Treatment  All of these complications require emergency

exploratory celiotomy to diagnose and correct the problem. Non-surgical methods to manage bladder rupture have been described and may be a consideration in certain cases.

Expected Outcome  If treated promptly, the outcome

following jejunal volvulus and bladder rupture would be expected to be good. If intestinal ischemia or peritonitis occurs, the prognosis is much more guarded. Gastric

rupture is a hypothetical risk, but if it occurred, the outcome would be poor due to difficulty in accessing the stomach for repair of the rupture and the spillage of gastric contents and subsequent peritonitis.

­Air Embolism Definition  One or more air bubbles get access to the circulatory system, causing blockade of one or multiple blood vessels. Risk Factors (attributed to presumptive venous air embolism) ●●

●●

Dorsal location of the urinary tract relative to the right ventricle Presence of denuded epithelium

Pathogenesi  Urinary tract endoscopy was proposed to cause venous air embolism in two cases reported in the literature  [5–7]. Please refer to the vascular air embolism section in Chapter  3: Complications of Intravascular Injection and Catheterization. Air was noted to be present within the renal pelvis during ultrasonographic examination performed 24 hours after the endoscopic procedure, which may suggest that air was absorbed through the renal vasculature  [6]. The dorsal location of the urinary tract relative to the right ventricle is suggested to create a pressure gradient that favors the movement of air into the vasculature [7]. This may be additionally facilitated by the presence of denuded epithelium, which could increase the risk of air entering the bloodstream [5–7]. Prevention  Prevention of venous air embolism during urinary tract endoscopy would include use of alternative means to distend the urethra and bladder, such as saline solution or carbon dioxide gas, pre-oxygenation with 100% oxygen, and anticoagulant therapy; however, the mucoid and crystalline nature of equine urine makes the use of saline to distend the bladder impractical  [6, 7]. These precautions may be warranted in cases thought to be at higher risk for venous air embolism, such as cases presenting for hematuria or severe cystitis cases with denuded mucosa [7]. Diagnosis  Refer

to Chapter  3: Complications Intravascular Injection and Catheterization.

of

Treatment  The clinical signs and treatment of vascular air embolism are described in detail as a complication of intravenous catheterization and readers are directed to that chapter.

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Complications of Endoscopy

Expected Outcome  In the cases described in the literature, and as described in Chapter 3, horses would be expected to recover and return to normal from this complication if recognized and insufflation was stopped. The horse

described in Gordon et  al.  [5] was euthanized following recovery from two occurrences of presumptive vascular air embolism, due to a poor prognosis for a malignant lesion that prompted the cystoscopy.

R ­ eferences 1 Sykes, B.W. and Jokisalo, J.M. (2014). Rethinking equine gastric ulcer syndrome. Part 1: Terminology, clinical signs and diagnosis. Equine Vet. Educ. 26: 543–547. 2 Bonilla, A.G., Hurcombe, S.D., Sweeney, R.W. et al. (2014). Small intestinal segmental volvulus in horses after gastroscopy: four cases (2011–2012). Equine Vet. Educ. 26: 141–145. 3 Kilcoyne, I. and Dechant, J.E. (2014). Complications associated with perineal urethrotomy in 27 equids. Vet. Surg. 43: 691–696. 4 Wurm Johansson, G., Nemeth, A., Nielsen, J. et al. (2013). Gastric rupture as a rare complication in diagnostic upper gastrointestinal endoscopy. Endoscopy. 45: E391.

5 Gordon, E., Schlipf, J.W., Husby, K.A. et al. (2015). Two occurrences of presumptive venous air embolism in a gelding during cystoscopy and perineal urethrotomy. Equine Vet. Educ. doi: 10.1111/eve.12507. 6 Romagnoli, N., Rinnovati, R., Lukacs, R.M. et al. (2014). Suspected venous air embolism during urinary tract endoscopy in a standing horse. Equine Vet. Educ. 26: 134–137. 7 Nolen-Walston, R. (2014). Venous air embolism during cystoscopy in standing horses. Equine Vet. Educ. 26: 138–140.

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5 Complications of Nasogastric Intubation Julie E. Dechant DVM, MS, DACVS, DACVECC School of Veterinary Medicine, University of California–Davis, Davis, California

­Overview

Risk Factors ●●

Nasogastric intubation is performed to check for gastric reflux, relieve gastric distension, or administer enteral fluids, laxatives, or medications. Nasogastric intubation is achieved by directing and maintaining the nasogastric tube into the ventral meatus of the nasal cavity, without traumatizing the nasal turbinates and the ethmoid turbinates. The tube is blindly manipulated within the nasopharynx to the esophageal opening, avoiding the dorsal pharyngeal recess and the salpingopharyngeal plica. Once in the esophagus, the nasogastric tube is gently advanced aborally to enter the cardia of the stomach. The blind manipulation and passage of the tube can result in trauma to the associated tissues along the intended pathway, and trauma to structures if the tube is misdirected. Misplacement of the tube can result in further problems (fragmentation of the tube or administration of fluid into the lungs) if not recognized.

­ ist of Complications Associated L with Nasogastric Intubation ●● ●● ●● ●● ●● ●●

Epistaxis Misplacement of tube Esophageal/pharyngeal trauma Fragmentation of tube Administration of fluid into lungs Sinusitis

E ­ pistaxis Definition  Epistaxis is the presence of hemorrhage from the nares.

●●

Inexperience, although hemorrhage may occur with skillful intubation in a compliant horse Non-compliant horse

Pathogenesis  Epistaxis is the most common complication from nasogastric intubation [1–3]. Hemorrhage can occur when the respiratory mucosa, nasal turbinates, or ethmoid turbinates are traumatized. Prevention  The risk of epistaxis may be minimized by careful and gentle technique and assuring advancement of tube into ventral nasal meatus using well-lubricated tubes that are in good condition and free of external defects or roughening. Tube diameter should be selected to be an appropriate size for the patient, with the dimensions of the ventral nasal meatus being most limiting. Although water often provides sufficient lubrication in most circumstances, additional lubrication using carboxymethylcellulose or lubricating gel at the end of the tube may reduce risk of epistaxis in small patients, patients with dry or friable mucosa, or animals with restricted nasal passages. Preemptive intranasal application of phenylephrine spray, which causes local vasoconstriction of vessels within the nasal mucosa, may be of benefit. Patients should be adequately restrained, which may require use of a nose twitch or sedation. Diagnosis  Epistaxis

occurs during placement immediately after removing the nasogastric tube.

or

Treatment  Mild elevation of the head may speed resolution of bleeding, because lowering the head increases venous congestion, which would delay hemostasis. Extreme elevation of the head should be avoided because it increases the risk of aspiration and pneumonia  [1]. Packing of the

Complications in Equine Surgery, First Edition. Edited by Luis M. Rubio-Martinez and Dean A. Hendrickson. © 2021 John Wiley & Sons, Inc. Published 2021 by John Wiley & Sons, Inc.

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affected nasal cavity is an option, but the technique may simply divert hemorrhage into the nasopharynx and not reduce the volume of bleeding. Intranasal application of phenylephrine or epinephrine may be useful in providing local vasoconstriction; however, ongoing bleeding may limit the amount and distribution of drug that is absorbed by the nasal mucosa. Expected Outcome  Bleeding may be minor or more significant, and is usually self-limiting  [2]. In rare circumstances, hemorrhage may be severe enough to require blood transfusion and the administration of drugs to promote coagulation and prevent fibrinolysis. It is recommended that horses should not be anesthetized while there is ongoing nasal hemorrhage, because the head is generally positioned lower than the heart during anesthesia, which would exacerbate hemorrhage, and the cardiovascular consequence of ongoing blood loss is less tolerated during the cardiovascular depressant effects of most anesthetic drugs.

­Misplacement of Tube Definition  The tube is inadvertently misdirected into tracheal lumen, guttural pouch or retroflexes at the back of the nasopharynx and enters the oral cavity, or exits out the contralateral nostril while advancing the tube. Risk Factors ●●

●●

●●

Uncooperative patients, inadequate restraint or assistance, and inexperience with the procedure are predominant risk factors. Excessively pliable nasogastric tubes increase the risk of misplacement or misdirection of the tube. Smaller diameter tubes may increase the risk of misplacement of the tube within the guttural pouch (Figure 5.1).

Pathogenesis  Misplacement of the nasogastric tube is a common complication of nasogastric intubation. The esophageal opening is directly dorsal to the arytenoid cartilages of the larynx and it is relatively easy to enter the trachea, especially in horses that do not swallow or are resisting the intubation procedure. Retroflexion of the tube into the oral cavity can occur at the leading edge of the tube when trying to enter the esophagus. Alternatively, it may happen along any part of the length of the tube if the esophagus spasms around the tube and prevents its advancement. Further efforts to advance the tube against esophageal resistance results in the pharyngeal part of the

Figure 5.1  Lateral radiograph of the pharyngeal region of a miniature horse undergoing a positive contrast esophagogram (black asterisks) showing the nasogastric tube coiled within the guttural pouch (white arrows). The nasogastric tube was subsequently repositioned within the esophagus. The intravenous catheter is labeled (white arrowhead). Source: University of California, Davis Veterinary Medical Teaching Hospital Diagnostic Imaging Service.

tube retroflexing into the oropharynx. Misplacement of the tube in the guttural pouch with subsequent perforation of the medial compartment has been described [4]. Prevention  Misdirection of the tube into the trachea can be minimized by flexing the horse’s head when the tube is in the nasopharynx. Rotation of the tube by 180 degrees after it has cleared the nasal passages may also be helpful. The tube can be marked with a permanent marker at the distance from the nares to the pharynx/larynx to help judge the proximity of the indwelling tube to the larynx. Retroflexion of the tube into the oral cavity may be minimized by using a tube with sufficient rigidity to reduce abrupt bending of the tube. Tubes with areas of focal weakness should be avoided. Sedation, especially with detomidine [5], may relax the esophagus and aid passage of the tube; however, the horse may have a reduced swallowing reflex. Endoscopic guidance should be considered when smaller diameter nasogastric tubes are placed  [4] or if repeated attempts to pass the nasogastric tube have failed. Diagnosis  Although horses may respond to intratracheal

placement of the nasogastric tube by coughing, some horses may not exhibit a cough reflex. Absence of coughing does not guarantee correct placement of the nasogastric

­Esophageal/Pharyngeal Traum  31

tube. Intratracheal positioning of the tube can be determined by lack of any resistance to advancement of the tube and free movement of air, if air is blown into the tube or suction is applied to the tube. The tube may be felt to be reverberating within the trachea if the trachea is gently shaken. More importantly, correct positioning of the tube within the esophagus can be confirmed by palpating air boluses within the esophagus when air is blown into the tube and negative pressure is obtained when suction is applied to the tube. Palpation or visualization of the tube within the cervical esophagus ensures correct positioning. If further confirmation is needed, a second individual can auscultate for air bubbling into the stomach by listening over the left 14th intercostal space while air is blown into the tube. Location of small diameter feeding tubes, which may not be easily palpable, can be confirmed with radiographs (Figure  5.2). Retroflexion of the tube into the oral cavity may be detected by recognizing that the horse is chewing and recognizing that the chewing involves the tube. During misdirection of the nasogastric tube into the contralateral nasal passage, there will be some resistance to passing the tube, but air will move freely in and out of the tube and it cannot be localized in the trachea or esophagus. In the case report describing trauma secondary to misplacement of the

tube into the guttural pouch, it was described that initial placement of a nasogastric tube was not able to be advanced beyond the nasopharynx, although subsequent passage of a larger diameter tube was successful. The horse developed signs of throatlatch swelling four hours later, which prompted referral and identification of lesion with endoscopy, ultrasound and radiography [4]. Treatment  As long as intratracheal placement is recognized and corrected before any fluids or medications are administered, there are minimal to no consequences. Erroneous administration of fluid or medication into the lungs is discussed as a separate complication. Retraction of the orally misplaced tube corrects the misplacement; however, the consequences range from abrasion of the tube to cracks or defects in the wall of the tube to complete transection of the tube  [5]. In the case report of guttural pouch perforation as a complication of nasogastric intubation, the associated signs of pharyngeal swelling and cellulitis was treated with antibiotics, non-steroidal antiinflammatory drugs, supportive fluid therapy, and feeding of pelleted mashes and soaked hay. Unfortunately, the horse was euthanized several days later due to ulcerative, necrotizing colitis [4]. Expected Outcome  If promptly recognized and corrected,

misplacement of the tube should not be considered a complication. It is merely a consequence of blindly guiding the tube into the esophagus. If misplacement of the tube is not corrected promptly, it can be associated with lifethreatening complications if there is resulting tissue trauma or infusion of medication into the lungs.

­Esophageal/Pharyngeal Trauma Definition  Pharyngeal trauma ranges from mild bruising to perforation of the dorsal pharyngeal wall. Esophageal trauma can include ulcerations, linear lacerations, and partial to full-thickness perforation of the wall at any point along its length. Risk Factors ●●

Figure 5.2  Lateral radiograph of the thorax of a neonatal foal to document the position of the indwelling nasogastric feeding tube. In this radiograph, the feeding tube is located within the trachea and extending within a caudal bronchus and into the dorsocaudal lung lobe. Correct esophageal positioning would be evidenced by dorsal positioning of the feeding tube relative to the trachea, especially at the carina (white arrowheads). Source: University of California, Davis Veterinary Medical Teaching Hospital Diagnostic Imaging Service.

●●

●●

Prolonged durations or repeated intubations Horses that resist intubation by retching and contracting their cervical musculature may be at greater risk for complications Smaller horse breeds [3]

Pathogenesis  Mild pharyngeal trauma and bruising may occur after nasogastric intubation. Pharyngeal perforation has also been described as a complication of nasogastric

32

Complications of Nasogastric Intubation

intubation [7]. Ulceration or perforation of the esophagus is a documented complication of nasogastric intubation. In one study, the primary cause of esophageal perforations was traumatic nasogastric intubation [8]. In another study, esophageal ulceration or perforation was the predominant complication attributed to nasogastric intubation  [3]. Pharyngeal and esophageal trauma can occur with a single intubation; however, prolonged durations or repeated intubations appear to be associated with greater risk of complications [3]. Prevention  It is proposed that pharyngeal and esophageal trauma might be minimized by selecting smaller tube size and sedating horses with an alpha-2 agonist, such as detomidine, to relax the esophagus [3]. It is important to note that smaller tube size may increase the risk of certain misplacements and sedation may impede the swallowing reflex. The risk of prolonged intubations in horses with persistent gastric reflux needs to be balanced against the risk of repeated, intermittent intubations. Diagnosis  In most cases, mild pharyngeal trauma and

bruising is subclinical and would only be recognized if the horse undergoes endoscopic inspection of the nasopharynx. Endoscopy was necessary to diagnose the pharyngeal trauma after horses developed clinical signs of ptyalism, dysphagia, bruxism, and coughing attributed to pharyngeal trauma [3]. Clinical signs of esophageal trauma have been reported to be indistinguishable from pharyngeal trauma [3]; however, other studies describe the concurrent presence of fever, cervical swelling, and cellulitis when esophageal perforation has occurred  [8, 9]. In some perforation cases, the cellulitis and infection may travel caudoventral along the fascial planes towards the mediastinum. Endoscopy is helpful in identifying esophageal ulcerations and perforations, although small perforations may be hidden within the esophageal folds in some cases  [9]. In those situations, ancillary diagnostic tests, such as radiology and ultrasound, may be helpful to support the diagnosis and document the extent of cellulitis.

Treatment  Treatment of pharyngeal trauma and esophageal

ulceration is antimicrobial therapy and anti-inflammatory drugs to manage cellulitis, if present, and feeding of soft feeds or mashes if the horse is dysphagic. Sucralfate may aid in healing of esophageal ulcerations. Tracheostomy may be necessary if pharyngeal or peri-esophageal swelling causes upper respiratory tract obstruction. Surgical debridement of esophageal perforations is recommended to establish ventral drainage and excise infected tissues. Broad spectrum

antibiotic therapy is required because of the significant degree of contamination and extension of infection along fascial planes. Nutritional and fluid support is a major challenge in these cases, because of the esophageal defect and the need for it to heal. The risks and benefits of indwelling nasogastric tubes versus esophagostomy tubes need to be considered in each individual case [9]. Expected Outcome  Prognosis for subclinical pharyngeal trauma and bruising is excellent, whereas prognosis for clinically evident pharyngeal trauma is guarded and depends on the ability to manage the cellulitis and avoid associated complications, such as antimicrobial associated colitis and laminitis  [3, 7]. Prognosis for survival after esophageal ulceration is good, although stricture may occur with extensive or circumferential ulcerations. Prognosis for esophageal perforations is guarded, because there is often a delay in treatment, resulting in extensive cellulitis and tissue damage subsequent to the leakage of saliva and feed into the periesophageal tissues with subsequent abscessation, mediastinitis, and tissue necrosis [8. 9].

­Fragmentation of Tube Definition  Fragmentation of the tube refers to complete

structural failure of the tube, resulting in discontinuity of the tube. Risk Factors ●● ●● ●●

Repeated use of tubes Retroflexion into oral cavity Exposure to sunlight, chemical agents, or environmental extremes

Pathogenesis  Nasogastric tubes can fragment if they are brittle, have defects, or become retroflexed into the oral cavity. Nasogastric tubes can become brittle over time and with repeated use, especially if exposed to sunlight, chemical agents, or temperature extremes [10]. Tubes may also fragment if a horse chews on a tube which retroflexes into the oral cavity [6]. These fragments may remain within the esophagus or stomach. Prevention  Nasogastric tubes should be frequently

inspected to ensure that they are in good condition and without any defects or damage. Care should be taken to avoid oral retroflexion of nasogastric tubes and immediate correction, if it occurs. Awareness and prompt recognition of the problem may reduce the chance of complete

­Administration of Fluid into Lung  33

transection of the tube. If the tube has been misdirected into the oral cavity, it should be removed and inspected for damage before continuing with nasogastric intubation. Diagnosis  Once it is recognized that the tube is incomplete,

it is essential to immediately locate the position of the fragmented segment of tube. This should include an oral examination, because some fragments may be retrieved orally  [11]. If this is not successful, external palpation of the neck, endoscopic examination of the esophagus and stomach, and cervical and thoracic radiographs may locate the fragment [6, 11]. Multiple fragments may be present, so it is important that the entire tube is retrieved [10, 11].

Treatment  Treatment requires removal of the fragmented tube to prevent further gastrointestinal obstruction and trauma. The method of removal depends on the location of the tube, available equipment, and the success of each technique. Manual extraction from the oral cavity can be performed if the tube is located in the oral cavity and is facilitated by general anesthesia to allow safe and thorough manual exploration  [11]. Homemade or commercially available snares can be used to endoscopically snare and retrieve tube fragments, either using standing sedation or general anesthesia [6, 10]. Surgical removal by esophagotomy or gastrotomy has been used in selected cases when other methods of retrieval were unsuccessful [6, 10]. Expected Outcome  If nasogastric tube fragments are not

removed, it is likely that they may cause future intestinal obstruction or injury and require emergency exploratory celiotomy (Figure 5.3).

­Administration of Fluid into Lungs Definition  Aspiration pneumonia in this circumstance is caused by administration of enterally administered fluids or medication into the lung. Risk Factors ●● ●● ●● ●●

Improper technique Inadequate restraint Incomplete passage into the stomach Improper removal of the tube

Pathogenesis  Administration of fluid into the lungs can be a consequence of misplacement of a tube into the trachea or it may result from spillage from a properly placed nasogastric tube. The severity of the resulting pulmonary

Figure 5.3  Intraoperative photograph showing the removal of a large nasogastric tube fragment (1.3 cm diameter, 90 cm long) through a full thickness enterotomy in the right dorsal colon. This horse presented with acute signs of colic, but had no known history of prior nasogastric intubation complications. It was presumed that the nasogastric tube fragment had been acquired prior to the current ownership of the horse and did not cause problems until it migrated to the transverse colon and caused obstruction. Source: Courtesy of Isabelle Kilcoyne.

pathology depends on the type and volume of fluid that enters the lung. There are several mechanisms by which nasogastric procedures can result in aspiration pneumonia. First, the nasogastric tube may be misplaced into the trachea by improper technique, inadequate restraint, or by impaired swallowing reflexes in obtunded patients (Figure 5.1) [12]. Second, incomplete passage of the tube into the stomach or esophageal intubation may allow reflux of administered medication or fluid from the esophagus and into the trachea  [12]. Third, rapid administration or administration of a large volume of fluid or medication into an already filled stomach can result in esophageal reflux and aspiration of that reflux into the lungs  [12]. Fourth, failure to completely empty the tube, failure to kink or occlude the tube while removing, or rapid removal of the tube may allow any residual fluid or medication within the tube to spill into the nasopharynx where it can be aspirated [12]. Prevention  Prevention of inadvertent administration of fluids into the lungs is an essential part of nasogastric intubation procedures. Please refer to the section describing misplacement of nasogastric tubes for specific preventative procedures. Careful attention to all precautions throughout the nasogastric intubation procedure will help to minimize complications.

34

Complications of Nasogastric Intubation

Diagnosis  Development of respiratory distress immediately

following a nasogastric tube procedure is highly suggestive of inadvertent pulmonary administration of fluid. Signs may be delayed by a few days in cases with a small amount of mineral oil aspiration. Diagnosis of contamination of the lungs with mineral oil, also described as mineral oil-induced pneumonitis or lipoid pneumonia, is based on a history of mineral oil administration, radiographic or ultrasonographic evidence of pneumonia, and the identification of oil in tracheal wash or bronchoalveolar lavage samples [13–17].

a small amount of clean water is inadvertently administered into the lungs, the horse should be placed on anti-inflammatory treatment and antimicrobial therapy to prevent pneumonia  [1]. Administration of larger volumes of fluid may require additional supportive care, such as furosemide to treat pulmonary edema, bronchodilators, and intranasal oxygen therapy. Inadvertent intratracheal administration of certain medications (e.g. deworming drenches)  [12] and mineral oil [13, 15–19] may have fatal consequences, even with aggressive treatment. These horses should be aggressively treated with antimicrobial therapy, antiinflammatory medications, bronchodilators, nebulization, and intra-nasal oxygen [13–17]. Repeated bronchoalveolar lavage and lung lobectomy has been reported to be helpful in people with mineral oil aspiration, but it has not been described in the equine case reports [16, 17]. There is one report of successful treatment of lipoid pneumonia, from aspiration of mineral oil, in which dexamethasone treatment was used  [14]; however, other authors have reported use of corticosteroids as part of their treatment efforts in cases with unsuccessful outcomes [15].

­Sinusitis Definition  Sinusitis is the accumulation of suppurative exudate within the paranasal sinuses of the horse and typically results in malodorous nasal discharge with or without pyrexia. Risk Factors ●● ●●

Treatment  If

Expected Outcome  A small amount of clean water inadvertently administered into the lungs may be tolerated; however, the horse should be placed on prophylactic treatment to prevent pneumonia  [1]. In contrast, a small amount of mineral oil aspirated into the lungs in nearly invariably fatal [13–17].

●●

Prolonged or repeated nasogastric intubation Contamination of the nasal cavity with blood or gastrointestinal reflux, especially during general anesthesia [18, 19]. Prolonged intubation is a significant risk factor in people [20]

Pathogenesis  Unilateral or bilateral sinusitis has been described as a rare complication of nasogastric intubation [18, 19]. Pathogenesis is assumed to be related to overwhelming of normal sinus defense mechanisms by impediment of normal sinus drainage (inflammation and swelling of mucosa secondary to indwelling tubes), increased bacterial load (prolonged intubation, use of a contaminated tube, or feed contamination of sinuses), or propagation of bacterial growth (blood contamination). Prevention  Nasogastric tube-associated sinusitis may be minimized by prophylactically lavaging the nasal passages if they are contaminated with gastrointestinal reflux during colic surgery and by using clean, disinfected nasogastric tubes for as short a time as possible [18]. Diagnosis  Clinical signs are the development of suppurative

nasal discharge and fever [18]. Radiographs of the paranasal sinuses and endoscopy of the upper respiratory tract can localize the disease to the paranasal sinuses.

Treatment  Treat with systemic antimicrobial therapy and

lavage of the affected sinuses via trephination. Sinusotomy via sinonasal flap may be necessary in selected cases.

Expected outcome  Prognosis with appropriate treatment

should be good.

­References 1 Fehr, J. (2013). Nasogastric intubation. In: Practical Guide to Equine Colic (ed. L.L. Southwood), 38–44. Ames: John Wiley & Sons, Inc.

2 Lopes, M.A.F. (2003). Administration of enteral fluid therapy: methods, composition of fluids and complications. Equine Vet. Educ. 15: 107–112.

  ­Reference

3 Hardy, J., Stewart, R.H., Beard, W.L. et al. (1992). Complications of nasogastric intubation in horses: nine cases (1987–1989). J. Am. Vet. Med. Assoc. 201: 483–486. 4 Gillen, A., Cuming, R., Schumacher, J. et al. (2015). Guttural pouch perforation caused during nasogastric intubation. Equine Vet. Educ. 27: 398–402. 5 Wooldridge, A.A., Eades, S.C., Hosgood, G.L. et al. (2002). Effects of treatment with oxytocin, xylazine butorphanol, guaifenesin, acepromazine, and detomidine on esophageal manometric pressure in conscious horses. Am. J. Vet. Res. 63: 1738–1744. 6 Cribb, N.C., Kenney, D.G., and Reid-Burke, R. (2012). Removal of a nasogastric tube fragment from the stomach of a standing horse. Can. Vet. J. 53: 83–85. 7 Rashmir-Raven, A.M., DeBowes, R.M., Gift, L.J. et al. (1991) What is your diagnosis? J. Am. Vet. Med. Assoc. 198: 1991–1992. 8 Craig, D.R., Shivy, D.R., Pankowski, R.L, et al. (1989). Esophageal disorders in 61 horses: results of nonsurgical and surgical management. Vet. Surg. 18: 432–438. 9 Kruger, K. and, Davis, J.L. (2013). Management and complications associated with treatment of cervical oesophageal perforations in horses. Equine Vet. Educ. 25: 247–255. 10 DiFranco, B., Schumacher, J., and Morris, D. (1992). Removal of nasogastric tube fragments from three horses. J. Am. Vet. Med. Assoc. 201: 1035–1037. 11 Baird, A.N. and True, C.K. (1989). Fragments of nasogastric tubes as esophageal foreign bodies in two horses. J. Am. Vet. Med. Assoc. 194: 1068–1070.

12 Stauffer, B.D. (1982). Stomach intubation accidents. J. Am. Vet. Med. Assoc. 181: 448. 13 Metcalfe, L., Cummins, C., Maischberger, E. et al. (2010). Iatrogenic lipoid pneumonia in an adult horse. Irish Vet. J. 63: 303–306. 14 Henninger, R.W., Hass, G.F., and Freshwater, A. (2006). Corticosteroid management of lipoid pneumonia in a horse. Equine Vet. Educ. 18: 205–209. 15 Bos, M., de Bosschere, H., Deprez, P. et al. (2002), Chemical identification of the (causative) lipids in a case of exogenous lipoid pneumonia in a horse. Equine Vet. J. 34: 744–747. 16 Davis, J.L., Ramirez, S., Campbell, N. et al. (2001). Acute and chronic mineral oil pneumonitis in two horses. Equine Vet. Educ. 13: 230–234. 17 Scarratt, W.K., Moon, M.L., Sponenberg, D.P. et al. (1998). Inappropriate administration of mineral oil resulting in lipoid pneumonia in three horses. Equine Vet. J. 30: 85–88. 18 Nieto, J.E., Yamout, S., and Dechant, J.E. (2014). Sinusitis associated with nasogastric intubation in 3 horses. Can. Vet. J. 55: 554–558. 19 Tremaine, W.H. and Dixon, P.M. (2001). A long-term study of 277 cases of equine sinonasal disease. Part 1: Details of horses, historical, clinical and ancillary diagnostic findings. Equine Vet. J. 33: 274–282. 20 Prabhakaran, S., Doraiswamy, V.A., Nagaraja, V. et al. (2012). Nasoenteric tube complications. Scand. J. Surg. 101: 147–155.

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36

6 Complications of Fluid Therapy Angelika Schoster Dr.med.vet, DVSc, PhD, DVSc, DACVIM/DECEIM1 and Henry Stämpfli DVM, Dr.med.vet, DACVIM2 1

Clinic for Equine Internal Medicine, University of Zurich, Switzerland Ontario Veterinary College, University of Guelph, Guelph, Ontario, Canada

2

­ ist of Complications Associated L with Fluid Therapy ●● ●●

●●

●●

●●

●●

Fluid overload using crystalloid solutions Complications associated with the type of crystalloid fluid infused –– Sodium imbalance –– Potassium imbalance –– Other electrolyte imbalances –– Complications due to administration of sodium bicarbonate –– Complications due to glucose/dextrose containing fluids Complications associated with intravascular plasma administration –– Immunological reactions –– Non-immunogenic complications –– Serum hepatitis Complications associated with administration of colloid therapy Complications of enteral fluid therapy –– Complications due to administration setup –– Complications due to volume of fluid used –– Complication due to type of fluid used Complications associated with administration of parenteral nutrition solutions –– Catheter associated complications –– Metabolic aberrations –– Complications due to withholding of enteral feeding

­ luid Overload Using Crystalloid F Solutions In healthy adult animals, the body is made of 60% of water. Two-thirds of total body water is intracellular (ICF,

intracellular fluid compartment) and one-third is extracellular (ECF, extracellular fluid compartment). ECF is composed of interstitial and intravascular fluid (one-third of body weight, ~8%)  [1, 2]. Overhydration can have severe negative impacts on health and should be avoided. Definition  Fluid overload occurs when the total body water is increased relative to the normal volume for a given patient. Fluid overload is caused by administration of excessive amounts of fluid or adequate amounts of fluid to a patient with impaired elimination, for example a patient with decreased urine output due to renal compromise. This condition is rare in adult horses with normal cardiac and renal function. Risk Factors  ●● ●● ●● ●●

Hypoproteinemia Renal failure, heart failure Systemic inflammation Blood product administration [3, 4]

Pathogenesis  If fluid plans are properly designed and followed, this complication is rare. It may occur more commonly in small patients (ponies and neonates) if the weight is estimated, as the margin of safety is smaller in these patients. Starling’s law governs fluid shifts across capillary membranes. Hydrostatic pressures maintain an outward pressure, while oncotic forces aim to retain fluid in its respective compartment. Hydrostatic pressures are derived from body water on either side of the capillary. If large amounts of fluid are introduced into the intravascular space, hydrostatic pressure of the vasculature will increase. When the hydrostatic pressure becomes high enough to overwhelm

Complications in Equine Surgery, First Edition. Edited by Luis M. Rubio-Martinez and Dean A. Hendrickson. © 2021 John Wiley & Sons, Inc. Published 2021 by John Wiley & Sons, Inc.

­Fluid Overload Using Crystalloid Solution 

counteracting forces in the interstitium, extravasation of fluid occurs. In addition, the main oncotic force of the vasculature, albumin, is often diluted in such situations. This lowers oncotic pressure in the vasculature bed, thus further promoting extravasation of fluid into the interstitium and resulting in edema formation [5]. In horses with hypoproteinemia (e.g. colitis, enteritis, colon torsion, post-peritoneal lavage), the oncotic pressure of the vasculature is decreased even without prior dilution. In cases such as acute non-oliguric renal failure, extravasation of fluid due to high hydrostatic pressure can also occur in patients with normal protein levels. Clinical signs of over-hydration (see Diagnosis below) become noticeable once the amount of total water exceeds a critical value, which is individually different. Prevention  A fluid plan should be formulated for each individual patient every 24 hours, taking into account dehydration, maintenance needs and ongoing losses. Care should be taken in animals with risk factors and response should be monitored closely. The weight of the animal should be measured if possible, not estimated, particularly in smaller horses (ponies, neonates). Before formulating a detailed fluid plan in severely hypovolemic patients, an initial resuscitation with a shock dose of a maximum of 90 ml/kg in bolus can be given. This amount can be administered safely in about 20–30 minutes to a 500 kg horse. In high-risk patients, such as neonates, horses with suspected non-oliguric renal failure or horses with severe systemic compromise or obvious signs of heart failure (distended jugular veins, jugular pulses, ventral edema, tachycardia, weak pulses), a more conservative approach is warranted and administration of 45–60 ml/kg over 30 minutes should be targeted initially. This should be followed by slowly replacing the remainder of the deficit over a 12–24 h period. Alternatively, hypertonic fluid (e.g. 5–7% hypertonic saline, 4 ml/kg) can be used as an initial bolus followed by crystalloid fluid therapy (minimum of 5–10 times the amount of hypertonic saline administered). A fluid deficit (dehydration or hypovolemia) can be assessed via clinical data such as heart rate, capillary refill time, moistness of mucous membranes, and skin tent, as well as laboratory data including hematocrit, plasma proteins and creatinine [6, 7]. Anything less than 5% of fluid loss cannot be diagnosed clinically, whereas severe dehydration of around 12% may result in death. Dehydration in percent (%) times body weight gives the amount of fluid in liters to be replaced over a specific time:

Fluid deficit L

%dehydration body weight kg

Ongoing losses due to diarrhea or reflux should ideally be measured. If this is not possible, then losses can be estimated. Maintenance fluid requirement is 2–3 ml/kg/h (50– 75  ml/kg/day) in adult horses and 3–4 ml/kg/h in foals (75–100ml/kg/day), who have a higher total tissue water amount. Additional fluid sources such as enteral fluids, or use of different fluids such as plasma, colloids, or parenteral nutrition solution with their high osmolality, have to be factored into the fluid equation. Once the desired amount of fluid for the next 24 hours is calculated it should be given as a continuous rate infusion (CRI). Ideally in all, but certainly in smaller animals (ponies or foal), a fluid pump should be used. The adequacy of fluid therapy should be monitored every 6–12 hours. The fluid plan should be adjusted accordingly every 12–24 hours. Monitoring parameters include hematocrit and plasma proteins, serum creatinine and lactate. Serial measurements have to be performed, as single hematocrit values can be influenced by splenic contractions and low protein concentrations can be due to primary hypoproteinemia rather than overhydration. Urine output is a good marker for hydration status. When adequate urine output (min, 1 mL/kg/h, approx. 500 mL/h or 12 L/day for a 500 kg horse) occurs after initiation of fluid therapy and urine specific gravity returns to normal (reference range 1,020– 1,040), dehydration is likely resolved and fluid rates should be reduced to cover maintenance and ongoing losses. Repeated weighing of the patient as an objective determination of adequate fluid administered has limited value. For instance, horses with colitis may accumulate fluid in the colon, and gain weight rapidly while still being dehydrated. Continuous daily weight gain should alert for fluid overload in a horse with normal hydration status; however, severely dehydrated horses usually appropriately gain weight. Other techniques providing a more accurate estimation of fluid therapy include central venous pressure monitoring, bioimpedance analysis and pulse pressure variation [8–11]. These techniques are not routinely used in practice and are usually restricted to large referral or university hospitals. Diagnosis  Diagnosis of fluid overload is based on clinical signs and laboratory data. Acute fluid overload often leads to signs of pulmonary edema, while chronic fluid overload is often associated with signs of heart failure. Pulmonary edema leads to impaired oxygenation; clinical signs include tachypnea, tachycardia, coughing, respiratory distress, “wet” lung sounds on auscultation and serous or frothy nasal discharge (see Figure 6.1). Signs observed with chronic fluid overload include lethargy, tachycardia, peripheral edema formation on the ventral midline (see Figure 6.2), distal limbs,

37

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Complications of Fluid Therapy

Figure 6.1  Frothy nasal discharge due to pulmonary edema from fluid overload in a horse.

Figure 6.3  Chemosis as a consequence of fluid overload in a horse.

the sheath in geldings or the head when carried low, and rarely chemosis (see Figure 6.3). Additional signs seen can be restlessness, shivering, colic, ascites, pleural effusion, and large amounts of urine voided. On laboratory analysis, hematocrit and plasma proteins are often below normal range. Arterial blood gas analysis can be performed to assess oxygenation in patients with suspected pulmonary edema. Blood pressure can be elevated. Other negative effects of fluid overload include interstitial tissue edema, gastrointestinal motility disturbances, acute respiratory distress syndrome, abdominal compartment syndrome, delayed wound healing and increased mortality [12, 13].

Treatment options depend on severity of the case. If mild signs of pulmonary (mild tachypnea but no signs of respiratory distress or nasal discharge) or of cardiovascular impairment (mildly elevated heart rate but no overt signs of heart failure) are present and renal function is normal, the kidneys are likely to excrete the excessive amounts of fluid as long as no additional excessive fluid amount is administered. If severe clinical signs of pulmonary, cardiovascular or any renal function impairment are present, additional treatments should be initiated. ●●

Treatment  Once fluid overload is recognized, measures should aim at reducing the total amount of body fluid. ●●

●●

●●

Discontinue or decrease administration of fluid, depending on whether the underlying clinical problem requires additional fluid therapy (e.g. electrolyte imbalances). Increase renal excretion of fluid: Furosemide 1–2 mg/kg IV as a bolus. In case of severe pulmonary edema, up to 4 mg/kg. Drain excessive fluid from pleural and peritoneal spaces if present. Reassess hydration status initially every 2–4 hours, later every 6–12 hours, using the clinical and laboratory parameters described above until hydration status is normal.

Expected Outcome  The outcome depends on the inciting

Figure 6.2  Ventral edema as a consequence of fluid overload in a horse.

cause and underlying disease. If the inciting cause (such as inadvertent over-administration to a healthy patient) can be resolved, prognosis is good. If renal failure is the cause for fluid overload, prognosis is poorer and guarded. Horses with pulmonary edema can die within a short period of time, or can recover fully depending on severity and initiation of treatment.

­Complications Associated with the Type of Crystalloid Fluid Infuse  39

­ omplications Associated C with the Type of Crystalloid Fluid Infused Fluid therapy can lead to acid–base and electrolyte imbalances when given to a healthy animal, but also overcorrections of pre-existing abnormalities can lead to severe side effects if not performed correctly. Sodium and potassium mainly, but also chloride, calcium, magnesium and phosphor homeostasis, are important. Many different crystalloid fluids are available commercially, containing varying concentrations of different electrolytes and base equivalents. Few formulations are currently available in 3–5 L bags, while 1 L bags usually are available but are often cost-prohibitive and cumbersome to be administered to a normal sized horse. Depending on the country and legislation, these fluids differ slightly in their composition. Every clinic/hospital/practitioner should attempt to get an overview of formulations available in his/her country for administration to horses and should know content and concentrations including osmolality of the fluids. Replacement fluid therapy should be considered separately from maintenance fluid therapy, especially the type of fluid chosen. In general, replacement fluids (e.g. Lactated Ringer’s, isotonic saline, Normosol-RTM, Plasmalyte ATM) are very close to serum concentrations for sodium, chloride and potassium, whereas maintenance fluids contain much lower amounts of sodium and chloride and higher amounts of potassium as well as other electrolytes and sometimes glucose (e.g. Normosol MTM).

Pathogenesis  Changes in blood sodium concentrations are often due to underlying diseases or incorrect fluid therapy and result from abnormal water and sodium intake or loss. Blood sodium is always in distribution equilibrium with the total ECF. Abrupt changes in blood sodium concentration cause shifts in the intracellular and interstitial fluid concentrations. In hyponatremia, water shifts from the extracellular fluid compartment intracellularly to maintain osmolal equality between the compartments. Water accumulation in brain cells leads to cerebral swelling and neurological abnormalities. Hyponatremia is uncommon in horses, but can occur in association with diarrhea, bladder rupture, acute renal failure, and severe sweat losses and more rarely with excessive water consumption. Adrenal insufficiency and rhabdomyolysis are rare causes of hyponatremia [14–18]. In hypernatremia, osmolality of the extracellular fluid increases. In acute cases, water shifts from the intracellular fluid compartment extracellular to maintain osmolal equality between the compartments. Cerebral cell dehydration can lead to neurological signs. Hypernatremia is rare in horses. Prevention  ●●

●●

●●

●●

Sodium Imbalance Definition  ●●

●●

Increased (hypernatremia) or decreased (hyponatremia) blood sodium levels (reference range: 139–147 mmol/L) Acute (40 h) conditions are recognized

Risk Factors  ●●

●● ●●

●● ●●

●●

●●

Administration of intravenous sodium-bicarbonate (hypernatremia) Administration of hypertonic saline (hypernatremia) Peritoneal lavage or colon lavage with water or low sodium fluids (hyponatremia) Reflux and diarrhea (usually hyponatremia) Renal disease, interfering with sodium excretion (usually hyponatremia, except if large amounts of sodium are administered when hypernatremia can occur) Small patients (neonates, ponies): these have a smaller margin of safety (both) Pre-existing blood sodium abnormalities (both)

●●

Monitor the amount of sodium administered via fluid therapy. Sodium levels (in combination with other electrolytes) should be measured every 24–48 h during fluid therapy. In hypo- or hypernatremic animals, the rate and speed of correction is crucial to avoid complications. If high or low sodium fluids are used, or correction of existing hypo- or hypernatremia is performed, plasma sodium concentrations should be measured every 12–24 hours. High risk patients (small patients, neonates undergoing abdominal or colon lavage with water) should have blood sodium levels measured 1–2 hours after the procedure.

When replacement fluid therapy is administered to a normonatremic animal, a fluid containing concentrations of sodium equal or close to plasma (~130–150 mmol/L) should be used, e.g. Lactated Ringer’s solution (130 mmol/L). For maintenance, solutions with lower sodium concentration (~40 mmol/L) can be used. As these are not widely available in 3–5 L bags, replacement fluid is often used for maintenance as well. As long as renal function is adequate, the increased sodium load is simply excreted by the kidney. In foals, or animals with impaired renal function, this should be taken into account and a true maintenance solution containing lower amounts of sodium and chloride (e.g. Normosol-MTM Na 40 mmol/L) should be considered.

40

Complications of Fluid Therapy

Diagnosis  Diagnosis is based on clinical signs and blood sodium concentrations. Clinical signs occur only in moderate to severe hyponatremia and include restlessness, focal and general seizures and death. Clinical signs of acute hyponatremia occur in humans at concentrations of 125 mmol/L [19], while concentrations as low as 110 mmol/L can be without clinical signs in chronic hyponatremia [20]. The concentrations at which horses show clinical signs have not been experimentally determined; however, it is known from case reports that foals with Na 24 h in foals), proteins should be added to glucose-only solutions to avoid muscle wasting. Proteins provide essential and non-essential amino acids. The caloric benefit of amino acids is controversial. Some authors recommend excluding the calories provided from amino acids from calculations to spare proteins from anabolism. However, this could lead to underestimating the caloric content of a solution by 15–20% and could lead to overfeeding. Physiologically, it is more likely that calories are used as needed (for production of proteins and all other processes), and providing an overall correct amount of calories is more useful than the concept of protein sparing  [69]. Adequate protein provision should be monitored through daily measurement of Blood Urea Nitrogen (BUN) and serum protein and serum albumin.

Figure 6.5  Blood from a patient with severe hyperlipemia as a consequence of reduced energy intake.

Solutions should be protected from direct sunlight to avoid denaturation of proteins. Commercial aminoacid solutions are usually hypertonic (up to 2,000 mosm/l) and safe infusion rates with gradual increase and the use of infusion pump need to be calculated individually. To avoid hyperlipidemia and its consequences, serum triglycerides should be measured before initiation of lipid containing PPN and monitored daily thereafter (reference range 0.1–0.5  mmol/L). If hyperlipidemia and hypertriglyceridemia are not controlled, they can lead to hepatic lipidosis. Visual inspection for signs of lipemia (see Figure 6.5) is not sensitive enough. The administration of lipid containing parenteral nutrition should be reduced or discontinued when triglycerides levels in blood increase above the reference range. Monitoring during PPN administration should include regular assessments of serum and urine glucose, triglycerides, electrolytes and BUN as explained above. Once stable levels are reached, once daily monitoring is adequate. Additionally, respiratory function should be monitored with blood gas analysis, as glucose administration leads to endogenous production of CO2. Foals should also be weighed daily to ensure anabolic state and adequate weight gain. The catheter site should be monitored four times daily for signs of thrombophlebitis. Parenteral nutrition should be discontinued gradually to avoid rebound hypoglycemia. Diagnosis and  Clinical Signs  Clinical signs are vague and

often masked by the underlying condition necessitating parenteral nutrition. Blood glucose, protein, triglyceride and cholesterol measurements need to be used for diagnosis.

Treatment  ●● ●●

Treatment of hyperglycemia: see above under Prevention Treatment of hyperlipemia: discontinue lipid solution. Exogenous insulin therapy can be considered in severe

  ­Reference

●●

●●

cases to stimulate the hormone sensitive lipase. In high-risk patients such as ponies, donkeys and obese individuals, as well as animals with pre-existing hypertriglyceridemia, administration of lipid-containing solutions should be avoided. Treatment of electrolyte abnormalities: see earlier in this chapter. Treatment of hypoproteinemia: adjustment of the parenteral solution to ensure that adequate amounts of amino acids are included.

Expected Outcome  Hyperglycemia has been shown to be

detrimental and to cause increased morbidity and mortality in human and equine patients. Recommendations are to maintain serum glucose concentrations within narrow margins and avoid hypo- or hyperglycemia [27]. Outcome of hyperlipidemia depends on the severity but can be fatal. Outcome of electrolyte abnormalities depends on severity but is usually good. Outcome of hypoproteinemia and muscle wasting depends on severity and the underlying disease necessitating parenteral nutrition. Literature on parenteral nutrition in horses is mostly available in the form of case reports, retrospective case series and conference proceedings [60, 62, 65, 67, 70–79]. There are few controlled studies available [70, 76, 80, 81]. Therefore, most information on application but also complications of parenteral nutrition is extrapolated from human medicine. This represents challenges as parenteral nutrition in humans differs from those in an equine setting with regards to administration, types of fluid, duration of therapy and metabolic side effects.

­ omplications Due to Withholding C of Enteral Feeding Definition  Withholding of enteral nutrition and use of

parenteral nutrition leads to a decrease in gut mass and structural protein, decreased motility and digestive

function and loss of mucosal integrity. Development of gastric ulcers also can occur. Risk Factors  Foals are at particular risk of developing gastric ulcers. Pathogenesis  Enterocytes need food. Enteral feeding is also less expensive, more physiological, improves immunity including gastrointestinal immunity and is easier and safer. Neonatal foals that receive PPN or TPN without additional enteral feeding are prone to development of gastric ulcers during that period and after re-feeding [70]. Prevention  Some human studies suggest that the route of administration is not as important as providing calories in itself; recommendations are still to institute early use of enteral nutrition if possible [82]. Current recommendations of the American Society for Parenteral and Enteral Nutrition are to avoid parenteral nutrition when the gastrointestinal tract can tolerate enteral nutrition  [83]. Gastric protectants should be administered (0.5 mg/kg Omeprazol IV or 4.4 mg/kg omeprazole PO) to prevent gastric ulcers in adult horses and foals. Sucralfate (12 mg/ kg PO q12 h) can be administered concurrently as mucosal protectant. H2 receptor antagonists (ranitidine 6.6 mg/kg q8 h PO) can be administered instead of omeprazole if it is unavailable or has proven to be ineffective in the patient [84]. Diagnosis and Clinical Signs  Clinical signs of gastric ulcers

include recurrent colic, salivation and bruxism.

Treatment  Enteral feeding should be reintroduced gradually. Some foals may also require help to develop normal nursing behavior after prolonged periods of being off feed. Expected outcome  Outcome is largely dependent on the underlying disease. Gastric ulcers in foals can perforate without prior clinical signs; in these cases prognosis is grave.

­References 1 Fielding, C.L., Magdesian, K.G., and Edman, J.E. (2011). Determination of body water compartments in neonatal foals by use of indicator dilution techniques and multifrequency bioelectrical impedance analysis. Am. J. Vet. Res. 72: 1390–1396. 2 Fielding, C.L., Magdesian, K.G., Elliott, D.A. et al. (2004). Use of multifrequency bioelectrical impedance analysis for estimation of total body water and extracellular and

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5 Woodcock, T.E. and Woodcock, T.M. (2012). Revised Starling equation and the glycocalyx model of transvascular fluid exchange: an improved paradigm for prescribing intravenous fluid therapy. Brit. J. Anaesth. 108: 384–394. 6 Brownlow, M.A. and Hutchins, D.R. (1982). The concept of osmolality: its use in the evaluation of “dehydration” in the horse. Equine Vet. J. 14: 106–110. 7 Rose, R.H. (2000). Fluid and electrolyte therapy: Assessment of fluid and electrolyte balance. In: Manual of Equine Practice, 2e (ed. R.J. Rose and D.R. Hodgson), 2. WB Saunders, Philadelphia. 8 Marik, P.E., Baram, M., and Vahid, B. (2008). Does central venous pressure predict fluid responsiveness? A systematic review of the literature and the tale of seven mares. Chest. 134: 172–178. 9 Magdesian, K.G., Fielding, C.L., Rhodes, D.M. et al. (2006). Changes in central venous pressure and blood lactate concentration in response to acute blood loss in horses. J. Am. Vet. Med. Assoc. 229: 1458–1462. 10 Fielding, C.L., Magdesian, K.G., Carlson, G.P. et al. (2007). Estimation of acute fluid shifts using bioelectrical impedance analysis in horses. J. Vet. Intern. Med. 21: 176–183. 11 Fielding, C.L. and Stolba, D.N. (2012). Pulse pressure variation and systolic pressure variation in horses undergoing general anesthesia. J. Vet. Emerg. Crit. Care. (San Antonio). 22: 372–375. 12 Fielding, L. (2014). Crystalloid and colloid therapy. Vet. Clin. N. Am. Equne Pract. 30: 415–425, viii–ix. 13 Cotton, B.A., Guy, J.S., Morris, J.A. Jr. et al. (2006). The cellular, metabolic, and systemic consequences of aggressive fluid resuscitation strategies. Shock. 26: 115–121. 14 Hardefeldt, L.Y. (2014). Hyponatraemic encephalopathy in azotaemic neonatal foals: four cases. Aust. Vet. J. 92: 488–491. 15 Lakritz, J., Madigan, J., and Carlson, G.P. (1992). Hypovolemic hyponatremia and signs of neurologic disease associated with diarrhea in a foal. J. Am. Vet. Med. Assoc. 200: 1114–1116. 16 Wong, D.M., Sponseller, B.T., Brockus, C. et al. (2007). Neurologic deficits associated with severe hyponatremia in 2 foals. J. Vet. Emerg. Crit. Care. 17: 275–228 17 Dunkel, B., Palmer, J.E., Olson, K.N. et al. (2005). Uroperitoneum in 32 foals: influence of intravenous fluid therapy, infection, and sepsis. J. Vet. Intern. Med. 19: 889–893. 18 Geor, R.J. (2007). Acute renal failure in horses. Vet. Clin. N. Am. Equine Pract. 23: 577–591, v–vi. 19 Arieff, A.I., Llah, F., and Massry, S.G. (1976). Neurological manifestations and morbidity of

hyponatremia: correlation with brain water and electrolytes. Medicine. 55: 121–129. 20 Biswas, M. and Davies, J.S. (2007). Hyponatraemia in clinical practice. Postgrad. Med. J. 83: 373–378. 21 Sterns, R.H., Riggs, J.E., and Schochet, S.S. Jr. (1986). Osmotic demyelination syndrome following correction of hyponatremia. New. E.g. J. Med. 314: 1535–1542. 22 Adrogue H.J. and Madias, N.E. (2000). Hyponatremia. New. Eng. Med. J. 342: 1581–1589. 23 Mohmand, H.K., Issa, D., Ahmad, Z. et al. (2007). Hypertonic saline for hyponatremia: risk of inadvertent overcorrection. C.J.A.S.N. 2: 1110–1117. 24 Groenendyk, S., English, P.B., and Abetz, I. (1988). External balance of water and electrolytes in the horse. Equine Vet. J. 20: 189–193. 25 Watson, Z.E., Steffey, E.P., VanHoogmoed, L.M. et al. (2002). Effect of general anesthesia and minor surgical trauma on urine and serum measurements in horses. Am. J. Vet. Res. 63: 1061–1065. 26 Epstein, V. (1984). Relationship between potassium administration, hyperkalemia and the electrocardiogram – an experimental study. Equine Vet. J. 16: 453–456. 27 Vincent, J.L. (2007). Metabolic support in sepsis and multiple organ failure: more questions than answers. Crit. Care Med. 35: S436–S440. 28 Eicker, S.W. and Ainsworth, D.M. (1984). Equine plasma banking: collection by exsanguination. J. Am. Vet. Med. Assoc. 185: 772–774. 29 Wilson, E.M., Holcombe, S.J., Lamar, A. et al. (2009). Incidence of transfusion reactions and retention of procoagulant and anticoagulant factor activities in equine plasma. J. Vet. Intern. Med. 23: 323–328. 30 Feige, K., Ehrat, F.B., Kastner, S.B. et al. (2003). Automated plasmapheresis compared with other plasma collection methods in the horse. J. Vet. Med. A. 50: 185–189. 31 Hardefeldt, L.Y., Keuler, N., and Peek, S.F. (2010). Incidence of transfusion reactions to commercial equine plasma. J. Vet. Emerg. Crit. Care (San Antonio). 20: 42–425. 32 More, S.J., Aznar, I., Bailey, D.C. et al. (2008). An outbreak of equine infectious anaemia in Ireland during 2006: Investigation methodology, initial source of infection, diagnosis and clinical presentation, modes of transmission and spread in the Meath cluster. Equine Vet. J. 40: 706–708. 33 Aleman, M., Nieto, J.E., Carr, E.A. et al. (2005). Serum hepatitis associated with commercial plasma transfusion in horses. J. Vet. Intern. Med. 19: 120–122.

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3 4 Chandriani, S., Skewes-Cox, P., Zhong, W. et al. (2013). Identification of a previously undescribed divergent virus from the Flaviviridae family in an outbreak of equine serum hepatitis. Proc. Nat. Acad. Sci. USA. 110: E1407–1415. 35 Ramsay, J.D., Evanoff, R., Wilkinson, T.E. Jr. et al. (2015). Experimental transmission of equine hepacivirus in horses as a model for hepatitis C virus. Hepatology. 61: 1533–1546. 36 Sacks, M. and Mosing, M. (2017). Volumetric capnography to diagnose venous air embolism in an anaesthetised horse. Vet. Anaesth. Analg. 44 (1): 189–190. doi:10.1111/vaa.12383 37 Westphal, M., James, M.F., Kozek-Langenecker, S. et al. (2009). Hydroxyethyl starches: different products – different effects. Anesthesiology, 111: 187–202. 38 Glover, P.A., Rudloff, E., and Kirby, R. (2014). Hydroxyethyl starch: a review of pharmacokinetics, pharmacodynamics, current products, and potential clinical risks, benefits, and use. J, Vet, Emerg, Crit, Care (San Antonio). 24: 642–661. 39 Schortgen, F., Girou, E., Deye, N. et al. (2008). The risk associated with hyperoncotic colloids in patients with shock. Intens. Care. Med. 34: 2157–2168. 40 Wiedermann, C.J., Dunzendorfer, S., Gaioni, L.U. et al. (2010). Hyperoncotic colloids and acute kidney injury: a meta-analysis of randomized trials. Crit. Care. 14: R191. 41 Dart, A.B., Mutter, T.C., Ruth, C.A. et al. (2010). Hydroxyethyl starch (HES) versus other fluid therapies: effects on kidney function. Cochrane Database of Systematic Reviews: 2010 (1): CD007594. doi: 10.1002/14651858.CD007594.pub2 42 Perner, A., Haase, N., Guttormsen, A.B. et al. (2012). Hydroxyethyl starch 130/0.42 versus Ringer’s acetate in severe sepsis. Ne. Eng. J. Med. 367: 124–134. 43 Myburgh, J.A., Finfer, S., Bellomo, R. et al. (2012). Hydroxyethyl starch or saline for fluid resuscitation in intensive care. New Eng. J. Med. 367: 1901–1911. 44 Gratwick, Z., Viljoen, A., Page, P.C. et al. (2017). A comparison of the effects of a 4% modified fluid gelatin and a 6% hydroxyethyl starch on haemodilution, colloid osmotic pressure, haemostasis and renal parameters in healthy ponies. Equine Vet. J 49 (3): 363–368.doi: 10.111/ evj.12594. 45 Fenger-Eriksen, C., Tonnesen, E., Ingerslev, J. et al. (2009). Mechanisms of hydroxyethyl starch-induced dilutional coagulopathy. J.T.H. 7: 1099–1105. 46 McKenzie, E.C., Esser, M.M., McNitt, S.E. et al. (2016). Effect of infusion of equine plasma or 6% hydroxyethyl starch (600/0.75) solution on plasma colloid osmotic pressure in healthy horses. Am. J. Vet. Res. 77: 708–714.

47 Epstein, K.L., Bergren, A., Giguere, S. et al. (2014). Cardiovascular, colloid osmotic pressure, and hemostatic effects of 2 formulations of hydroxyethyl starch in healthy horses. J. Vet. Intern. Med. 28: 223–233. 48 Blong, A.E., Epstein, K.L., and Brainard, B.M. (2013). In vitro effects of three formulations of hydroxyethyl starch solutions on coagulation and platelet function in horses. Am. J. Vet. Res. 74: 712–720. 49 Bellezzo, F., Kuhnmuench, T., and Hackett, E.S. (2014). The effect of colloid formulation on colloid osmotic pressure in horses with naturally occurring gastrointestinal disease. B.M.C. Vet. Res. 10 Suppl 1: S8. 50 Brunisholz, H.P., Schwarzwald, C.C., BettschartWolfensberger, R. et al. (2015). Effects of 10% hydroxyethyl starch (HES 200/0.5) solution in intraoperative fluid therapy management of horses undergoing elective surgical procedures. Vet. J. 206: 398–403. 51 Reilly, C. (2011). Retraction. Notice of formal retraction of articles by Dr. Joachim Boldt. Brit. J. Anaesth. 107: 116–117. 52 Lopes, M.A., White, N.A. 2nd, Donaldson, L. et al. (2004). Effects of enteral and intravenous fluid therapy, magnesium sulfate, and sodium sulfate on colonic contents and feces in horses. Am. J. Vet. Res. 65: 695–704. 53 Lopes, M.A., Walker, B.L., White, N.A. 2nd. et al. (2002).Treatments to promote colonic hydration: enteral fluid therapy versus intravenous fluid therapy and magnesium sulphate. Equine Vet. J. 34: 505–509. 54 Hallowell, G.D. (2008). Retrospective study assessing efficacy of treatment of large colonic impactions. Equine Vet. J. 40: 411–413. 55 Monreal, L., Garzon, N., Espada, Y. et al. (1999). Electrolyte vs. glucose-electrolyte isotonic solutions for oral rehydration therapy in horses. Equine Vet. J. Supplement: 425–429. 56 Collatos, C. and Romano, S. (1993). Cecal impaction in horses – causes, diagnosis, and medical-treatment. Comp. Cont. Educ. Pract. 15: 976–982. 57 Lester, G.D., Merritt, A.M., Kuck, H.V. et al. (2013). Systemic, renal, and colonic effects of intravenous and enteral rehydration in horses. J. Vet. Intern. Med. 27: 554–566. 58 Ousey, J.C. (1994). Total parenteral nutrition in the young foal. Equine Vet. Educ. 16: 2. 59 Krause, J.B. and McKenzie, H.C. 3rd. (2007). Parenteral nutrition in foals: a retrospective study of 45 cases (2000–2004). Equine Vet. J. 39: 74–78. 60 Lopes, M.A. and White, N.A. 2nd. (2002). Parenteral nutrition for horses with gastrointestinal disease: a retrospective study of 79 cases. Equine Vet. J. 34: 250–257.

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61 Hansen, T.O. (1986). Parenteral nutrition in foals. Proceedings of the 32nd Annual Convention of the American Association of Equine Practitioners AAEP, 4. 62 Myers, C.J., Magdesian, K.G., Kass, P.H, et al. (20098. Parenteral nutrition in neonatal foals: clinical description, complications and outcome in 53 foals (1995–2005). Vet. J. 181: 137–144. 63 Jeejeebhoy, K.N. (2004). Permissive underfeeding of the critically ill patient. Nutrit. Clin Pract 19: 477–480. 64 Carr, E.A. and Holcombe, S.J. (2009). Nutrition of critically ill horses. Vet. Clin. N. Am. Equine Pract. 25: 93–108, vii. 65 Magdesian, K.G. (2010). Parenteral nutrition in the mature horse. Equine Vet. Educ. 22: 364–371. 66 Waitt, L.H. and Cebra, C.K. (2009). Characterization of hypertriglyceridemia and response to treatment with insulin in horses, ponies, and donkeys: 44 cases (1995– 2005). J. Am. Vet. Med. Assoc. 234: 915–919. 67 Durham, A.E. (2006). Clinical application of parenteral nutrition in the treatment of five ponies and one donkey with hyperlipaemia. Vet. Record. 158: 159–164. 68 Han, J.H., McKenzie, H.C., McCutcheon, L.J. et al. (2011). Glucose and insulin dynamics associated with continuous rate infusion of dextrose solution or dextrose solution and insulin in healthy and endotoxin-exposed horses. Am. J. Vet. Res. 72: 522–529. 69 Klein, C.J., Stanek, G.S., and Wiles, C.E. 3rd. (1998). Overfeeding macronutrients to critically ill adults: metabolic complications. J. Am. Diet. Assoc. 98: 795–806. 70 Ousey, J.C., Prandi, S., Zimmer, J. et al. (1997). Effects of various feeding regimens on the energy balance of equine neonates. Am. J. Vet. Res. 58: 1243–1251. 71 Hoffer, R.E., Barber, S.M., Kallfelz, F.A. et al. (1977). Esophageal patch grafting as a treatment for esophageal stricture in a horse. J. Am. Vet. Med. Assoc. 171: 350–354. 72 McKenzie, H.C. 3rd., and Geor, R.J. (2009). Feeding management of sick neonatal foals. Vet. Clin. N. Am. Equine Pract. 25: 109–119, vii. 73 Furr, M.O. (2002). Intravenous nutrition in horses. Proceedings of the 20th Annual ACVIM Forum American College of veterinary Internal Medicine: 2.

74 Greatorex, J.C. (1975). Intravenous nutrition in the treatment of tetanus in horses. Vet. Record. 97: 498. 75 Dunkel, B. and McKenzie, H.C. 3rd. (2003). Severe hypertriglyceridaemia in clinically ill horses: diagnosis, treatment and outcome. Equine Vet. J. 35: 590–595. 76 Hansen, T.O., White, N.A. 2nd, and Kemp, D.T. (1988). Total parenteral nutrition in four healthy adult horses. Am. J. Vet. Res. 49: 122–124. 77 Suann, C.J. (1982). Esophageal resection and anastomosis as a treatment for esophageal stricture in the horse. Equine Vet. J. 14: 163–164. 78 Spurlock, S.L. and Ward, M.V. (1990). Providing parenteral nutritional support for equine patients. Vet. Med-US. 85: 883. 79 Bercier, D.L. (2003). Nutrition support in critical illness. Proceedings of the 49th Annual convention of the American Association of Equine Practitioners AAEP 6. 80 Durham, A.E., Phillips, T.J., Walmsley, J.P. et al. (2003). Study of the clinical effects of postoperative parenteral nutrition in 15 horses. Vet. Record. 153: 493–498. 81 Durham, A.E., Phillips, T.J., Walmsley, J.P. et al. (2004). Nutritional and clinicopathological effects of post operative parenteral nutrition following small intestinal resection and anastomosis in the mature horse. Equine Vet. J. 36: 390–396. 82 Kreymann, K.G., Berger, M.M., Deutz, N.E. et al. (2006). ESPEN Guidelines on Enteral Nutrition: Intensive care. Clin. Nutrit. 25: 210–223. 83 McClave, S.A., Taylor, B.E., Martindale, R.G. et al. (2016). Guidelines for the Provision and Assessment of Nutrition Support Therapy in the Adult Critically Ill Patient: Society of Critical Care Medicine (SCCM) and American Society for Parenteral and Enteral Nutrition (ASPEN). J.P.E.N. 40: 159–211. 84 Sykes, B.W., Hewetson, M., Hepburn, R.J. et al. (2015). European College of Equine Internal Medicine Consensus Statement – Equine Gastric Ulcer Syndrome in Adult Horses. J. Vet. Intern. Med./Am. Coll. Vet. Int. Med. 29: 1288–1299.

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7 Complications Associated with Hemorrhage Margaret C. Mudge VMD DACVS, DACVECC The Ohio State University, Columbus, Ohio

O ­ verview

Coagulopathy (congenital or acquired) Pre-existing bleeding (e.g. hemoabdomen, epistaxis) with surgical procedures to explore the cause of bleeding Surgical/surgeon factors: ○○ Technical failures (ligature slippage, poor choice of hemostatic device, lack of anatomic knowledge) ○○ Long duration of surgery in a bleeding area (e.g. complex tumors, sinusotomy) ○○ Inadvertent disruption of vasculature ○○ Medications administered (e.g. hemodilution with intravenous fluids, anticoagulation with heparin) ○○ ○○

Intra- and post-operative bleeding can occur with many equine procedures. The difference between bleeding and hemorrhage is generally based upon the severity of the blood loss. In many cases, hemorrhage can be predicted based upon the location of the surgical procedure. This chapter will discuss how to treat and prevent intra- and post-operative hemorrhage.

­ ist of Complications Associated L with Hemorrhage ●●

●●

Intraoperative hemorrhage ○○ Fluid therapy and blood transfusion ○○ Adjunctive systemic treatment Postoperative hemorrhage

­Intraoperative Hemorrhage Definition  Intraoperative hemorrhage is considered a complication if it is unexpected, severe enough to warrant a blood transfusion or leads to moderate/severe anemia, obscures the surgical field, or puts the animal at risk of additional intraoperative or postoperative morbidity. Early consequences of hemorrhage include shock, anemia, and difficulty visualizing the surgical site. Late complications include seroma formation, surgical site infection, and delayed healing. Risk Factors  ●●

Patient factors: ○○ Highly vascular areas (e.g. tumor removal, gonadectomy, paranasal sinus surgery)

●●

Pathogenesis  Bleeding is part of almost every surgery, but is usually well controlled by the patient’s normal mechanisms of hemostasis, along with surgical control of bleeding through pressure and ligation of vessels. The initial response to disruption of a blood vessel is vasoconstriction, followed by platelet activation, adhesion, and aggregation. Activation of clotting factors is initiated by tissue factor, with the end result being a fibrin clot. Platelet abnormalities, coagulation factor deficiencies, and excessive fibrinolysis can all result in abnormal or uncontrolled bleeding. The correlation of coagulation profile findings and bleeding complications has been evaluated in dogs and cats after ultrasound-guided biopsies  [1]. Bleeding complications were seen in thrombocytopenic cases, and in cats with prolonged aPTT and dogs with prolonged OSPT. Authors of a retrospective study in horses undergoing percutaneous liver biopsy did not find a correlation between bleeding complications and an abnormal coagulation profile; however, only 3 horses (9% of monitored horses) had a decrease in packed cell volume (PCV) [2]. Hereditary hemostatic defects are uncommon in horses. Platelet dysfunction can occur secondary to Glanzmann

Complications in Equine Surgery, First Edition. Edited by Luis M. Rubio-Martinez and Dean A. Hendrickson. © 2021 John Wiley & Sons, Inc. Published 2021 by John Wiley & Sons, Inc.

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thromasthenia, a membrane glycoprotein defect that has been described in a variety of breeds [3]. Von Willebrand disease can also cause prolonged mucosal bleeding times. Coagulation factor deficiencies, such as hemophilia A (factor VIII deficiency) have also been described and result in prolonged bleeding times. Acquired hemostatic defects are more common, and can be related to immune-mediated destruction of platelets, liver disease, uremia, or bone marrow disease. Transient coagulopathies can occur in horses with gastrointestinal disease or other critical illness, as upregulation of inflammation leads to systemic activation of coagulation [4]. There is limited information in the veterinary literature regarding risk factors for surgical hemorrhage. There is even less evidence for the efficacy of specific treatments or preventative measures in reducing hemorrhage in veterinary surgical procedures. Size has been shown to be a factor in ovariohysterectomy in dogs, with a 2% intraoperative hemorrhage rate in dogs weighing less than 50 pounds and 79% hemorrhage rate in dogs of 50 pounds or more [5]. The use of active suction drains has been reported as a potential risk factor for postoperative hemorrhage in dogs, but this has not been reported in horses [6]. Patient positioning has been shown to have a significant effect on intraoperative blood loss in humans. Reverse Trendelenburg positioning for human patients undergoing endoscopic sinus surgery resulted in decreased blood loss and improved visualization of the surgical field [7, 8]. Type of anesthesia has also been shown to have an effect on bleeding during endoscopic sinus surgery in human patients, with less bleeding under total intravenous anesthesia compared to inhalation anesthesia  [9]. Although the effect of positioning on blood loss has not been evaluated in horses, surgeons have observed decreased blood loss with standing paranasal sinus surgery compared to recumbent surgery in the horse [10]. Reverse Trendelenburg positioning has been used by this author during recumbent paranasal sinus surgery with a subjective decrease in blood loss (Figure 7.1). The intravenous or topical administration of tranexamic acid during major human orthopedic surgery is associated with a significant reduction in blood loss and units of blood transfused, without an increase in venous thromboembolic events  [11]. Several topical hemostatic agents have been evaluated for use in endoscopic sinus surgery, but none has consistently reduced hemorrhage compared to no treatment [12]. Surgeon experience may also be a factor in surgical hemorrhage. Involvement of a surgical resident in noncardiac surgeries on humans resulted in higher transfusion rates (56–78% higher) compared to surgeries performed by an attending surgeon without a resident. This may be related

Figure 7.1  A horse is positioned in reverse Trendelenburg in preparation for paranasal sinus surgery. Source: Margaret Mudge.

to surgeon skill, duration of surgery, or clinical judgment with respect to the need for transfusion [13]. Prevention  Coagulopathy is exceedingly uncommon in

otherwise healthy equine patients presenting for elective surgery. It would not be cost-effective to perform coagulation testing on all patients undergoing major surgery, but a thorough patient history, physical examination, and consideration of any underlying disease can help direct further testing. The horse may have a history of excessive bleeding during elective surgery, such as castration, or there may be a history of hematomas or bleeding at venipuncture sites. Medications such as nonsteroidal anti-inflammatory drugs (NSAIDs) may alter coagulation, although NSAIDs are commonly given prior to surgery in horses without clinical signs of excessive bleeding [14]. Herbal supplements have been shown to alter platelet function and coagulation in human patients. Commonly used mediations that increase the risk of bleeding include garlic, ginkgo biloba, green tea, and fish oil [15]. Physical exam may reveal mucous membrane petechiation, which should prompt a complete blood count, and potentially platelet function testing. Ideally, any anemia should be corrected before surgery, especially if blood loss is anticipated. Although erythropoietin will increase red blood cell production, the administration of recombinant human erythropoietin has led to development of erythropoietin antibodies and severe anemia in horses, so cannot be recommended [16]. Delaying the surgery or administering whole blood or packed RBC transfusions are the best methods for correcting preoperative anemia. Clinicopathologic findings of hepatic failure (e.g. icterus, photosensitization, abnormal liver enzymes, increased

­Intraoperative Hemorrhag  59

serum bile acids) should cause the clinician to delay surgery, perform coagulation testing, and consider transfusion with fresh frozen plasma. Horses with colic, especially with obstructive surgical or inflammatory medical conditions, frequently have clinicopathologic evidence of coagulopathy with increased d-dimer and prolonged PT/PTT  [17]. While there is no definitive treatment to prevent hemorrhage in these horses, consideration should be given to avoiding large volumes of synthetic colloids, and instead treating with fresh frozen plasma if colloids are needed. The surgeon should be prepared with appropriate hemostatic equipment. Surgical stapling devices such as the LDS™ and electrothermal bipolar vessel-sealing device (Ligasure™, Medtronic, Minneapolis, MN) can occlude vessels up to 7 mm in diameter [18]. Other stapling devices, such as the TA™ staplers (Medtronic), can be used to compress larger bundles of tissue. Electrocautery is effective for vessels up to 2 mm diameter [19]. For distal limb surgeries, especially extensive wound or foot debridements, the use of a tourniquet should be considered to provide better ­visualization and limit blood loss Figure 7.2). Patient positioning should also be considered, for example, reverseTrendelenburg or standing position for paranasal sinus surgery. Preparation for intraoperative hemorrhage also includes securing blood products or blood donor horses. In cases of known red blood cell alloantibodies or previous transfusion reactions, preoperative autologous donation (PAD) should be considered  [20]. PAD involves collecting the patient’s blood 2–4 weeks prior to surgery. Approximately 15–20% of the patient’s blood volume can be collected (6–8

liters for a 500 kg horse). Acute normovolemic hemodilution is another technique that could be considered when allogeneic blood is not available. This technique involves removal of the patient’s blood just before anesthesia with replacement of volume by crystalloid fluids [21]. Human patients who require blood transfusion during surgery have an increased risk of death, and are more likely to have septic and wound complications [22]. Hemorrhage during trauma surgery carries a high risk of transfusion and death, so in many cases, “damage control surgery” is advocated. An initial laparotomy is performed to control the damage (e.g. intestinal leakage, devitalized bowel, bleeding vessel), and packing with temporary closure are performed until the patient is stable enough to undergo definitive repair [23]. Diagnosis and  Monitoring  The diagnosis of intraoperative hemorrhage is based on the volume of blood loss, along with changes in vital signs (tachycardia, hypotension, prolonged capillary refill time) and decreasing PCV and TS. Intraoperative blood loss is usually readily apparent, but can be overlooked if it is not collected and measured. Suction canister volume should be recorded, and PCV of the fluid can be measured to determine the volume of blood lost. Careful monitoring under anesthesia is necessary, as the heart rate and hematocrit may not change, even with severe blood loss. Arterial blood pressure and PaO2, along with mucous membrane color and capillary refill time, may be more accurate reflections of blood loss  [24]. Central venous pressure and blood lactate concentration have also been shown to correlate with acute blood loss in standing, unsedated horses [25]. Treatment  Local treatment  The initial response to intraoperative

Figure 7.2  A tourniquet is applied over the metatarsophalangeal joint to limit blood loss and improve visualization during surgery of the digit. Source: Courtesy of Frank Nickels.

hemorrhage should be to apply firm pressure to the bleeding area. Direct mechanical pressure is a very effective way to limit blood loss during and after surgery. If bleeding vessels can be visualized, they should be clamped and ligated. Collagen sponges, microfibrillar collagen, gelatin sponges, oxidized regenerated cellulose, and bone wax are all topical mechanical hemostatic agents that apply pressure to the area of bleeding  [26]. Topical thrombin and fibrin-based sealants promote formation of fibrin clots, and are applied onto the bleeding areas [27]. Surgical sealants such as polyethylene glycol polymers are used as an adjunct for vascular reconstruction, but are quite expensive [28]. A tourniquet can be used on the distal limb in order to improve visualization of transected vessels. In the case of diffuse bleeding, such as after debridement of exuberant granulation tissue, pressure bandages can be used on the distal limb. If substantial bleeding is encountered during

60

Complications Associated with Hemorrhage

paranasal sinus surgery, the sinus should be packed firmly with gauze packing and the sinusotomy bone flap can be temporarily stapled closed [29]. Chilled saline and topical vasoconstrictive agents such as epinephrine or phenylephrine can also be used as topical adjuncts (alone or on gauze packing) in sinus surgery to promote local vasoconstriction and reduce bleeding [30]. When blood loss from the paranasal sinuses cannot be controlled with direct pressure, temporary bilateral carotid artery occlusion can be used to limit blood loss ([31]. One of the most important factors in limiting blood loss is making a quick decision to limit blood loss and postpone the remainder of the surgery until bleeding is controlled. In the case of paranasal sinus surgery, the packing can be removed during a standing procedure 24 to 48 hours later, with reevaluation of the sinus and completion of the procedure under better visualization. Fluid therapy and blood transfusion 

Initial stabilization for acute blood loss is accomplished with intravenous crystalloid fluids. A starting point for resuscitation should be an initial bolus of approximately 20  ml/kg. Overzealous resuscitation can result in further bleeding due to an increase in blood pressure and dilution of clotting factors. The goals of fluid therapy should be to bring the mean arterial blood pressure to within a range of 60–70 mmHg, and maintain tissue perfusion  [25]. Blood lactate can be used to help determine response to fluid therapy, with the aim to normalize lactate (60/min, CRT >3 sec, cold extremities, depressed mentation) despite adequate volume resuscitation, oxygen extraction ratio greater than 40%, lactate greater than 4 mmol/l, and acute hemorrhage with a PCV less than 20%. In acute blood loss situations, the volume of blood lost can be estimated based on the severity of shock. For example, a horse that is severely tachycardic with decreased pulse pressure, pale mucous membranes, and altered

­ entation can be estimated to have lost approximately 30% m of its blood volume  [25]. Up to half of the volume lost should be replaced by a whole blood transfusion. In cases of normovolemic anemia, the following formula can be used to estimate transfusion volume: Blood transfusion volume (ml): Body weight kg 80 ml / kg

Desired PCV Actual PCV Donor PCV

.

The target PCV will depend on whether the horse is at risk of continued bleeding and whether there are any comorbidities that might decrease perfusion. This author will typically target a PCV of 25%, although the total blood transfusion volume will often be limited by how much blood the donor horse can give. Donor horses are the most common source of blood for transfusion, but autologous salvaged blood should also be considered. Cell salvage devices can be used to collect blood from surgical sites or drains. Blood is suctioned from the surgical site, filtered, centrifuged, washed, and returned to a bag for reinfusion into the patient [35]. This technique has been reported in canine patients, and could be used in equine patients if the equipment is available [36]. Blood can be collected and transfused directly into the patient without processing, but the cell salvage system reduces contaminants. A leukocyte depletion filter is needed when there may be contamination of blood with neoplastic cells or bacteria. When blood is lost into a body cavity (hemothorax or hemoabdomen), it can also be left to be reabsorbed by the patient. The immediate hypovolemia must be addressed with IV fluids, but the majority of shed blood may be reabsorbed via lymphatics within 48 hours  [37]. If PCV falls below 20% or the horse continues to have signs of shock despite fluid resuscitation, a blood transfusion may still be needed. Allogeneic transfusion from a donor horse is most common, but collection of blood from the abdominal cavity and reinfusion has also been reported [38]. Adjunctive systemic treatment 

The mainstays of systemic treatment for acute hemorrhage are fluid therapy and blood transfusion. There are a number of procoagulant medications that can also be used to enhance hemostasis in the horse [39]:

●●

●●

Formalin – Proposed to enhance endothelial or platelet activation, reported dose of 10–100 ml of 10% formalin in 1 L isotonic saline Aminocaproic acid – Lysine derivative that inhibits fibrinolysis by binding plasminogen activators and enhancing antiplasmin activity. The previously reported doses are 10–40 mg/kg IV q6h slow in saline or 3.5 mg/kg/min for 15 min then 0.25 mg/kg/min constant rate infusion.

­Postoperative Hemorrhag  61 ●●

●●

●●

●●

Tranexamic acid – Similar mechanism of action as aminocaproic acid; 5 g IV every 12 hours or 10 g PO every 6 hours New research suggests that as little as 1/20 of the published doses of aminocaproic acid and tranexamic acid may be effective in horses [40]. Conjugated estrogens  –  May polymerize mucopolysaccharides in vessel walls or decrease antithrombin activity, 0.6 mg/kg IV every 24 hours Yunnan baiyao – Chinese herbal medication with demonstrated hemostatic efficacy, possibly due to activation of platelets, enhanced expression of surface glycoproteins on platelets [41].

Expected Outcome  The acute risks of intraoperative hemorrhage include rapid shock and death, particularly if a large vessel is ruptured, such as a portal vein rupture during reduction of an epiploic foramen entrapment. There are no specific reports on intraoperative mortality due to hemorrhage in equine patients.

­Postoperative Hemorrhage Definition  Postoperative hemorrhage can occur immediately

after surgery or can be delayed by several days after surgery. Hemorrhage is most commonly from the surgical site, but can occur in distant areas if a coagulopathy has developed.

Risk Factors  Same as for intraoperative hemorrhage (see

above)

Pathogenesis  The pathogenesis of postoperative hemorrhage is the same as for intraoperative hemorrhage. Inadequate hemostasis may not be recognized at the time of surgery, possibly due to lower blood pressure under anesthesia, positioning (e.g. lower pressure in the distal limb of a horse in dorsal recumbency), or a temporary clot that becomes dislodged after surgery.

passage. Tachycardia, tachypnea, and pale mucous membranes may signal ongoing blood loss, and serial PCV/TS can help to determine the severity of blood loss. TS should decrease within minutes to hours of blood loss, but PCV may remain normal even during terminal blood loss, due to the effects of splenic contraction [24]. Internal bleeding into the abdomen or thorax may not be apparent until the horse begins to show signs of shock or discomfort. In a recent retrospective study of postoperative abdominal hemorrhage, clinical signs included tachycardia, decreasing PCV/TP, abdominal discomfort, and incisional drainage. The hemoabdomen was confirmed by ultrasound or abdominocentesis  [42]. Swirling, echogenic fluid is characteristic of hemoabdomen, and abdominocentesis will confirm the diagnosis (Figure 7.3). Blood loss into the intestinal lumen can be more difficult to detect until it is passed in the feces. Intraluminal blood loss should be suspected in horses that have had an enterotomy or large colon resection, and that have an acute, severe decrease in PCV along with tachycardia and melena within 72 hours of surgery [43]. Treatment  See “Fluid therapy and blood transfusion” and “Adjunctive systemic treatment” sections above. Reoperation  Reoperation is often the last resort for postoperative hemorrhage, but should be considered early if there is unexpected postoperative hemorrhage and if there is a chance that a ligature may have slipped. A return to surgery may be needed if the patient is deteriorating despite medical therapy, although these patients are likely to be unstable under anesthesia [44]. If bleeding was detected at surgery but was inaccessible, or if the source of bleeding is unlikely

Prevention  Same as for intraoperative hemorrhage (see

above)

Diagnosis and Monitoring  Acute blood loss of 30% of blood

volume will result in cardiovascular shock due to hypovolemia and reduced oxygen delivery to the tissues. Signs of shock include tachycardia, tachypnea, prolonged capillary refill time, cool extremities, depressed or anxious mentation, and hypotension. In horses, splenic contraction will increase the PCV, so the decrease in PCV will typically lag behind the decrease in total solids (TS). Postoperative hemorrhage may be apparent if there is blood leaking from the surgical drain, incision, or nasal

Figure 7.3  Transabdominal ultrasound image showing cellular echogenic free fluid consistent with hemoabdomen. Source: Courtesy of Teresa Burns.

62

Complications Associated with Hemorrhage

to be accessible through the same surgical approach, an alternate approach is indicated. For example, a hemoabdomen post-castration may be best treated through a standing laparoscopic approach [38]. In a case series at a level 1 human trauma center, reoperation for bleeding in trauma patients was prompted by direct signs, such as external bleeding or bleeding from drains, in 74% of patients. Indirect signs that led to reoperation included hemodynamic instability, decrease in hematocrit, and abdominal distention [44].

Expected Outcome  Mortality in horses with hemorrhage after emergency celiotomy was reported to be 35%. Causes of death were hemorrhagic shock, septic peritonitis, and adhesions [42]. In a report of post-castration complications, less than 2% of horses undergoing routine castration suffered from significant hemorrhage. In all horses, bleeding occurred within 4 hours of surgery, and all were treated by packing with sterile laparotomy sponges which were removed at 24–48 hours. One horse received aminocaproic acid [45].

­References 1 Bigge, L.A., Brown D.J., and Penninck D.G. (2001). Correlation between coagulation profile findings and bleeding complications after ultrasound-guided biopsies: 434 cases (1993–1996). J. Am. Anim. Hosp. Assoc. 37: 228–233. 2 Johns I.C. and Sweeney R.W. (2008). Coagulation abnormalities and complications after percutaneous liver biopsy in horses. J. Vet. Intern. Med. 22 (1): 185–189. 3 Brooks, M.B. (2008). Coagulopathies in horses. Vet. Clin. N. Am. Equine Pract. 30 (2): 437–452. 4 Dallap Schaer, B.L. and Epstein K. (2009). Coagulopathy of the critically ill equine patient. J. Vet. Emer. Crit. Care. 19 (1): 53–65. 5 Berzon, J.L. (1979). Complications of elective ovariohysterectomies in the dog and cat at a teaching institution: clinical review of 853 cases. Vet. Surg. 8 (3): 89–91. 6 Lynch, A.M., Bound, N.J., Halfacree, Z.J. et al (2011). Postoperative haemorrhage associated with active suction drains in two dogs. J. Small Anim. Pract. 52 (3): 172–174. 7 Ko, M.T., Chuang, K.C., and Su, C.Y. (2008). Multiple analyses of factors related to intraoperative blood loss and the role of reverse Trendelenburg position in endoscopic sinus surgery. Laryngoscope. 118: 1687–1691. 8 Hathorn, I.F., Habib, A.R., Manji, J. et al. (2013). Comparing the reverse Trendelenburg and horizontal position for endoscopic sinus surgery: a randomized controlled trial. Otol. – Head Neck Surg. 148 (2): 308–313. 9 Wormald, P.J., van Renen, G., Perks, J. et al (2005). The effect of total intravenous anesthesia compared with inhalational anesthesia on the surgical field during endoscopic sinus surgery. Am. J. Rhin. 19 (5): 514–520. 10 Quinn, G.C., Kidd, J.A., and Lane, L.G. (2005). Modified frontonasal sinus flap in standing horses: surgical findings and outcomes of 60 cases. Vet. Surg. 37 (2): 138–142.

11 Kim, C., Park, S.S., and Davey, J.R. (2015). Tranexamic acid for the prevention and management of orthopedic surgical hemorrhage: current evidence. J. Blood Med. 6: 239–244. 12 Halderman, A.A., Sindwani, R., and Woodard, T.D. (2015). Hemorrhagic complications of endoscopic sinus surgery. Otol. Clin. N. Am. 48: 783–793. 13 Glance, L.G., Mukamel, D.B., Blumberg, N. et al. (2014). Association between surgical resident involvement and blood use in noncardiac surgery. Transfusion. 54 (3): 691–700. 14 Schafer A.I. (1995). Effects of nonsteroidal antiinflammatory drugs on platelet function and systemic hemostasis. J. Clin. Pharm. 35 (3): 209–219. 15 Wang, C.Z., Moss, J., and Yuan, C.S. (2015). Commonly used dietary supplements on coagulation function during surgery. Medicines (Basel). 2 (3): 157–185. 16 Piercy, R.J., Swardson, C.J., and Hinchcliff, K.W. (1998). Erythroid hypoplasia and anemia following administration of recombinant human erythropoietin to two horses. J. Am. Vet. Med. Assoc. 212 (2): 244–247. 17 Cesarini, C. Monreal, L., Armengou, L. et al. (2014). Progression of plasma D-dimer concentration and coagulopathies during hospitalization in horses with colic. J. Vet. Emerg. Crit. Care. 24 (6): 672–680. 18 Covidien (2008) LigaSure Atlas Hand Switching Instruments. Boulder, CO. 19 Sankaranarayanan, G., Resapu, R.R., and Jones, D.B. et al. (2013). Common uses and cited complications of energy in surgery. Surg. Endos. 27 (9): 3056–3072. 20 Mudge, M.C., Macdonald, M.H., and Owens, S.D. et al. (2005). How to perform pre-operative autologous blood donation in equine patients. Proceedings of the 51st Annual Convention of the American Association of Equine Practitioners. 51: 263–264. 21 Thompson, K.R., Rioja, E., Bardell, D. et al. (2015). Acute normovolarmic haemodilution in a Clydesdale gelding

 ­Reference

prior to partial resection of the left ventral concha under general anesthesia. Equine Vet. Educ. 27 (6): 295–299. 22 Glance, L.G., Dick, A.W., Mukamel, D.B. et al. (2011). Association between intraoperative blood transfusion and mortality and morbidity in patients undergoing noncardiac surgery. Anesthesiology. 114 (2): 283–292. 23 Hammond, K.L. and Margolin, D.A. (2006). Surgical hemorrhage, damage control, and the abdominal compartment syndrome. Clin. Colon Rect. Surg. 19: 188–194. 24 Wilson, D.V., Rondenay, Y., and Shance, P.U. (2003). The cardiopulmonary effects of severe blood loss in anesthetized horses. Vet. Anaesth. Anal. 30: 80–86. 25 Magdesian, K.G., Fielding, C.L., Rhodes, D.M. et al. (2006). Changes in central venous pressure and blood lactate concentration in response to acute blood loss in horses. J. Am. Vet. Med. Assoc. 229 (9): 1458–1462. 26 Schonauer, C., Tessitore, E., Barbagallo, G., et al. (2004). The use of local agents: bone wax, gelatin, collagen, oxidized cellulose. Europ. Spine. J. 13: S89–S96. 27 Sileshi, B., Achneck, H.E., and Lawson, J.H. (2008). Management of surgical hemostasis: topical agents. Vascular. 16 (1): S22–28. 28 Garcia-Morales, L.J., Racmchandani, M., and Loebe, M. (2014). Intraoperative sealant application during cardiac defect repair. Texas Heart Inst. J. 41 (4): 440–442. 29 Hart S.K., Sullins K.E. (2011). Evaluation of a novel post-operative treatment for sinonasal disease in the horse (1996–2007). Equine Vet. J. 43 (1): 24–29. 30 Zhao, Y.C. and Psaltis, A.J. (2016). Hemostasis in sinus surgery. Curr. Op. Otol. Head Neck Surg. 24 (1): 26–30. 31 Wyn-Jones, G., Jones, R.S., and Church, S. (1986). Temporary bilateral carotid artery occlusion as an aid to nasal surgery in the horse. Equine Vet. J. 18 (2) 125–128. 32 Tennent-Brown. B.S., Wilkins. P.A., Lindborg. S. et al/ (2010). Sequential plasma lactate concentrations as prognostic indicators in adult equine emergencies. J. Vet. Intern. Med. 24 (1): 198–205. 33 Rasmussen. K.C., Secher. N.H., and Pedersen. T. (2016). Effect of perioperative crystalloid or colloid fluid therapy on hemorrhage, coagulation competence, and outcome: A systematic review and stratified meta-analysis. Medicine. 95 (31): 1–10. 34 Gratwick, Z., Viljoen, A., Page, P.C. et al. (2016). A comparison of the effects of a 4% modified fluid gelatin

and a 6% hydroxyethyl starch on haemodilution, colloid osmotic pressure, haemostasis and renal parameters in healthy ponies. Equine Vet. J. {early view, doi: 10.1111/ evj.12594] 35 Waters, J.H. (2013). Intraoperative blood recovery. A.S.A.I.O.J. 59 (1): 11–17. 36 Kellett-Gregory, L.M., Seth, M., Adamantos, S. et al. (2013). Autologous canine red blood cell transfusion using cell salvage devices. J. Vet. Emerg. Crit. Care. 23 (1): 82–86. 37 Florey, H. and Witts, L.J. (1928). Absorption of blood from the peritoneal cavity. Lancet. June 30: 1323–1325. 38 Waguespack, R., Belknap, J., and Williams, A. (2001). Laparoscopic management of postcastration hemorrhage in a horse. Equine Vet. J. 33 (5): 510–513. 39 Wong, D.M., Brockus, C., Alcott, C. et al. (2009). Modifying the coagulation cascade: available medications. Compend. Equine. June: 224–236. 40 Fletcher, D.J., Brainard, B.M., Epstein, K. et al. (2013). Therapeutic plasma concentrations of epsilon aminocaproic acid and tranexamic acid in horses. J. Vet. Internal. Med. 27 (6): 1589–1595. 41 Tang, Z.L., Wang, X., Yi, B. et al. (2009). Effects of the preoperative administration of Yunnan Baiyao capsules on intraoperative blood loss in bimaxillary orthognathic surgery: A prosective, randomized, double-blind, placebo-controlled study. Int. J. Oral Maxillo. Surg. 38 (3): 261–266. 42 Gray, S.N., Dechant, J.E., LeJeune, S.S. et al. (2015). Identification, management and outcome of postoperative hemoperitoneum in 23 horses after emergency exploratory celiotomy for gastrointestinal disease. Vet. Surg. 44: 379–385. 43 Doyle, A.J., Freeman, D.E., Rapp, H. et al. (2003). Life-threatening hemorrhage from enterotomies and anastomoses in 7 horses. Vet. Surg. 32: 553–558. 44 Hirshberg, A., Wall, M.J., Ramchandani, M.K. et al. (1993). Reoperation for bleeding in trauma. Arch. Surg. 128: 1163–1167. 45 Kilcoyne, I., Watson, J.L., Kass, P.H. et al. (2013). Incidence, management, and outcome of complications of castration in equids: 324 cases (1998–2008). J. Am. Vet. Med. Assoc. 242 (6): 820–825.

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64

8 Complications of Blood Transfusion Margaret C. Mudge VMD,DACVS, DACVECC The Ohio State University, Columbus, Ohio

O ­ verview

I­ mmune Reactions

Blood transfusion can be a necessary treatment for intraoperative or postoperative hemorrhage, but transfusion of blood products is not without risk. There are 8 recognized equine blood types with at least 30 different factors within 7 of these groups. There is no recognized “universal donor” and the incidence of adverse reactions to equine blood transfusion is much higher than the incidence for human transfusions. The reported incidence of transfusion reactions in horses transfused with whole blood or pRBCs is 16%, with a 2% incidence of fatal anaphylactic reaction  [1]. Immune reactions may involve recipient antibodies to donor red blood cell (RBC) antigens, donor antibodies to recipient RBC antigens, or reactions to plasma proteins, white blood cells, or platelets. Nonimmune reactions can occur when there is excessive overall fluid volume administered or when blood is stored improperly. See Chapter  6: Complications of Fluid Therapy, for information about complications associated with plasma administration.

Hemolytic Transfusion Reactions

­ omplications Associated with Blood C transfusion ●● ●● ●● ●● ●● ●●

Immune reactions Allergic and febrile reactions Transfusion-related acute lung injury Nonimmune reactions Transfusion-transmitted infections RBC storage lesion

Definition  Acute hemolytic transfusion reactions can

involve destruction of red blood cells within 24 hours of transfusion, and more often within several hours of transfusion. The hemolysis can involve the donor red blood cells (RBCs) or the recipient RBCs. Hemolysis can be intravascular or extravascular. Delayed hemolytic transfusion reactions occur within 5 days of the transfusion.

Risk Factors  ●●

●● ●●

Incompatible blood types, especially in a horse that has been previously transfused or exposed to a different blood type (e.g. broodmare) and has developed alloantibodies Crossmatch-incompatible blood Improper storage of blood products (non-immune reaction)

Pathogenesis  Acute hemolytic reactions typically occur

when there is major incompatibility (donor RBCs and recipient plasma), resulting in rapid destruction of the transfused RBCs. Hemolysis of recipient red blood cells can occur if there are RBC antibodies in the donor plasma. Delayed hemolytic reactions occur >24 hours after transfusion, likely due to RBC antibody production shortly after transfusion. Clinical signs of acute hemolysis include hemoglobinemia, hemoglobinuria, and anemia. In severe cases, shock and cardiovascular collapse may occur. Clinical signs with delayed hemolytic reaction are similar to those with acute hemolysis, although usually less severe. Acute renal failure may occur secondary to pigment nephropathy.

Complications in Equine Surgery, First Edition. Edited by Luis M. Rubio-Martinez and Dean A. Hendrickson. © 2021 John Wiley & Sons, Inc. Published 2021 by John Wiley & Sons, Inc.

­Allergic and Febrile Reaction  65

Acute hemolytic transfusion reactions occur in approximately 1 out of 76,000 transfusions in humans [2]. In a retrospective study of blood transfusions in canine patients, there was a complication rate of approximately 25%, with hemolysis in 6% [3]. Prevention  Ideally, all blood donors should be tested for

RBC antibodies, and blood typing should be used to find the optimal blood donor. Blood typing is not practical in an emergency situation, and due to the large number of blood types, an ideal donor may not be available. While anti-Aa antibodies are thought to be the most immunogenic, anti-Ca antibodies appear to be the most common in horses  [4]. There is a stall-side test available (Alvedia, Limonest, France) to detect Ca-positive horses, but Aa and Qa tests are not available. A complete crossmatch is recommended to determine donor-recipient incompatibility. In an emergency, most horses can safely be given a blood transfusion without crossmatch, since they are unlikely to have preexisting RBC antibodies. A crossmatch is strongly recommended for horses that have previously been exposed to red blood cells either through blood transfusion or transplacental exposure. The major crossmatch detects incompatibility between the donor RBCs (RBC antigens) and the recipient plasma (RBC antibodies). The minor crossmatch detects incompatibility between the recipient RBCs and the donor plasma. Crossmatch can be performed by traditional tube incubation and microscopic evaluation to assess for agglutination. Ideally, complement should be added to assess for hemolysis. Recently, a microgel assay and modified rapid gel assay have been evaluated for use in horses  [5]. Crossmatch incompatibility is associated with decreased RBC survival time as well as increased risk of febrile reaction [6]. If there is a history of transfusion reaction or if a crossmatch-compatible donor cannot be identified, autologous transfusion options, such as preoperative autologous donation or cell salvage, should be considered (see Chapter 7: Complications Associsted with Hemorrhage). Diagnosis and  Monitoring  Whole blood and packed RBC

transfusions should be monitored very closely during the first 10–20 minutes, checking temperature, heart rate, and respirations. The transfusion should be slowed or stopped if there are any signs of allergic reaction such as muscle fasciculations, sweating, or urticaria. Signs of acute hemolytic reaction include a sudden decrease in packed cell volume (PCV), hemoglobinuria, hemoglobinemia, and systemic inflammatory response syndrome. Delayed hemolytic reactions result in an unexpected decrease in PCV more than 24 hours after transfusion.

Treatment  Stop the transfusion if it is still in progress. Note the adverse reaction in the medical record and discontinue any orders for further blood transfusion from that donor [7]. Signs of shock or hypotension should be treated with IV fluids. Crystalloid fluids should be continued to maintain renal perfusion and reduce the risk of pigment nephropathy. If there is minor incompatibility (donor plasma and recipient RBCs), the red blood cells can be washed to remove the plasma fraction and blood transfusion may continue with careful monitoring. If the patient remains anemic and requires additional blood transfusion, crossmatch is strongly recommended with new donors. Expected Outcome  The expectations after blood transfusion are for improved oxygenation of tissues. A decrease in heart rate, decrease in lactate, and increase in PCV are reasonable expectations after transfusion, but the rise in PCV is not predictable. In a retrospective report of horses receiving blood transfusions, heart rate and respiratory rate improved significantly after transfusion, but PCV did not increase significantly in horses with hemorrhagic anemia receiving blood transfusions  [1]. It is likely that these horses were transfused during or soon after the episode of hemorrhage, so the pre-transfusion PCV may have been relatively high due to splenic contraction and incomplete volume resuscitation. Acute hemolytic reactions can be severe and may lead to organ failure and death. If recognized early, outcome can be good, especially if a compatible donor is identified. Horses may develop RBC antibodies after transfusion, without any clinical signs. These horses may develop acute hemolysis with subsequent transfusions, and broodmares may have RBC antibodies in their colostrum, leading to neonatal isoerythrolysis in the foal [8].

­Allergic and Febrile Reactions Definition  Febrile nonhemolytic transfusion reaction (FNHTR) is a fever ( 1°C increase from baseline) that occurs within 4 hours of transfusion and that is not associated with hemolysis or signs of allergic reaction. Risk Factors  ●● ●● ●●

Hypersensitivity to donor leukocytes Crossmatch-incompatible blood In humans, blood product storage is associated with accumulation of proinflammatory cytokines and FNHTR

Pathogenesis  Fever and allergic reactions are the most common complications of blood and plasma transfusion in

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Complications of Blood Transfusion

veterinary patients  [1, 9]. Leukocytes in the transfused blood may incite febrile reaction. Acute allergic reactions can also occur, most often a type I immune-mediate hypersensitivity to plasma components. In human patients, febrile nonhemolytic reactions occur in 0.1–1.0% of transfusions and incidence of allergic reaction is reported at 1–3% [2]. In a retrospective study of blood transfusions in canine patients, there was a complication rate of approximately 25%, with fever (12%) and hemolysis (6%) being the most common [3]. Prevention  In an experimental study with healthy horses, crossmatch incompatibility was predictive of febrile reaction, so using crossmatch compatible blood should limit the risk of FNHTR [6]. Plasma proteins are thought to be one stimulus allergic transfusion reactions, so washing the RBCs may reduce the risk of allergic reaction. This author has used the technique of washing donor RBCs to eliminate an allergic reaction in a horse that had a moderate allergic reaction to blood from multiple different crossmatch-compatible donors. Leukoreduction has been shown to lower the risk of inflammatory reaction in an experimental study with healthy dogs, so this could also be considered if a febrile reaction is noted [10]. Premedication with antihistamines has been shown to decrease the incidence of acute allergic reactions in dogs receiving transfusions [11]. Diagnosis and Monitoring  Clinical signs of allergic reaction can include urticaria, piloerection, facial swelling, and fever. Severe anaphylactic allergic reactions will cause hypotension and shock, and may cause death. FNHTR is characterized by fever without other clinical signs. However, fever is also associated with acute hemolytic reaction, allergic reaction, and bacterial contamination, so careful investigation and close monitoring are warranted whenever fever is associated with transfusion. Treatment  Febrile reactions are usually self-limiting. Treatment with antipyretics such as nonsteroidal antiinflammatory drugs (e.g. flunixin meglumine, 1.1 mg/kg IV) is indicated with high or symptomatic fevers. When in doubt, the transfusion should be stopped while the cause of the fever is investigated. Mild allergic reactions, such as urticaria, can be treated with antihistamines (e.g. diphenhydramine, 1.1 mg/kg IM) and temporary interruption of the transfusion. Any signs of anaphylactic reaction warrant immediate discontinuation of the transfusion and treatment with epinephrine (0.01–0.02 mg/kg IV). Expected Outcome  FNHTR is usually self-limiting. There is

a risk of recurrence with subsequent transfusions. Mild

allergic reactions can usually be treated successfully. Anaphylactic reactions may be fatal.

T ­ ransfusion-Related Acute Lung Injury Definition  Transfusion-related acute lung injury (TRALI) is a new onset of bilateral pulmonary infiltrates within 6 hours of transfusion. TRALI follows the criteria for acute lung injury (ALI), defined as acute onset respiratory difficulty with evidence of pulmonary capillary leakage, no evidence of left atrial hypertension, and PaO2/FiO2 of less than 300 mmHg [12]. TRALI is an important cause of transfusion-related mortality in humans. TRALI has been described in dogs but has not been reported in horses. Nonetheless, it is an important potential adverse reaction to consider and include in the list of differential diagnoses for dyspnea or hypoxemia after transfusion. Risk Factors  ●●

●●

●●

Leukocyte antibodies in the donor may react with leukocyte antigens in the recipient, leading to sequestration and activation of neutrophils in lung tissue. Activation of cytokines and lipids may also cause damage to the pulmonary vascular endothelium. Activation of neutrophils related to infection, inflammation, or trauma may be the “first hit” prior to the “second hit” of the transfusion.

Pathogenesis  Activation of neutrophils (see above) leads to damage to the pulmonary capillary endothelium, with subsequent capillary leak. Priming of the neutrophils may occur from an initial event (e.g. trauma, surgery, infection). Activation of the neutrophils in the pulmonary endothelium then occurs secondary to transfusion-related immune stimulation. Prevention  Leukocyte antibodies in donor blood can be reduced by processing whole blood into packed RBCs and by washing RBCs. Diagnosis  Clinical signs of TRALI include hypoxemia,

cyanosis, tachypnea, and tachycardia, usually within 6 hours of transfusion. Volume overload, allergic reaction, and systemic inflammatory response syndrome should also be considered as differential diagnoses.

Treatment  Hypoxemic patients should be treated with supplemental oxygen. Conservative fluid therapy is indicated to reduce the risk of volume overload.

­Transfusion-Transmitted Infection 

Expected Outcome  TRALI is usually self-limiting in

humans, with recovery in 48 to 96 hours, although mortality is reported as high as 25% [13]. The incidence of TRALI in dogs appears to be low (3.7%) and not significantly different than the incidence of ALI in critically ill dogs that have not received transfusions [14].

N ­ onimmune Reactions Volume Overload Definition  Volume overload, or transfusion-associated circulatory overload (TACO), is recognized when signs of respiratory distress and pulmonary edema occur after a large volume transfusion. Risk Factors  ●● ●●

●●

●●

Large volume of whole blood given to normovolemic patient Total dose (ml/kg) of blood products was a risk factor in a study of dogs receiving packed RBC transfusions [15]. Large volume of crystalloid or colloid fluids administered in addition to blood transfusion Preexisting conditions, such as heart failure and renal failure

Pathogenesis  Volume overload is uncommon in adult

horses receiving blood transfusions, but may occur with smaller patients such as miniature horses and foals  [16]. Massive transfusion, defined as transfusion of one blood volume or more within 24 hours or 50% of one blood volume within 3 hours, may lead to additional complications [17]. Massive transfusion can cause hypocalcemia associated with citrate toxicity. Liver failure has been reported in neonatal foals receiving large volume transfusions to treat neonatal isoerythrolysis, likely due to iron overload [18].

Prevention  Volume overload can be avoided with careful calculation of total fluid volume planned for treatment of the patient. In normovolemic patients, packed RBCs should be used, when available. Diagnosis  Clinical signs include dyspnea and cyanosis.

Signs of pulmonary edema may be seen on thoracic ultrasound or radiographs.

Treatment  Discontinue the transfusion (if still in progress) and administer supplemental oxygen. Furosemide (1.1 mg/ kg IV) should be administered as a diuretic. Expected Outcome  Prognosis is good if the condition is

recognized early and treated appropriately, assuming there

are not underlying clinical conditions such as heart failure, renal failure, or sepsis.

T ­ ransfusion-Transmitted Infections Definition  Transfused blood may transmit infection due to unrecognized donor infection or due to bacterial overgrowth in the blood product. Risk Factors  ●●

●●

Improper collection and storage of blood, including skin contamination during collection, refrigeration without strict temperature control, break in sterility during warming or administration of blood Blood-borne disease in donor horse

Pathogenesis  Bacterial contamination can occur at many points during the collection, storage, and administration of blood products. Horses are most often transfused with fresh whole blood, so the risk of substantial bacterial contamination is low since the blood is not stored. Donor horses may transmit viral, bacterial, and protozoal diseases, such as equine infectious anemia (EIA), piroplasmosis, and equine parvovirus. Prevention  The USDA issues standards for equine plasma labelled for treatment of failure of passive transfer of immunity and treatment of specific diseases. These standards include testing plasma donors for EIA, piroplasmosis, dourine, glanders, and brucellosis. The USDA recommends additional testing for equine viral arteritis, West Nile virus, and equine parvovirus. The USDA does not have regulatory oversight of whole blood or packed RBCs, but the guidelines for plasma donors are logical for blood donors as well. Blood donors should not give blood if they are showing any signs of illness, including fever. The blood collection site (usually jugular vein) should be clipped and prepared with a surgical scrub, especially if blood will be stored. Sterile technique should be used with needle or catheter placement and a closed collection system should be used to limit potential for bacterial contamination. Stored blood should not be used if there are any signs of contamination or disruption of the bag. Do not leave blood products at room temperature for more than 4–6 hours. Diagnosis  Bacterial contamination and production of

toxins may result in immediate clinical signs of systemic inflammatory response syndrome in the transfused patient. Fever, tachypnea, and tachycardia can occur for a variety of

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reasons during transfusion, and regardless of the suspected cause, the transfusion should be stopped. Unfortunately, transmission of viral or protozoal disease will not be immediately apparent, so prevention through donor testing is strongly recommended. Treatment  The transfusion should be stopped if there are any signs of reaction or suspicion of contamination. Any remaining donor blood can be cultured if bacterial contamination is suspected. Expected Outcome  Outcome will depend on the underlying

infection. In humans, approximately 10% of transfusionrelated deaths were due to transfusion-transmitted infections [19].

­RBC Storage Lesion Definition  The storage lesion refers to red blood cell and biochemical changes that occur during blood storage. These include hemolysis, decreased red blood cell deformability, increased 2,3-diphosphoglycerate (DPG) levels, increased potassium and lactate, and decreased glucose. Risk Factors  ●●

●●

Long duration of storage. The RBCs continue to break down throughout the storage period. Improper collection or storage. Collection into glass bottles inactivates platelets and increases hemolysis. Improper storage solution will not support RBC metabolism and will lead to more rapid RBC breakdown.

Pathogenesis  The morphologic and biochemical changes in stored blood occur, even in storage solutions that provide dextrose and balance pH. Ongoing RBC metabolism and

breakdown lead to an increase in potassium and lactate and a decrease in 2,3-DPG  [20]. As the cell membrane deteriorates, increased hemolysis can be detected and hemoglobin microparticles are released. Large-volume transfusion of stored blood can introduce high levels of potassium and lactate. As storage time increases, post-transfusion viability of the RBCs decreases. The post-transfusion lifespan of equine autologous RBCs stored for 28 days was 59 days, compared to a lifespan of 99  days for fresh, biotinylated blood [21]. Prevention  Fresh whole blood is most often used for equine transfusions, so “storage lesion” (hyperkalemia, hyperlactatemia, decreased 2,3-DPG) is not usually a concern. When collecting blood intended for storage, use CPDA-1 storage bags to support RBC viability. Use a dedicated blood bank refrigerator at 4°C. Diagnosis and Monitoring  Stored blood should be discarded

if hemolysis is evident, and storage of equine blood beyond 28 days is not recommended. Horses receiving stored blood should be monitored for hemolysis, hyperkalemia, and poor tissue oxygenation, along with other transfusion reactions.

Treatment  There is no specific treatment indicated for animals that receive older units of RBCs. The decrease in 2,3-DPG is reversible, so the limitations of oxygen delivery should not be long-lasting. Additional blood transfusion may be needed if RBC viability has been severely compromised by storage. Outcome  The biochemical and functional changes that occur during RBC storage are similar across species. In dogs, age of the stored RBCs is associated with the risk of transfusion-related hemolysis, but not with fever or mortality [3].

Expected

R ­ eferences 1 Hurcombe, S.D., Mudge, M.C., and Hinchcliff, K.W. (2007). Clinical and clinicopathologic variables in adult horses receiving blood transfusions: 31 cases (1999–2005). J. Am. Vet. Med. Assoc. 231 (2): 267–274. 2 Weinstein, R. (2012). Clinical Practice Guide on Red Blood Cell Transfusion. Washington, DC: American Society of Hematology. 3 Maglaras, C.H., Koenig, A., Bedard, D.L. et al. (2017). Retrospective evaluation of the effect of red blood cell product age on occurrence of acute transfusion-related complications in dogs: 210 cases (2010–2012). J. Vet. Emerg. Crit. Care. 27 (1): 108–120.

4 Bailey, E. (1982). Prevalence of anti-red blood cell antibodies in the serum and colostrum of mares and its relationship to neonatal isoerythrolysis. Am. J. Vet. Res. 43 (11): 1917–1921. 5 Casenave, P., Leclere, M, Beauchamp, G. et al. (2019). Modified stall-side crossmatch for transfusions in horses. J. Vet. Intern. Med. May 18: 1–9 [Epub ahead of print]. 6 Tomlinson, J.E., Taberner, R.C., Boston, S.D. et al. (2015). Survival time of cross-match incompatible red blood cells in adult horses. J. Vet. Intern. Med. 29 (6): 1683–1688. 7 Tocci, L.J. (2010). Transfusion medicine in small animal practice. Vet. Clin. N. Am. Small Anim. Pract. 40: 485–494.

  ­Reference

8 Wong, P.L., Nickel, L.S., Bowling, A.T. et al. (1986). Clinical survey of antibodies against red blood cells in horses after homologous blood transfusion. Am. J. Vet. Res. 47: 2566–2571. 9 Prittie, J.E. (2003). Tirggers for use, optimal dosing, and problems associated with red call transfusions. Vet. Clin. Small Anim. Pract. 33: 1261–1275. 10 McMichael, M.A., Smith, S.A., Galligan, A. et al. (2010). Effect of leukoreduction on transfusion-induced inflammation in dogs. J. Vet. Intern. Med. 24 (5): 1131–1137. 11 Bruce, J.A., Kriese-Anderson, L., Bruce A.M. et al. (2015). Effect of premedication and other factors on the occurrence of acute transfusion reactions in dogs. J. Vet. Emerg. Crit. Care. 25 (5): 620–630. 12 Wilkins, P.A., Otto, C.M., Baumgardner, J.E. et al. (2007). Acute lung injury and acute respiratory distress syndromes in veterinary medicine: consensus definitions: the Dorothy Russell Havemeyer Working Group on ALI and ARDS in Veterinary Medicine. J. Vet. Emerg. Crit. Care. 17 (4): 333–339. 13 Frazier, S.K., Higgins, J., Bugajski, A. et al. (2017). Adverse reactions to transfusion of blood products and best practices for prevention. Crit. Care Nurs. Clins. N. Am. 29: 271–290. 14 Thomovsky, E.J. and Bach, J. (2014). Incidence of acute lung injury in dogs receiving transfusions. J. Am. Vet. Med. Assoc. 244 (2): 107–174.

15 Holowaychuk, M.K., Leader, J.L., and Monteith, G. (2014). Risk factors for transfusion-associated complications and nonsurvival in dogs receiving packed red blood cell transfusions: 211 cases (2008–2011). J. Am. Vet. Med. Assoc. 244 (4): 431–437. 16 Tennent-Brown, B. (2011). Plasma therapy in foals and adult horses. Compendium. 33 (10): E1–E4. 17 Beer, K.S. and Thomer, A. (2019). Massive transfusion. In: Textbook of Small Animal Emergency Medicine (ed. K.J. Drobatz, K. Hopper, E. Rozanski, et al.), 1156–1160. John Wiley & Sons. 18 Polkes, A.C., Giguere, S., Lester, G.D. et al. (2008). Factors associated with outcome in foals with neonatal isoerythrolysis (72 cases, 1988–2003). J. Vet. Intern. Med. 22 (5): 1216–1222. 19 U.S. Food and Drug Administration (2016). Fatalities reported to FDA following blood collection and transfusion: Annual summary for fiscal year 2016. Available at: www.fda.gov/media/111226/download. 20 Mudge, M.C., MacDonald, M.H., Owens, S.D. et al. (2004). Comparison of 4 blood storage methods in a protocol for equine pre-operative autologous donation. Vet. Surg. 33 (5): 475–486. 21 Owens, S.D., Johns, J.L., Walker, N.J. et al. (2010). Use of an in vitro biotinylation technique for determination of posttransfusion survival of fresh and stored autologous red blood cells in Thoroughbreds. Am. J. Vet. Res. 71 (8): 960–966.

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9 Complications Associated with Sutures Ian F. Devick DVM, MS, DACVS-LA1 and Dean A. Hendrickson DVM, MS, DACVS2 1

 Weatherford Equine Medical Center, Weatherford, Texas  College of Veterinary Medicine and Biomedical Sciences, Colorado State University, Fort Collins, Colorado

2

O ­ verview Suture serves as a fundamental part of veterinary surgery and is mainly used for tissue apposition of a wound/ incision and vessel ligation for hemostasis. The first known documented reference to suturing of a wound dates back to a papyrus from 1600 BC  [1]. Obviously, since that time there has been enormous advances made in the development of suture materials, resulting in a vast number of different suture materials and sizes available to veterinarians today. Briefly, suture material is classified by degradation behavior (absorbable vs. nonabsorbable), composition (natural vs. synthetic), and structure (monofilament vs. multifilament)  [2]. Degradation behavior, composition, and structure along with suture surface characteristics and suture size influence additional suture characteristics, including flexibility, elasticity, capillarity, memory, tensile strength, knot holding capacity, and relative knot security [2]. There is no one suture material that is ideal for every situation and it is important for the veterinarian to understand the advantages and disadvantages of the different sutures physical and biological characteristics. However, it is equally important to understand the wound/ incision location, tissue tension, contamination, vascular supply, and the healing rate of the given tissues when making the selection of an appropriate suture in the effort to decrease risk of suture-related complications  [3]. The cruciality of the proper surgical technique and the suture pattern selection for the given wound/incision, along with pertinent peri-operative management (antibiotics, NSAIDs, bandaging, drain placement, immobilization, and confinement) cannot be overstated in preventing wound and incisional suture complications [3].

Suture-related complications include dehiscence, infection without dehiscence, tissue reaction, suture ligation slippage, and suture cut-out. When specific to the alimentary, urogenital, respiratory, musculoskeletal, and ophthalmologic systems, these complications will be discussed in detail in the respective chapters. Suture cut-out as a complication without incisional dehiscence can occur as a separate complication in the realm of tendon repairs and certain upper airway procedures which are discussed in their respective chapters.

­ ist of Complications Associated L with Sutures ●● ●● ●● ●●

Dehiscence Infection without dehiscence Suture reactions Ligature loop failure

­Dehiscence Definition   Wound or incisional dehiscence can be defined

as separation of a previously apposed wound or incision. Dehiscence may be superficial or deep and partial or complete.

Risk Factors ●● ●● ●● ●● ●●

Infection Suture placement Poor knotting technique Inappropriate suture material Premature suture removal

Complications in Equine Surgery, First Edition. Edited by Luis M. Rubio-Martinez and Dean A. Hendrickson. © 2021 John Wiley & Sons, Inc. Published 2021 by John Wiley & Sons, Inc.

­Dehiscenc  ●● ●● ●● ●● ●● ●●

Improper suture needle selection Inadequate suture line tension Excessive suture line tension Dead space Suturing of nonviable tissue Inappropriate support and immobilization of a suture line

activity within 5 mm of the wound edges, leading to an increased risk of suture cut-through and dehiscence of the wound [5]. Poor knotting technique

A poor knot-tying technique can result in the knot untying and wound dehiscence [5].

Pathogenesis  Infection

All sutures produce a local tissue reaction to some degree, which increases the susceptibility to development of an incisional infection [4]. Infection can be the primary reason causing dehiscence or can be a sequelae to dehiscence [5]. Bacteria release proteolytic enzymes that inhibit wound healing, therefore inducing wound disruption and dehiscence [5]. ●●

●●

●●

●●

●●

●●

Tissue integrity and perfusion, local wound repair responses, and bacterial challenge, influence the presence of an infection of the suture line [6]. Degree of bacterial contamination is a useful predictor of incisional/wound infection potential [7]. Improper wound cleansing with cytotoxic substances or overzealous scrubbing can result in unnecessary tissue inflammation, edema, and necrosis, all leading to an increased risk of incisional infection and dehiscence [8]. Inadequate or traumatic debridement of necrotic, devitalized, heavily contaminated tissue and organic debris increases risk of incisional infection and dehiscence. Use of a larger suture size than necessary results in unnecessary foreign material present within the wound/ incision, altering the tissue structure, weakening the repair, and therefore decreasing the capacity to resist infection [3, 9]. Physical and biochemical characteristics of the suture serve as an important factor in the initiation, severity, and persistence of incisional infections  [4]. Bacteria have a higher affinity for braided suture compared to monofilament suture  [4]. Removal of bacteria by the body’s defense mechanism is slower with braided suture [4]. The use of barbed sutures has been shown to increase the risk of incisional infections [10], Suture pattern choice can contribute to prolonged edema and erythema from decrease in microvascular flow, resulting in delayed healing, decreased incisional tensile strength, and risk of incisional complications [11].

Suture placement

Sutures that are placed too close to the wound margins risk suture cut-through due to an initial elevated collagenase

Inappropriate suture material

Selection of an inappropriate suture material with insufficient tensile strength for the given tissues or that significantly decreases in tensile strength (resorption time) faster than tissue healing occurs for the respective tissue, increases the risk of dehiscence [5]. Interactions between the suture material and tissue can alter the characteristics of the suture and lead to suture failure [9]. Barbed sutures have been shown to increase the incidence of postoperative incisional dehiscence and erythema as wound complications [12]. Premature suture removal

Suture removal prior to appropriate wound healing may result in dehiscence [5]. Improper suture needle selection

The type of needle and size in relation to the suture can increase the risk of suture cut-through, especially when there is tension present or tissues are compromised [5]. Inadequate suture line tension

Loosely placed sutures due to inadequate surgical technique or as a result of anticipated edema formation, as well as a suture line placed in a region of already present edema, increases the risk of wound edge retraction and incisional gapping when the edema resolves [5]. Excessive suture line tension

The use of excessive suture tension or use of an inappropriate suture pattern for mild to moderate tension along a suture line to appose tissues can result in suture cutthrough leading to dehiscence. Excessive suture tension can affect the local blood flow, which increases the inflammatory response resulting in tissue ischemia and pressure necrosis  [3, 6, 7]. The use of suture stents or quills in an attempt to diffuse the tension from the suture to a larger surface area can also affect microvascular supply and result in tissue pressure necrosis under the stent or quill, especially when placed under a pressure bandage or cast [3].

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Dead space

Dead space is created in some traumatic wounds where tissues have been lost or dissection planes have been created. Dead space is created surgically after tissue debridement, mass removal, or undermining has been performed to relieve tension for the closure. As a result, seroma or hematoma formation may manifest, increasing the risk of incisional infection and possible dehiscence [4]. Suturing of nonviable tissue  The degree of tissue compromise and viability of recently traumatized tissues can be difficult to predict. If a traumatic wound is closed too promptly, without allowing or anticipating the potential ensuing development of tissue necrosis to occur, the development of delayed necrosis may lead to dehiscence [5]. Inappropriate support and immobilization of a suture line

Excessive motion for any given suture line increases the risk of tension on the wound edges and possible dehiscence [5]. The repetitive motion of an incision causes chronic inflammation from microvascular, collagen deposits, and epithelialization disruption  [7]. However, complete immobilization can result in disorganized new collagen and decreases incisional tensile strength  [7]. Inadequate support and/or immobilization of a suture line as well as inadequate confinement can have detrimental effects on the wound/incision healing process and result in dehiscence. Prevention  Effective apposition of the wound/incision edges, atraumatic tissue handling, minimal disruption to blood supply, appropriate suture pattern, material, needle, and placement are essential requirements for a positive healing outcome [3, 5]. Adequate perioperative care is also an important factor in incisional healing and appropriate use of antibiotics, NSAIDs, diagnostics, bandaging, and confinement are important. Appropriate bandaging and NSAID uses can prevent excessive edema formation. It is important to inflict the least amount of trauma achievable to obtain the goal of the surgery [9]. The wound strength is more dependent on the tissue’s ability to hold the suture than on the given suture strength [2]. Suture placement from the wound edge is recommended an equal distance from the incision/wound edge as the thickness of the skin edge at that location [3]. Due to the normal inflammatory phase of healing, sutures should be placed at least 5 mm from the wound/incision edge to prevent dehiscence [3]. Spacing between sutures is variable, depending on wound/incision location and relative local tension but it is advised to use the minimum number of sutures necessary to achieve tissue apposition [3]. In

general, this corresponds to fewer sutures in thicker skin and areas of low tension and more sutures in regions of thin skin and higher tension [3]. Suture pattern choice can contribute to prolonged edema and erythema, such as with a simple continuous suture pattern when compared to a simple interrupted suture pattern [11]. This edema can result in delayed healing and risk of complications [11]. Physical and biological characteristics should be considered when selecting suture material and size, and the suture material should be compatible with the tissue type being sutured and the anticipated post-operative incisional tension [5, 9]. The suture should be as strong as the normal tissue through which it is placed [2, 3]. The rate of loss in tensile strength of the suture material and the gain in wound strength of the sutured tissues over time should coincide {2, 3]. Monofilament suture material has the advantages of low tissue drag and low tendency to foster infection  [15]. There has been no beneficial effect in the use of antibiotic-coated suture material in preventing suture-related complications [16]. Tension forces are converted to shear forces at the suture knot, thus making the knot the weakest point of the suture loop [9]. Secure square knots are important in preventing dehiscence and the appropriate number of throws for good knot security depends on the suture material characteristics and the nature of the suture pattern (interrupted vs. continuous) [3]. A surgeon’s throw is only indicated when needed to appose the tissues, otherwise it is contraindicated, especially in deeper layers such as facial, subcutaneous, organs, joint capsule, paratenon, etc.  [3] Unnecessary throws on a knot or the use of a surgeon’s throw makes a bulkier knot and increases suture material within the tissues, thus increasing the risk of delayed wound healing, pressure necrosis, suture extrusion, and infection [3, 17]. Wound/incision location and the tissue layer being sutured will have important influence on the appropriate suture pattern indicated  [3]. There is a wide variety of suture patterns (interrupted vs. continuous, inverting vs. everting, and tension sutures) and each have advantages and disadvantage which must be considered when determining an appropriate pattern for the given location, tension, and organ or tissue layer being sutured  [3]. Interrupted sutures increase the amount of suture material in the wound/incision when buried and increase surgery time and cost [3]. Continuous patterns lack the ability to vary tension along the suture line and knot or suture failure can be catastrophic to the entire length of the apposed tissues [3]. Also, simple continuous and horizontal suture patterns can compromise the vascular supply to the wound/ incision edge resulting in increased inflammation and edema formation  [3, 11]. Depending on the wound/ incision location, inversion, eversion, or edge-to-edge may

­Dehiscenc 

be advantageous. Inversion is advantageous in preventing leakage in hollow viscera closure but also will reduce the luminal diameter of viscera, which can lead to complications which are discussed in the respective chapters. Slight eversion is recommended when there is a tendency for the skin edges to invert and the slight eversion results in positive cosmetic outcome  [3]. A continuous intradermal pattern results in the best cosmetic outcome and does not require suture removal; however, there is a potential for suture fistula formation if improper technique was used and the epidermis was included in the closure. Incised wounds have limited tensile strength during the inflammatory phase of wound healing and apposition is primarily achieved by the suture  [9]. Excessive tension placed on the suture line should be avoided, as the tissue’s ability to hold suture has more influence on the repair than the strength of the suture material itself [2, 3]. For wounds/ incisions under tension it is discouraged to use a larger suture size; instead it is recommended to increase the number of sutures and use of appropriate tension relieving sutures in the suture line [2, 3]. Other options of tension relieving techniques, such as undermining, walking sutures, tension-relieving incisions, mesh expansion, tissue flaps or plasties, can be used to prevent occurrence of dehiscence from tension [3, 6, 7]. Staggered suture removal in areas of tension is also recommended to prevent incisional dehiscence [6]. Even the least reactive suture materials act as foreign material and decrease the ability of the wound to resist infection, thus suture number, suture size, and number of knots should be minimized [3, 9]. However, there is usually a variety of sutures that can be used with a favorable outcome in most situations, so surgeon preference can be considered in suture selection [9]. Hematoma and seroma formation can be prevented by adequate intraoperative hemostasis, atraumatic surgical technique, and closure of dead space created  [5]. Drains should be placed intraoperatively if seroma formation is anticipated [5]. As well adequate compression, bandaging should occur in indicated areas to prevent hematoma or seroma formation. Proper placement is essential and they should not be used as a substitute for proper wound cleansing, debridement, and lavaging  [3]. Drains are not benign, so close monitoring and aseptic technique during bandage changes is important to prevent retrograde bacterial migration and excessive tissue irritation  [3]. To prevent complications associated with drains, they should be removed as soon as possible, such as when there is a decrease in drainage or change from purulent or serosanguinous to serous and non-odoriferous, and is typically at 2–4 days but varies depending on location and wound environment [3].

Severely traumatized tissues or tissues suspected of blood supply loss should not be closed too soon and should be closely monitored until viability is ensured [5]. In some circumstances it is recommended to suture the tissues initially before viability is ensured, such as if it is over a joint or there is exposed cortical bone. An understanding and acceptance of tissue necrosis and future partial dehiscence in these circumstances may be of more benefit to overall healing and these expectations should be discussed in advance with the owner. Confinement should be used effectively to adequately immobilize excessive motion. Confinement and exercise may range from a cross tied patient to stall confinement to paddock turnout to pasture turnout, depending on the surgery and postoperative time frame. Horses should be introduced to exercise appropriately for the given surgical procedure performed and to allow for continued remodeling and strengthening of the incision. Incisional dressing and bandaging provide a barrier to environmental contamination but can also play a key role in decreasing motion of the surgical site. The location and surgical procedure performed will determine whether a light bandage, compression bandage, stent bandage, or no bandage is appropriate. In areas of high motion, such as over a joint, casting or splinting may be considered necessary for that specific case [7]. Ensuring proper postoperative nutrition for the patient’s metabolic needs will help prevent a delay in wound healing due to protein and vitamin deficiencies [7, 18]. Ensuring more focused or localized neoplastic treatment with radiation therapy and protection of adjacent healthy tissues is important in preventing unnecessary complications with wound healing [19, 20]. General recommendations are difficult to make based on the current literature, but in wounds with suspected incomplete tumor resection, it has been thought to delay intra-tumoral chemotherapy until wound healing has begun (7–14 days) to decrease the risk of dehiscence  [5, 21]. Diagnosis  Dehiscence can occur from the immediate

postoperative period up to several weeks after surgery. Dehiscence during the anesthetic recovery or soon after surgery can be a result of self-induced trauma or inadequate steps to immobilize the region, confine the patient, or relieve tension on the suture line as appropriate. Most commonly, incisional dehiscence will occur 4–5 days postoperatively [5]. Clinical signs that may develop prior to dehiscence include serosanguineous discharge or in the case of an infection, a purulent odorous discharge. Tissue swelling, heat, and necrosis of the sutured tissue edges along with pain to palpation may also be evident prior to

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dehiscence. Dehiscence is diagnosed at the time where there is superficial or deep and partial or complete separation of the previously sutured wound or incision. Identifying any primary cause for the dehiscence before assuming it was a result of infection is important, since with incisional disruption and dehiscence there is often secondary infection present  [5]. Clinical signs associated with incisional infections include incisional swelling, heat, pain, and drainage of a purulent nature [13]. If there is a suspected infection present, regardless of whether it was the primary cause or secondary to another cause, a deep swab should be obtained of the infected area after aseptic preparation [6]. The swab is then submitted for aerobic and anaerobic bacteriological culture and sensitivity testing. In some cases, a fungal culture is recommended. The degree of bacterial contamination will help determine the most appropriate wound management, thus qualitative and quantitative cultures can be beneficial [7]. If a foreign body and sequestra is the underlying cause of the dehiscence, it can be identified or ruled out with a number of diagnostics, including manual exploration and probing, ultrasound, contrast or plain radiographs, CT, or MRI of the wound [7]. If self-mutilation was the cause of the dehiscence, it is usually diagnosed through observation or evidence of a rough anesthetic recovery, rubbing, biting, or pawing [6]. Cytological or histopathological examination may be indicated to identify an underlying cause such as neoplasia [5]. Treatment  Treatment will vary depending on the identified cause of incisional dehiscence and whether it is a partial or completed dehiscence. Location, size, tissue viability, reason for the dehiscence, owner expectations and financial concerns will all play a critical role in how the dehisced sutured line is treated. Examination of the dehisced incision and determination of cause is the first step in determining a course of treatment. Early and meticulous evaluation of the dehisced incision along with appropriate management using a combination of timely surgical and medical treatments are used to promote the best healing outcome [6]. If there is no suspicion of infection then the dehisced sutures are removed, the wound cleansed, without the use of antiseptics, debrided, lavaged, and primary closure can be performed  [5]. If excessive tension is suspected, additional steps are taken as needed, such as incorporating tension relieving suture patterns, walking sutures, or tension relieving techniques such as tissue undermining, relief incisions, or plasties can be performed [7]. If excessive motion is thought to be involved, increasing incisional support through bandaging, splinting, or casting is recommended. In addition, stricter confinement may be

necessary, such as cross-tying, smaller stall confinement, no hand-walking, etc. Partial dehiscence or intentional partial dehiscence, in the case when dependent sutures are removed to allow for adequate drainage, can be managed with appropriate wound care including cleansing, debridement, lavaging, and appropriate wound dressings. Passive or active drains are incorporated to ensure adequate drainage and obliteration of dead space if discharge, fluid, or gas build-up within the repair was suspected to have contributed to the dehiscence. Drains will function by channeling undesired discharge, fluid, gas, or debris and usually promotes faster healing and decreases the chance of dehiscence reoccurring [3]. Incorporation of a compression bandage when applicable will help with the elimination of dead space. Common isolates from infected equine wounds include Streptococcus spp, Staphylococcus spp, Enterobacteriaceae, Pseudomonas spp, and anaerobes [6]. With the suspicion of infection of the suture line, a course of broad-spectrum antibiotics and or regional limb perfusions are recommended and initiated until culture and sensitivity results have been obtained. Delayed primary closure, secondary closure, or second intention healing are recommended in cases where there is a presence of infection, necrotic or compromised tissue, or if additional debridement is needed  [5]. The degree of bacterial contamination, determined by qualitative and quantitative culture, will help identify the most appropriate wound management  [7]. Appropriate wound care and wound dressings are essential and are dictated by the wound characteristics and phase of wound healing. Sequesta formation may not be evident on radiographs until 3–4 weeks after injury [6, 7, 14]. Similarly, healing is delayed in most horses with foreign bodies present and are prone to dehiscence of the suture line and development of a persistent draining tract  [6, 14]. Prolonged medical treatments are usually unsuccessful in resolving the infection and the drainage returns once treatment is discontinued. Complete removal of the fistulous tract, sequestrum and debridement of the underlying bone or removal of the foreign body usually results in a positive outcome  [6]. The dehisced incision may be managed by primary closure or second intention healing  [6]. In dehisced cases not managed by closure, skin grafting can improve the cosmetic appearance [6, 7]. In the case of self-mutilation, applying cayenne pepper or similar substances on the outside of the bandage may deter the behavior in some horses. Medicating with tranquilizers or other calming agents may also be indicated in horses not tolerant of stall confinement. Different bandaging techniques can be tried in certain cases, such as

­Suture Reaction 

with head surgeries where the use of a stockinette or nothing in place of an Elastikon bandage may be more beneficial for the outcome of the incision healing. Systemic diseases that could be playing a factor in delayed wound healing and dehiscence should be addressed, diagnosed, and treated accordingly. Incisions over areas of motion should be immobilized appropriately, depending on the predicted amount of movement. This may be achieved with a bandage or a splint or cast in certain circumstances [7]. Expected Outcome  The prognosis after treatment and/or repair of a dehisced wound is usually good as long as the initiating factors are recognized and eliminated. However, outcome will be impacted by blood supply and location of the dehisced wound. Dehisced incisions that are left to heal by second intention are at increased risk of decreased cosmetic appearance (hairless scar formation) and tissue strength, depending on size and location of the dehisced wound. Owners should be notified that financially the cost of extended periods of proper wound dressings, bandaging, and recheck examinations required for wound healing by second intention can easily exceed the cost of repairing the dehiscence via primary or secondary closure when indicated.

­Infection Without Dehiscence Surgical site and suture line infections can lead to wound dehiscence as discussed earlier. However, suture-related surgical site infections do not always lead to dehiscence, although risk factors, diagnosis, treatment, and prevention are similar to that of dehisced wounds due to infection. Details are discussed in Chapter  17: Complications Associated with Surgical Site Infections.

­Suture Reactions Definition  Suture-related tissue reaction is a local

inflammatory response induced by the suture material.

Risk Factors ●● ●● ●● ●● ●●

Suture material Inappropriately large suture Excessive suture material Inappropriate suture technique Excessive tension

Pathogenesis  Tissues react to all suture material regardless

of the type of suture material used  [9]. Excessive tissue reaction to suture results in edema, tissue friability, and subsequent suture failure  [9]. Usually, the inflammatory

reaction is most prominent at the knot site, since the knot represents the major foreign body mass and density, and causes the most mechanical trauma to the tissues [22]. Suture material

Both the physical (monofilament vs. multifilament) and the chemical composition influence the reaction that takes place within the tissues [23]. Monofilament suture material withstands contamination better than multifilament suture material, while also having less tissue reactivity properties [23, 24]. Multifilament material results in more tissue trauma and has more capillary action, which may increase the potential for bacterial contamination  [5]. Although bacteria can adhere to any suture material, multifilament suture surfaces tend to adhere to higher numbers of bacteria when compared to monofilament suture  [4, 23]. Antibacterial-coated suture may be responsible for increased risk of development of incisional edema [16]. Chronic granulomatous or abscess formation is a reaction that can occur secondary to suture material placement, which may result in a discharging sinus  [9]. Surgical gut is a capillary multifilament suture that elicits a marked foreign body reaction when implanted in tissues because it is composed of collagen  [23, 24]. In contrast, synthetic monofilament absorbable sutures such as polydioxanone, polyglyconate, and polyglecaprone 25 as well as synthetic multifilament absorbable sutures such as polyglycolic acid and polyglactin 910, cause a mild inflammatory response characterized by the presence of macrophages and fibroblasts at the wound site  [23, 24]. Alternatively, synthetic nonabsorbable sutures such as nylon and polypropylene are biologically inert and cause minimal tissue reaction [23, 24]. Steel is biologically inert and incites no inflammatory reaction, except for that caused by inflexible suture ends [23, 24]. Inappropriately large suture

Using larger suture size than necessary results in unnecessary foreign material present within the wound/incision, altering the tissue structure, causing excessive tissue reaction, weakening the incision line and therefore decreasing the capacity to resist infection [3, 9]. Knot size depends on suture size and number of throws. Suture size is the principle influence on knot volume and tissue reactivity; an increase in suture size increases tissue reaction more than adding an extra throw to a knot [22]. Excessive suture material

Suture material acts as a foreign body and induces a tissue reaction in the incisional line [25]. Inflammatory reactions to sutures are most pronounced close to the knots because they have the largest amount of foreign material [22].

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Inappropriate suture technique

The suturing technique and excessive and inappropriate handling of the tissues and unnecessary needle sticks will increase tissue inflammation and edema formation [23]. Excessive tension can affect the local blood flow and increase the inflammatory response resulting in tissue ischemia and pressure necrosis [3, 7]. Prevention  Appropriate surgical knowledge and technique

for the given suture(s) location is crucial in limiting the occurrence of tissue reactions to sutures. Physical and biological characteristics of suture materials should be considered when selecting a suture material and size [5, 9]. Even the least reactive suture materials act as foreign material, thus minimizing the amount of suture material within the tissues without compromising the closure should be the objective in incisional closures [9]. Therefore, decreasing the amount of suture material within the tissues is achieved by minimizing the number of sutures, using the smallest adequate suture size, having the fewest number of knots achievable, keeping the number of throws in a knot to a minimum, avoiding a surgeon’s throw when possible, and not having excessively long suture tails [3, 9, 23]. Suture absorption time and the gain in wound strength of the sutured tissues over time should coincide  [2, 3]. Monofilament suture material is recommended instead of multifilament if the circumstances allow [23]. Diagnosis  Tissue reaction to suture material is usually

diagnosed with observation of tissue edema or swelling filled with clear fluid around an individual suture or entire suture line [23]. Erythema in light-colored skin or heat and pain to palpation are other clinical signs that can assist in the diagnosis of tissue suture reaction. There may also be present a draining tract to the skin if the suture reaction is of deeper tissues [23]. Ultrasound is not usually needed for the diagnosis but can be useful in identifying problematic suture fragments or segments. Suture reactions can also result in other observed incisional complications including infection, wound disruption, and chronic sinus formation and it can be difficult to determine whether tissue suture reaction or suture line infection were the initiating causes that disrupted wound healing.

Treatment  Treatment of tissue reactions to suture will vary, depending on the degree of clinical signs. If the suture reaction is mild, then typically no treatments are required. For more advanced suture reactions or if the reaction does not resolve within 1–2 weeks, then removal of the suture(s) or entire suture line is indicated.  [23]. Samples of the affected tissues should then be submitted for bacterial

culture and histopathological assessment  [23]. Once the problematic sutures have been removed, the wound can be closed with a more inert suture material or left to heal by second intention, depending on the circumstances of the case. Granulomatous or abscess formation, and suture sinuses will usually heal without detrimental complication once the inciting suture is removed [9]. Expected Outcome

Tissue suture reactions can result in increased morbidity to the patient, prolonged wound healing time, decreased cosmetic appearance of the surgical site, and an increase in the treatment costs. However, the prognosis is usually good after removal of the problematic suture(s) [9, 23].

­Ligature Loop Failure Definition  Ligation suture loops are commonly used for hemostasis of an isolated vessel, vascular pedicle, or other structure and have the potential to fail via suture slippage or suture breaking. Risk Factors ●● ●● ●● ●● ●●

Suture material Suture size Inappropriate ligation knotting Inappropriate ligation placement Tissue bulk

Pathogenesis  Suture material, ligation technique, number of ligatures, and manipulation of the vessel or pedicle are all factors that should be considered when performing a ligation  [26]. Ligation knot slippage or breakage is a significant contributor to ligation failure and occurrence is likely underestimated [27]. Suture material

The use of multifilament suture for laparoscopic ligating loops does not maintain the shape of the loop well due to low stiffness of the suture material and may result in inadequate placement of the ligating loop [28, 29]. Suture size

Selection of suture that is too small will result in suture loop breakage, typically at the knot where suture tension forces have been converted to shear forces, making the knot the weakest point of the suture loop [9]. Inappropriate ligation knotting

The square knot is used commonly for vessel ligation but, however, performs poorly when compared to a slip knot, modified transfixing ligature, or single-double other side knot  [26]. When using a square knot, it is dependent on

­Ligature Loop Failur 

there being no slippage of the first throw until the second throw has secured the knot [26]. Every knot type is at risk of not providing appropriate vessel occlusion and hemostasis if the surgical technique is not sufficient. Inappropriate ligation placement

Transection of the vessel/pedicle too close to the ligature can result in ligature slippage [29]. Tissue bulk

Tissue bulk of a pedicle or tissue surrounding a vessel can inhibit the ability to achieve adequate occlusion of the vessel and result in hemorrhage. Prevention  The importance of meticulous and proper placement of ligatures is essential for healing and preventing surgical complications. Whether it is open surgery or laparoscopy, ligatures are placed for the same reasons; however, there may be differences in the mechanics of the procedure  [28]. Effective surgical techniques when performing ligation and vessel occlusion for hemostasis are essential in prevention of unnecessary hemorrhage [26]. Suture needs to be of sufficient size to withstand the tensile forces placed on the loop and shear forces at the knot. Regardless of the knotting technique used, the use of monofilament suture is recommended because it appears to be stronger and provides more efficient hemostasis then multifilament suture  [30]. Monofilament suture is also advised for laparoscopic ligating loops because the shape of the loop is usually maintained reasonably well by the increased stiffness  [28, 29]. Ligature loops should be tied table-side rather than pre-tied and sterilized because sterilization can weaken the suture material and predispose to ligation failure  [28]. A 4-S modified Roeder knot using monofilament suture is recommended for maximal ligature loop strength [28]. The performance of the single knot loop has been shown to be biomechanically superior to a double knot loop in tensile breaking strength because with the single knot loop the forces are equally divided over the whole ligature, whereas with a double knot loop the two loops of the ligature will have different tensions after every knot  [27]. A transfixation ligature can be performed to prevent slippage of the ligature; however, postoperative bleeding may still occur due to ligature failure of one of the double knot loops  [27]. Sliding knots have been shown to be quicker and behave similar to or better than a surgeon’s knot in establishing hemostasis of arteries [30].

Tissue bulk can be overcome by dividing it into smaller sections (“divide and conquer method”) or multiple ligatures can be placed around a bulky structure to improve the hemostasis  [26]. Clamping to crush the tissue and reduce its bulk, as well as “flashing” the clamp adjacent to the ligature being placed, are additional techniques for improving vessel occlusion and ligature security [26]. Diagnosis  Ligature

loop failure can be observed intraoperatively under direct visualization or via laparoscopy. Postoperatively, incisional swelling or hemorrhage from the incision line can develop. Ultrasound and/or aspirate of the swelling are the most common diagnostics used to differentiate a hematoma from seroma or edema formation. Diagnosis of hemorrhage into a body cavity, such as pedicle ligation failure and development of a hemoperitoneum, are discussed in their respective chapters.

Treatment  When ligation failure occurs intraoperatively,

the cause of the failure should be determined as to whether it is ineffective occlusion (knot slippage), loop slippage, or suture breakage and measures used to correct the failure. The use of ligating clips, staples, electrocautery and other electrosurgical instrumentation can be used in appropriate situations to provide hemostasis after ligature failure  [28, 29]. If there is hematoma formation then treatment options differ depending on the degree and location. With mild hemorrhage and hematoma formation no treatment may be needed. For more significant hemorrhaging and hematoma formation there are multiple treatment options. If there is active hemorrhaging then the incision may need to be opened and hemostasis achieved via intraoperative methods discussed. Alternatively, compression or a compression bandage can be an effective means of hemostasis and prevention of hematoma formation.

Expected Outcome  The prognosis is dependent on the

degree of hemorrhage but incisional vessel ligation failure usually has a good outcome once time has been allowed for the hematoma to resolve. However, hematoma formation can increase morbidity to the patient, prolong wound healing time, and can increase treatment costs. Also, even mild hemorrhages can have an impact on the safety and efficiency of a given procedure, as well as effect outcome, depending on the situation [28].

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­References 1 Mackenzie, D. (1973). The history of sutures. Med. Hist. 17 (2): 158–168. 2 Kümmerle, J.M. (2012). Suture materials and patterns. In: Equine Surgery, 4e (ed. J.A. Auer and J.A. Stick), 181–202. St. Louis, Elsevier. 3 Céleste, C. (2008). Selection of suture materials, suture patterns, and drains for wound closure. In: Equine Wound Management, 2e (ed. T.S. Stashak and C.L. Theoret), 193–224. Ames: Wiley-Blackwell. 4 Katz, S., Izhar, M., and Mirelman, D. (1981). Bacterial adherence to surgical sutures. A possible factor in suture induced infection. Ann. Surg. 194 (1): 35–41. 5 Claeys, S. (2016). Dehiscence. In: Complications in Small Animal Surgery, 1e (ed. D. Griffon and A. Hamaide), 57–63. Ames: Wiley-Blackwell. 6 Hanson, R.R. (2009). Complications of equine wound management and dermatologic surgery. Vet. Clin. N. Am. Equine Pract. 24 (3): 66–696. 7 Hendrickson D. and Virgin, J. (2005). Factors that affect equine wound repair. Vet. Clin. N. Am. Equine Pract.: Wound Manag. 21 (1): 33–44. 8 Hendrickson, D.A. (2012). Management of superficial wounds. In: Equine Surgery, 4e (ed. J.A. Auer and J.A. Stick), 306–317. St. Louis: Elsevier. 9 Stashak, T.S. and Yturraspe, D.J. (1978). Consideration for selection of suture materials. Vet. Surg. 7 (2): 48–55. 0 Campbell, A.L., Patrick, D.A., Liabaud, B. et al. (2014). 1 Superficial wound closure complications with barbed sutures following knee arthroplasty. J. Arthroplasty. 29 (5): 966–969. 11 Speer, D.P. (1979). The influence of suture technique on early wound healing. J. Surg. Res. 27 (6): 385–391. 12 Cortez, R., Lazcono, E., and Miller, T. (2015). Barbed sutures and wound complications in plastic surgery: an analysis of outcomes. Aesthet. Surg. J. 35 (2): 178–188. 13 Mair, T.S. and Smith, L.J. (2005). Survival and complication rates in 300 horses undergoing surgical treatment of colic. Part 2: Short-term complications. Equine Vet. J. 37 (4): 303–309. 14 Booth, L.C. and Feeney, D.A. (1982). Superficial osteitis and sequestrum formation as a result of skin avulsion in the horse. Vet. Surg. 11 (1): 2–8. 15 Kawcak, C.E. and Baxter, G.M. (1996). Surgical materials and wound closure techniques. Vet. N. Am.: Equine Pract. 12 (2): 195–205. 16 Bischofberger, A.S., Brauer, T., Gugelchuck, G. et al. (2010). Difference in incisional complications following exploratory celiotomies using antibacterial-coated suture material for subcutaneous closure: Prospective randomized study in 100 horses. Equine Vet. J. 42 (4): 304–309. 17 Sanders, R.E., Kearney, C.K., Buckley, C.T. et al. (2015). Knot security of 5 metric (USP 2) sutures: Influence of knotting technique, suture material, and incubation time

for 14 and 28 days in phosphate buffered saline and inflamed equine peritoneal fluid. Vet. Surg. 44 (6): 723–730. 8 Schroeder, D., Gillanders, L., Mahr, K. et al. (1991). 1 Effects of immediate postoperative enteral nutrition on body composition, muscle function, and wound healing. J. Paren. Ent. Nutr. 15 (4): 376–383. 19 Haubner, F., Ohmann, E., Pohl, F. et al. (2012). Wound healing after radiation therapy: review of the literature. Rad. Oncol. 7: 162. 20 Théon, A.P. and Pascoe, J.R. (1994). Iridium-192 interstitial brachytherapy for equine periocular tumors: treatment results and prognostic factors in 115 horses. Equine Vet. J. 27 (2): 117–121. 21 Théon, A.P., Wilson, W.D., Magdesian, K.G. et al. (2007). Long-term outcome associated with intratumoral chemotherapy with cisplatin for cutaneous tumors in equids: 573 cases (1995–2004). J. Am. Vet. Med. Assoc. 230 (10): 1506–1513. 22 van Rijssel, E.J.C., Brand, R., Admiraal, C. et al. (1989). Tissue reaction and surgical knots: the effect of suture size, knot configuration, and knot volume. Obstet. Gynecol. 74 (1): 64–68. 23 Laitinen-Vapaavuori, O. (2016). Suture reactions. In: Complications in Small Animal Surgery, 1e (ed D. Griffon and A. Hamaide), 64–65. Ames: Wiley-Blackwell. 24 Boothe, H.W. (2003). Surgical materials, tissue adhesives, staplers, and ligating clips. In: Textbook of Small Animal Surgery 3e (ed. D. Slatter), vol. 1, 235–244. Philadelphia: Saunders, Elsevier Science. 25 Varma, S., Johnson, L.W., Ferguson, H.L. et al. (1981). Tissue reaction to suture materials in infected surgical wounds: a histopathologic evaluation. Am. J. Vet. Res. 42 (4): 563–570. 26 Leitch, B.J., Bray, J.P., Kim, N.J.G. et al. (2012). Pedicle ligation in ovariohysterectomy: an in vitro study of ligation techniques. J. Small Anim. Pract. 53 (10): 592–598. 27 Rijkenhuizen, A.B.M., Sommerauer, S., Fasching, M. et al. (2013). How securely is the testicular artery occluded in the spermatic cord by using a ligature? Equine Vet. J. 45 (5): 649–652. 28 Caron, J.P. (2012). Equine laparoscopy: hemostasis. Compendium: Cont. Educ. Vet. 34 (12): E1–E4. 29 Rodgerson, D.H. and Hanson, R.R. (2000). Ligature slippage during standing laparoscopic ovariectomy in a mare. Can. Vet. J. 41 (5): 395–397. 30 Gandini, M., Giusto, G., Comino, F. et al. (2014). Parallel alternating sliding knots are effective for ligation of mesenteric arteries during resection and anastomosis of the equine jejunum. BioMed. Cent. Vet. Res. 10 (1): S1–DS10.

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10 Complications of Bone Graft Harvesting, Handling, and Implantation Lynn Pezzanite DVM, MS DACVS1 and Laurie R. Goodrich DVM, PhD, DACVS2 1 

Department of Clinical Sciences and Translational Medicine Institute, College of Veterinary Medicine and Biomedical Sciences, Colorado State University, Fort Collins, CO Department of Clinical Sciences, Colorado State University, Fort Collins, Colorado

2 

O ­ verview Bone grafts are most frequently used in equine surgery to facilitate healing following long bone fracture, arthrodesis, and comminuted phalangeal fractures  [1]. Autogenous cancellous bone grafts are the most frequently used type of graft in the equine patient [1, 2, 3]. Bone grafts may be categorized according to their origin and location. Grafts may be harvested and applied to a different site in the same individual (autograft), to a genetically different individual of the same species (allograft), or to a member of a different species (xenograft). Grafts may be applied to an anatomically similar location (orthotopic) or different implantation site (heterotopic). In general, bone grafts serve the function of osteoconduction or osteoinduction, depending on the type of graft [1, 4]. Osteoconduction refers to the matrix of the graft acting as a scaffold into which mesenchymal cells grow. Osteoinduction refers to a process through which signals are sent to influence new bone formation (osteogenesis) as a result of differentiation of mesenchymal cells or recruitment of viable osteoblasts and osteocytes on the surface of the bone graft. Bone morphogenetic proteins (BMPs) are molecules found within bone marrow and are responsible for signaling the differentiation of mesenchymal cells into cartilage and bone [5]. Their presence is thought to play an important role in this process. Grafts may be composed of entirely cancellous or cortical bone, or a combination of both types. Cancellous bone grafts have been shown to have osteogenic, osteoinductive, and osteoconductive properties  [1, 5, 6]. Cancellous and cortical autografts differ histologically in three respects: 1) cancellous grafts revascularize more rapidly and com-

pletely; 2) creeping substitution of cancellous bone involves an appositional bone formation phase followed by a resorptive phase; and 3) cancellous grafts repair completely with time, while cortical grafts remain admixtures of necrotic and viable bone [6]. All grafts are eventually replaced with host tissue by a process called creeping substitution, which is defined as remodeling by osteoclastic resorption and creation of new vascular channels with osteoblastic bone formation [4, 5, 7]. The successful integration of a bone graft depends on the interaction of six factors: 1) host bed; 2) viability of the bone graft; 3) volume of bone to be grafted; 4) growth factor activity of the host be; 5) metabolic activity index; and (6) homostructural function of the bone graft  [1, 8, 9]. The condition of the host bed in terms of local blood flow, stability and bone marrow activity determines acceptance of the graft. Cancellous and vascularized corticocancellous bone grafts are more viable and have greater rates of acceptance in comparison to grafts with reduced vascularity. Larger volumes of bone graft take longer to be incorporated into host tissue, and therefore have a greater likelihood for development of complications such as nonunions or fatigue failure. Proliferation of perivascular connective tissue in the host bed, which facilitates osteogenesis, is induced by growth factor activity. The metabolic activity index (MAI) is correlated to the capacity of the host bed to incorporate bone grafts and repair fractures. The MAI is determined by heart rate, blood flow, metabolic rate, respiratory rate and body temperature. The MAI of horses has not been determined, but is extrapolated from other species  [9]. The homostructural or support function of the bone graft influences incorporation of the bone graft. Complete incorporation of the graft into host tissue may take years [9].

Complications in Equine Surgery, First Edition. Edited by Luis M. Rubio-Martinez and Dean A. Hendrickson. © 2021 John Wiley & Sons, Inc. Published 2021 by John Wiley & Sons, Inc.

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­ ist of Complications Associated L with Bone Grafts ●● ●● ●● ●● ●● ●● ●● ●●

Intraoperative Complications Reduced viability of graft Early Postoperative Complications Morbidity associated with incision at donor site Fracture at donor site Pneumothorax/hemothorax Late Postoperative Complications Suboptimal integration of bone graft

­Intraoperative Complications Reduced Viability of the Graft Definition  Reduced viability of the graft, defined as death of cells within the graft itself, affects integration of the graft into the host bed. Risk Factors ●● ●●

●●

Suboptimal handling of the graft Prolonged time between harvesting and implantation of the graft Lack of a second surgical team to harvest the graft

Pathogenesis  Reduced viability of the graft results from a combination of prolonged time between harvesting and implantation of the graft, dehydration or compaction of the graft, or exposure of the graft to air, saline-soaked sponges, or antibiotics prior to implantation. Reduced cell survival is attributed to a combination of mechanical damage, desiccation, or osmotic challenge, depending upon the circumstances [10, 11]. Prevention  Cell survival may be maximized by several techniques during harvesting and implantation. A separate surgical team in addition to the surgeons repairing the fracture is advantageous, in order to harvest the cancellous bone graft while the surgical procedure is begun to reduce lag time between harvesting and implantation. It is recommended to have blood-soaked sponges ready to store the harvested bone or marrow following collection and prior to implantation (Figure  10.1). Blood may be obtained via intravenous catheter from the jugular or cephalic vein. Exposure of graft tissue to air, coverage with saline-soaked sponges, or exposure of the graft tissues to antibiotics during harvesting should be avoided. Aseptic technique during implantation is essential for successful incorporation of the graft.

Figure 10.1  Loosely arranged cancellous bone graft in blood-soaked sponge following collection from tuber coxae.

The bone graft material should be lightly packed into the recipient site to allow for appropriate oxygenation of the graft and to reduce mechanical damage to the cells [1, 10]. Osteogenesis occurs as a result of the activity of viable osteoblasts on the surface of the bone graft. Loosely arranged bone grafts are more desirable due to the greater surface area created, with more living cells available resulting in greater osteogenic activity. Avoiding dehydration and compaction of the bone graft results in a greater number of surviving cells and improved viability of the graft [8]. Diagnosis  Reduced viability of the bone graft may

contribute to lack of incorporation of the graft into host tissue, resulting in prolonged fracture repair or increased rate of fracture repair failure. However, lack of viability of the graft itself may not be apparent unless infection of the recipient site occurs or fracture repair failure occurs postoperatively as a result of implant fatigue. Diagnostic imaging (e.g. radiography, ultrasonography or CT) may be utilized to recognize infection or fracture repair failure earlier if indicated based upon clinical signs.

Monitoring

Monitoring for host acceptance of the graft involves monitoring for morbidity at the recipient site (e.g. infection) as well as clinical and radiographic evidence of bone healing. Radiographic signs consistent with infection or lack of incorporation of the graft include evidence of malunion of

­Early Postoperative Complication 

the fracture site or lucency around the implants. Complete integration of the bone graft into host tissue may take years  [9]. Autogenous cancellous bone grafting enhances and stimulates bone healing, and utilization of bone grafts in long bone fracture repair should decrease fracture healing time and fracture repair failure as a result of implant fatigue. Treatment

Treatment following reduced viability of a bone graft is typically not necessary unless infection of the recipient site occurs due to lack of adherence to aseptic technique. Aggressive treatment of infection of the graft bed or fracture site is recommended, typically with a combination of local and systemic antibiotic therapy. In addition, revision of the fracture repair and local lavage may be performed. Expected outcome

Lack of incorporation of the bone graft may contribute to prolonged fracture repair as well as infection of the recipient site if aseptic technique is not followed appropriately. In the event of persistent infection, removal of orthopedic implants may be necessary following fracture repair and bone healing.

­Early Postoperative Complications Morbidity Associated with Incision at Donor Site Definition  The most common complications associated

with the incision for bone graft harvest include incisional infection, seroma, and drainage with peri-incisional edema  [3, 12–13]. Incisional dehiscence may result in osteomyelitis, particularly when the sternum and proximal tibia are used as donor sites [13]. Risk factors  Harvest site location

Pathogenesis  Case selection in the bone graft harvest site is important in minimizing complications. Several donor sites for cancellous bone grafts in the horse have been described, principally the tuber coxae, sternum, rib, proximal medial aspect of the tibia, and proximal humerus, each with its advantages and disadvantages, which are summarized in Table 10.1 [3, 12, 14–17]. Similar amounts of cancellous bone may be obtained from the sternum, tuber coxae, tibia and humerus, while the rib yields smaller quantities in comparison [2, 17]. Case-specific factors dictate intraoperative access to the donor site, amount of graft material required, as well as other case-specific factors including pre-existing soft tissue trauma or decubital ulcers [12, 16, 17].

Utilization of the sternum as a graft donor site is associated with minor complications, including peri-incisional edema, serum exudate, and wound dehiscence due to the ventral location and tension [16]. Incisional dehiscence, which may result in osteomyelitis, is reported, particularly when the sternum and proximal tibia are used as donor sites due to tension and location [13]. Prevention  Location of the donor site is selected based upon the location of the surgical site and therefore anesthetic recumbency selected, which dictates intraoperative access to the site and amount of graft material required. While multiple donor sites may supply an adequate quantity of bone graft material, each donor site carries its own risks and benefits in terms of early postoperative sequellae. Donor site selection is made after taking into account the known risks associated with each site as well as case specific factors such as location of the lesion, soft tissue trauma or presence of decubital ulcers. Whenever possible, avoiding sites at greatest risk of complication is recommended (Table 10.1). Adherence to aseptic technique is advised to reduce morbidity associated with the bone graft donor site incision. The sternum and tibia have also been reported to be more prone to dehiscence due to tension in these areas during anesthetic recovery, and so avoidance of these sites as donor sites for bone graft harvest may reduce incisional site complications. Diagnosis  Incisional infection, seroma, or edema is

diagnosed by clinical examination with evidence of drainage or swelling at the incision site.

Monitoring  Monitor the graft donor incision site for

increased drainage, swelling or dehiscence that may indicate seroma formation or infection. Complete integration of the bone graft into host tissue may take years  [9]. Autogenous cancellous bone grafting enhances and stimulates bone healing, and utilization of bone grafts in long bone fracture repair should decrease fracture repair failure as a result of implant fatigue.

Treatment  Incisional infection or seroma at the donor site may be treated successfully with facilitated drainage of the incision site and antimicrobial therapy. Expected outcome  Incisional complications, such as incisional infection, seroma, and drainage with periincisional edema or superficial incisional infection, are usually self-limited and carry a good prognosis [3, 12, 13]. Osteomyelitis is a more serious condition but usually responds well to local debridement and antimicrobial therapy.

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Table 10.1  Summary of bone graft donor sites Donor Site

Advantages

Tuber coxae [2, 23, 17]

●● ●● ●● ●●

Sternum [16, 21, 37, 38, 39]

●● ●●

●●

●●

●●

Tibia [12, 19]

●●

●●

Humerus [3]

●●

Rib [25]

●●

Fourth coccygeal vertebra [15]

●● ●●

Periosteum [15]

●●

●●

●●

Provide ample grafting material Good visualization for surgical approach Low rate of postoperative incisional complications Remains the most commonly used donor site

●● ●● ●●

Time-consuming Requires patient in lateral recumbency Decubital ulcers or soft tissue trauma over the tuber coxae may preclude its use

Use in cases where patient in dorsal recumbency ●● Risk of puncturing thoracic or pericardial cavities exists Reduces risk of pathological fracture associated with harvesting from the tibia and humerus Absence of skin tension and dependency of this location facilitates drainage if incisional infection or dehiscence occur Cancellous bone obtained is equivalent in amount and microscopic appearance to that obtained from other sites such as the tuber coxae, proximal tibia, and rib No instability or fractures of the sternum have been reported, even when more than one sternebra is accessed in order to obtain the desired amount of cancellous bone May be accessed with patient in dorsal or lateral recumbency Useful in cases where smaller amounts of graft material (1 hour, was associated with better recovery quality than a lower dose of romifidine or xylazine [15]. However, in a study of perioperative morbidity and mortality in horses, sedation with an alpha-2 adrenergic agonist during recovery appeared to

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show some association with improved recovery scores but, in the final model, it was found to be less important than other factors [16].

suffer injuries, which can range from minor wounds to fatal injuries leading to the euthanasia of the animal (e.g. fracture of a long bone).

Prevention  When low doses of alpha-2 adrenergic agonists are used in the recovery period, they prolong the time of recumbency and improve the quality of recovery  [14]. However, if the dose is too high, they may cause excessive ataxia. Romifidine causes a lower degree of ataxia compared with equipotent doses of xylazine and detomidine [2]. An alternative route of administration such as intramuscular may be considered as drugs are absorbed slowly and side effects, like ataxia, might be less dramatic. An adequate dose for the weight of the patient should be used. If the horse has been on an intravenous infusion of any alpha-2 adrenergic agonist intraoperatively, the administration of any more sedation for the recovery period should be gauged carefully, as the residual amount of drug after stopping the infusion may cause sufficient sedation during this phase. All alpha-2 adrenergic agonists increase diuresis, which is of similar degree and duration among agents [2]; therefore, emptying the bladder at the end of the surgical procedure before the recovery phase may improve comfort and prevent early attempts to stand up.

Ketamine: excitement and emergence hallucination Definition  Ketamine side effects include

Diagnosis  Horses recovering from general anesthesia

present some degree of ataxia due to the residual effects of anesthetic drugs. Ataxia contributes to the uncoordinated and sometimes unsuccessful attempts to stand during this phase. Once standing, ataxic horses sway from side to side and sometimes fall back down. This contributes to the high mortality and morbidity observed in horses during the recovery period.

Treatment  Partial antagonism of the alpha-2 adrenergic

agonist, with yohimbine or atipamezole, can help to improve the ataxia. However, if the horse is excessively ataxic it may be dangerous for personnel to enter the recovery room. Moreover, if antagonized excessively this may cause excitement, which can also lead to fatalities during the recovery. Keeping a quiet and dark environment while the horse is recovering is essential to avoid early attempts to stand up, when the ataxia is more pronounced. Expected outcome  The ataxia seen in recovery due to

sedation with alpha-2 adrenergic agonists is self-limited by the metabolism of the drug. Xylazine produces the shortest effects, lasting for about 15–20 minutes. Excessive sedation and ataxia may be responsible for morbidity and mortality during the recovery. Horses may

muscular tremors, rigidity, involuntary limb movements, excitement, ataxia and hallucinations, which may lead to increased morbidity and mortality during the recovery of horses [17]. Risk Factors ●● ●●

●●

High plasma ketamine concentrations Length of the ketamine infusion. Accumulation of ketamine and its metabolites can lead to prolonged recoveries with poor quality [18]. Hepatic and renal disease can cause a delay in the metabolism and excretion, respectively, of ketamine and its accumulation in plasma.

Pathogenesis  Ketamine is a dissociative anesthetic with actions on several receptors, but the antagonism of the N-methyl-D-aspartate (NMDA) receptors in the central nervous system (CNS) is mainly responsible for its anesthetic, analgesic, psychotomimetic and neuroprotective effects. It is widely used in horses in combination with benzodiazepines and/or alpha-2 adrenergic agonists as an induction agent and in total intravenous anesthesia, producing rapid and smooth induction with minimal cardiovascular depression and good analgesia. Intraoperative constant rate infusions (CRI) of ketamine are used in equine anesthesia as part of the balanced anesthesia concept aiming to improve analgesia, reduce the amount of inhaled agent and preserve cardiovascular function [19]. It seems that recovery from ketamine anesthesia in the horse depends on rapid redistribution of the drug from the central compartment and this explains the abrupt recovery from ketamine anesthesia often observed in the horse. The exact dose or circulating concentration of ketamine at which excitement or abnormal behavior occurs may vary between horses and has not been identified. Fielding et al. [29] concluded in their study that the use of subanesthetic doses of ketamine in standing horses up to 0.8 mg/ kg/h for 6 hours did not cause signs of excitement, but an analgesic effect was not obtained with the method of analgesic testing used. Prevention  The administration of a ketamine CRI intraoperatively for longer than 2 hours is not recommended. Administration of ketamine CRIs in horses with hepatic and/or renal disease should be avoided.

­Postop complication 

The administration of S-ketamine instead of racemic ketamine (R-/S- ketamine) decreases the adverse effects observed during the recovery phase [20]. The quality of recovery from anesthesia was better when an intravenous infusion of S-ketamine was used instead of racemic ketamine during isoflurane anesthesia in clinical horses undergoing arthroscopy [20]. Diagnosis  The presence of excitement in the recovery

period with nystagmus, ataxia, restlessness and hyperreactivity to sound and noise. Sometimes “box-walling” has been described.

Treatment  If ketamine has been administered as a CRI during anesthesia and the horse shows signs of excitement early during the recovery phase, it is recommended to sedate the horse with an alpha-2 adrenergic agonist. Keeping the horse in a quiet and dark environment will avoid stimulation and early attempts to stand. Expected outcome  With time the drug will be metabolized

and the horse will recover slowly from the side effects caused by the accumulation of ketamine and its metabolites. The outcome should be good if the horse does not suffer from major injuries. Lidocaine: ataxia and visual dysfunction Definition

Prevention  When using lidocaine as a CRI during anesthesia, it is recommended to stop the infusion 30 minutes before the end of surgery to avoid ataxia during the recovery period  [24]. This study showed that using intraoperative lidocaine as a CRI at a dose of 50 microg/kg/ min and discontinuing the CRI 30 minutes before the end of surgery reduced the degree of ataxia during the recovery period [24]. Diagnosis  Signs of neurotoxicity caused by lidocaine

include rapid eye blinking, ataxia, progressing to sedation, muscle twitching, seizures and unconsciousness  [21]. Tremors and signs of visual dysfunction, including staring and inspecting the walls and floor closely, in some horses that received a CRI of lidocaine during anesthesia were observed [25].

Treatment  No specific treatment exists for lidocaine neurotoxicity. The patients recover rapidly from the effects of lidocaine after discontinuation due to its short terminal half-life (40 min) in the horse [26]. Expected outcome  The outcome should be good if the

horse does not suffer from major injuries.

­Postop complications Opioids: Excitement

Ataxia and alterations in behaviour related to visual dysfunction may be observed after overdosing with lidocaine  [21]. Horses show rapid and intermittent eye blinking, anxiety and attempts to inspect closely located objects.

Definition  Opioids can produce excitement, seen as box walking, restlessness and dysphoria when administered alone in pain-free horses.

Risk Factors

●●

●●

●●

Lidocaine administration until the end of anesthesia has a significant negative effect on the degree of ataxia exhibited by horses in the recovery period. Liver disease can impair lidocaine metabolism and hepatic clearance, therefore it will not be metabolized and so accumulates.

Pathogenesis  Lidocaine is a local anesthetic commonly used intravenously as a CRI as part of balanced anesthetic protocols in equine anesthesia. The beneficial effects include analgesia and inhalational anaesthetic-sparing effect  [22, 23]. However, lidocaine at high plasma concentrations can cause neurotoxicity and cardiotoxicity (see Chapter  14: Complications of Loco-Regional Anesthesia).

Risk Factors

●●

Administration of high doses of opioids without the concurrent administration of a sedative drug Administration of opioids in pain-free horses

Pathogenesis  Horses possess a unique opioid receptor profile and density compared to other species and are sensitive to opioid-induced CNS stimulatory and locomotor effects. Excitement may result indirectly from increased release of norepinephrine and dopamine. This may explain the mechanism why noradrenergic and dopaminergic blocking drugs like phenothiazines suppress the opioid induced excitement  [12]. However, increased locomotor activity produced by opioids seems to be associated with opioid receptors. The propensity of an opioid analgesic to promote locomotion may be greater with mu (e.g., morphine) than with kappa agonists (e.g. butorphanol) [27]. Kappa agonism more commonly causes ataxia and

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staggering [28]. Opioids were studied in varying numbers of pain-free horses in one of the most commonly cited references on opioid-induced locomotion in horses [32]. It is important to note that there is marked individual variation in responses. The median effective dose of morphine that causes an increase in locomotion activity in pain-free animals is 0.91 mg/kg, which is considerably higher than the doses used clinically to produce analgesia [30]. Prevention  Using appropriate clinical doses of opioids in

combination with a sedative drug will prevent this excitement [30]. Diagnosis  Increased locomotor activity, box walking, head

jerking, disorientation and/or ataxia

Treatment  The use of sedative agents like acepromazine or apha-2 adrenergic agonists can calm and sedate the horse, solving the excitement and increased locomotor activity. The use of the opioid antagonist naloxone (0.015 mg/kg) entirely prevented locomotor responses to morphine and fentanyl  [31]. Naloxone will revert the analgesics effects of any opioid, therefore it should be used with caution in painful horses and only in severe cases or overdose. Expected outcome  The outcome is good as these effects are usually mild and easy to control with the administration of a sedative.

Ileus Definition  Gastrointestinal propulsive motility depends on a complex interaction between neural, hormonal, vascular and neuromuscular pathways. Disruption of this intrinsic interaction leads to absence of propulsive aboral movement of food material, also called ileus. Risk Factors ●●

●●

●● ●●

●● ●● ●●

The use of high doses of either opioids or alpha-2 adrenergic agonists The use of opioids in pain-free horses may predispose to ileus Prolonged starvation (>18 h) Recent changes in management such as exercise, diet and transport increase the risk in hospitalized horses. Stress response to anesthesia, surgery and pain Local inflammation and edema of the intestine Endotoxemia

Pathogenesis  Alpha-2 adrenergic agonists decrease intestinal motility, which may predispose to ileus. Studies in rats using clonidine showed that the activation of presynaptic alpha-2A subtype receptors was responsible for the slower motility  [33]. In horses, xylazine-induced vasoconstriction of the cecal vasculature decreases arterial blood flow to the lateral cecal artery, decreasing normal local motility for up to 120 minutes with a full sedative dose (1.1 mg/kg, IV) and for 30 minutes with a low dose (0.275 mg/kg) [34]. The gastrointestinal effects of opioids may also predispose to post-anesthetic colic or ileus. All opioids, including mu and kappa agonists, reduce gastrointestinal motility [30]. Morphine (0.5 and 1.0 mg/kg) and fentanyl (10 or 50 mg) intravenously initially stimulated, but then inhibited ceco-colic electrical and mechanical activity for up to 3 hours in three pain-free ponies [38]. A decrease in gastrointestinal motility was detected 1 to 2 hours after intramuscular administration of morphine at doses of 0.05 and 0.1 mg/kg and after intravenous administration at a dose of 0.1 mg/kg  [39]. In another study, morphine administered at 0.5 mg/kg twice daily decreased propulsive motility and moisture content in the gastrointestinal tract lumen for up to 6 hours after each dose [37]. Epidural morphine has also been shown to temporarily reduce GI motility but it did not cause ileus or colic in a small group of healthy unfasted  horses  [40]. A single intravenous injection of butorphanol was associated with decreased borborygmi, and decreased defecation; however, the administration of butorphanol as a continuous intravenous infusion over 24 hours was associated with minimal side effects including minimal gastrointestinal effects [41]. The literature indicates a multifactorial etiology for perianesthetic ileus and an equivocal contribution of morphine and other opioid analgesics. Therefore, care should be taken when extrapolating these data to clinical situations of horses with painful conditions and in which other factors may also affect GI motility. Prevention  Continuous intravenous infusions of low doses may reduce the intensity of gastrointestinal side effects as compared with intravenous bolus administration. Avoid high doses of opioids and alpha-2-adrenergic agonists and reduce the dose of opioids and/or alpha-2 adrenergic agonists to the minimum effective dose. In painful horses the effective management of pain is important and the use of clinical doses of opioids (e.g. 0.1–0.3 mg/kg of morphine) is recommended, as the analgesic effect may override theoretical concerns of decreased gastrointestinal motility. Using pain scales may help to identify the patients that are in pain and in need of analgesia, allowing a more correct dosage and avoiding overdosing.

 ­Reference

Diagnosis  It is out of the scope of this chapter to detail the

diagnosis and treatment of ileus in horses, as it is a multifactorial disease, but if high doses of opioids and/or alpha-2 agents have been administered or they have been used for prolonged periods of time, they could be a contributing factor.

Treatment  Naloxone, a full opioid antagonist, induces a marked propulsive activity in the colonic segment producing onset diarrhea, restlessness, abdominal checking, tachycardia and tachypnea in healthy horses not pre-treated with opioids  [42]. In vitro, naloxone has prokinetic effects at the ileo-eco-colonic junction  [43]. Naloxone also reverses the analgesic effects of opioids.

N-methylnaltrexone, a peripheral opioid antagonist that does not cross the blood–brain barrier, therefore not reversing opioid-induced analgesia. has been studied in horses  [44]. At doses of 0.75 mg/kg intravenously, N-methylnaltrexone partially prevented the effects of morphine on the gastrointestinal tract. Alvimopan, a peripherally acting mu-opioid receptor antagonist, is an emerging treatment for human postoperative ileus. It partially prevents the gastrointestinal effects caused by morphine while preserving the central analgesic effects [35, 36]. Expected outcome  The prognosis of ileus is guarded. The outcome will depend on the etiology and the clinical status of the horse.

­References 1 Yamashita, K., Tsubakishita, S., Futaok S. et al. (2000). Cardiovascular effects of medetomidine, detomidine and xylazine in horses. J. Vet. Med. Sci. 62 (10): 1025–1032. 2 England, G.C.W., Clarke, K.W., and Goossens, L. (1992). A comparison of the sedative effects of three α2adrenoceptor agonists (romifidine, detomidine and xylazine) in the horse. J. Vet. Pharmacol. Ther. 15 (2): 194–201. 3 Wilson, D.V., Bohart, G.V., Evans, A.T. et al. (2002). Retrospective analysis of detomidine infusion for standing chemical restraint in 51 horses. Vet. Anaesth. Analg. 29 (1): 54–57. 4 Singh, S., Young, S.S., McDonell, W.N. et al. (1997). Modification of cardiopulmonary and intestinal motility effects of xylazine with glycopyrrolate in horses. Can. J. Vet. Res. 61 (2): 99. 5 Neto, F.J.T., McDonell, W.N., Black, W.D. et al. (2004). Effects of glycopyrrolate on cardiorespiratory function in horses anesthetized with halothane and xylazine. Am. J. Vet. Res. 65 (4): 456–463. 6 Pimenta, E.L.M., Teixeira Neto, F.J., Sá, P.A. et al. (2011). Comparative study between atropine and hyoscine-Nbutylbromide for reversal of detomidine induced bradycardia in horses: Hyoscine and atropine in horses. Equine Vet. J. 43 (3): 332–340. 7 Perotta, J.H., Canola, P.A., and Lopes, M.C. (2002). Hyoscine-N-butylbromide premedication on cardiovascular variables of horses sedated with medetomidine. Vet. Anaesth. Analg. 41 (4): 357–364. 8 Pignaton, W., Luna, S.P.L., Teixeira Neto, F.J., et al. (2016). Methadone increases and prolongs detomidineinduced arterial hypertension in horses, but these effects are not mediated by increased plasma concentrations of

arginine vasopressin or serum concentrations of catecholamines. J. Equine Vet. Sci. 37: 39–45. 9 Guedes, A.G., Rudé, E.P., and Rider, M.A. (2006). Evaluation of histamine release during constant rate infusion of morphine in dogs. Vet. Anaesth. Analg. 33 (1): 28–35. 10 Barke, K.E. and Hough, L.B. (1993). Opiates, mast cells and histamine release. Life Sci. 53 (18): 1391–1399. 11 Thompson, W.L. and Walton, R.P. (1964). Elevation of plasma histamine levels in the dog following administration of muscle relaxants, opiates and macromolecular polymers. J. Pharmacol. Ex. Ther. 143: 131–136. 12 Mircica, E., Clutton, R.E., Kyles, K.W. et al. (2003). Problems associated with perioperative morphine in horses: a retrospective case analysis. Vet. Anaesth. Analg. 30 (3):147–155. 13 Clutton, R.E. (1987). Unexpected responses following intravenous pethidine injection in two horses. Equine Vet. J. 19 (1): 72–73. 14 Santos, M. (2003). Garcia-Iturralde, P., Herran, R. et al. Effects of alpha-2 adrenoceptor agonists during recovery from isoflurane anaesthesia in horses. Equine Vet. J. 35 (2): 170–175. 15 Woodhouse, K.J., Brosnan, R.J., Nguyen, K.Q. et al. (2013). Effects of postanesthetic sedation with romifidine or xylazine on quality of recovery from isoflurane anesthesia in horses. J. Am. Vet. Med. Assoc. 242 (4): 533–539. 16 Senior, J.M., Pinchbeck G.L., Allister, R. et al. (2007) Reported morbidities following 861 anaesthetics given at four equine hospitals. Vet. Rec. 160 (12): 407–408.

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1 7 Wakuno, A., Aoki, M., Kushiro, A. et al. (2017). Comparison of alfaxalone, ketamine and thiopental for anaesthetic induction and recovery in Thoroughbred horses premedicated with medetomidine and midazolam. Equine Vet. J. 49 (1): 94–98. 18 Young, L.E., Bartram, D.H., Diamond, M.J. et al. (1993). Clinical evaluation of an infusion of xylazine, guaifenesin and ketamine for maintenance of anaesthesia in horses. Equine Vet. J. 25 (2): 115–119. 19 Bettschart-Wolfensberger, R. and Larenza, M.P. (2007). Balanced anesthesia in the equine. Clin. Tech. Equine Pract. 6 (2): 104–110. 20 Larenza, M.P., Kutter, A.P.N., Kummer, M. et al. (2009). Evaluation of anesthesia recovery quality after low-dose racemic or S-ketamine infusions during anesthesia with isoflurane in horses. Am. J. Vet. Res. 70 (6): 710–718. 21 Meyer, G.A., Lin, H.C., Hanson, R.R. et al. (2001). Effects of intravenous lidocaine overdose on cardiac electrical activity and blood pressure in the horse. Equine Vet. J. 33 (5): 434–437. 22 Dzikiti, T.B., Hellebrekers, L.J., and Dijk, P. (2003). Effects of intravenous lidocaine on isoflurane concentration, physiological parameters, metabolic parameters and stress-related hormones in horses undergoing surgery. J. Vet. Med. Ser. A. 50 (4): 190–195. 23 Murrell, J.C., White, K.L., Johnson, C.B. et al. (2005). Investigation of the EEG effects of intravenous lidocaine during halothane anaesthesia in ponies. Vet. Anaesth. Analg. 32 (4): 212–221. 24 Valverde, A., Gunkelt, C., Doherty, T.J. et al. (2005). Effect of a constant rate infusion of lidocaine on the quality of recovery from sevoflurane or isoflurane general anaesthesia in horses. Equine Vet. J. 37 (6): 559–564. 25 Valverde, A., Rickey, E., Sinclair, M. et al. (2010). Comparison of cardiovascular function and quality of recovery in isoflurane-anaesthetised horses administered a constant rate infusion of lidocaine or lidocaine and medetomidine during elective surgery. Equine Vet. J. 42 (3): 192–199. 26 Engelking, L.R., Blyden, G.T., Lofstedt, J. et al. (1987). Pharmacokinetics of antipyrine, acetaminophen and lidocaine in fed and fasted horses. J. Vet. Pharmacol. Ther. 10 (1): 73–82. 27 Mama, K.R., Pascoe, P.J., and Steffey, E.P. Evaluation of the interaction of Mu and Kappa opioid agonists on locomotor behavior in the horse. Can. J. Vet. Res. 57 (2): 106–109. 28 Nolan, A.M., Besley, W., Reid, J. et al. (1994). The effects of butorphanol on locomotor activity in ponies: a preliminary study. J. Vet. Pharmacol. Ther. 17 (4): 323–326.

29 Fielding, C.L., Brumbaugh, G.W., Matthews, N.S. et al. (2006). Pharmacokinetics and clinical effects of a subanesthetic continuous rate infusion of ketamine in awake horses. Am. J. Vet. Res. 67 (9): 1484–1490. 30 Clutton, R.E. (2010). Opioid analgesia in horses. Vet. Clin. N. Am. Equine Pract. 26 (3): 493–514. 31 Combie, J., Shults, T., Nugent, E.C. et al. (1981). Pharmacology of narcotic analgesics in the horse: selective blockade of narcotic-induced locomotor activity. Am. J. Vet. Res. 42 (5): 716–721. 32 Taylor, P.M., Hoare, H.R., de Vries, A. et al. (2016). A multicentre, prospective, randomised, blinded clinical trial to compare some perioperative effects of buprenorphine or butorphanol premedication before equine elective general anaesthesia and surgery. Equine Vet. J. 48 (4): 442–450. 33 Zadori, Z., Shujaa, N., Fulop, K. et al. (2007). Pre- and postsynaptic mechanisms in the clonidine- and oxymetazoline-induced inhibition of gastric motility in the rat. Neurochem. Int. 51 (5): 297–305. 34 Rutkowski, J.A., Eades, S.C., and Moore, J.N. (1991). Effects of xylazine butorphanol on cecal arterial blood flow, cecal mechanical activity, and systemic hemodynamics in horses. Am. J. Vet. Res. 52 (7): 1153–1158. 35 Lassen, K., Soop, M., Nygren, J. et al. (2009).Consensus review of optimal perioperative care in colorectal surgery: Enhanced Recovery After Surgery (ERAS) Group recommendations. Arch. Surg. Chic. Ill. 144 (10): 961–969. 36 Wang, S., Shah, N., Philip, J. et al. (2012). Role of alvimopan (entereg) in gastrointestinal recovery and hospital length of stay after bowel resection. P T Peer-Rev J. Formul. Manag. 37 (9): 518–525. 37 Boscan, P., Van Hoogmoed, L.M., Farver, T.B. et al. (2006). Evaluation of the effects of the opioid agonist morphine on gastrointestinal tract function in horses. Am. J. Vet. Res. 67 (6): 992–997. 38 Roger, T,. Bardon, T., and Ruckebusch, Y. (1985). Colonic motor responses in the pony: relevance of colonic stimulation by opiate antagonists. Am. J. Vet. Res. 46 (1): 31–35. 39 Figueiredo, J.P., Muir, W.W., and Sams, R. (2012). Cardiorespiratory, gastrointestinal, and analgesic effects of morphine sulfate in conscious healthy horses. Am. J. Vet. Res. 73 (6): 799–808. 40 Martin-Flores, M., Campoy, L., Kinsley, M.A. et al. (2014). Analgesic and gastrointestinal effects of epidural morphine in horses after laparoscopic cryptorchidectomy under general anesthesia. Vet. Anaesth. Analg. 41 (4): 430–437.

 ­Reference

4 1 Sellon, D.C., Monroe, V.L., Roberts, M.C. et al. (2001). Pharmacokinetics and adverse effects of butorphanol administered by single intravenous injection or continuous intravenous infusion in horses. Am. J. Vet. Res. 62 (2): 183–189. 42 Kamerling, S.G., Hamra, J.G., and Bagwell, C.A. (1990). Naloxone-induced abdominal distress in the horse. Equine Vet. J. 22 (4): 241–243.

43 Ruckebusch, Y. and Roger, T. (1988). Prokinetic effects of cisapride, naloxone and parasympathetic stimulation at the equine ileo-caeco-colonic junction. J. Vet. Pharmacol. Ther. 11 (4): 322–329. 44 Boscan, P., Van Hoogmoed, L.M., Pypendop, B.H. et al. (2006). Pharmacokinetics of the opioid antagonist N-methylnaltrexone and evaluation of its effects on gastrointestinal tract function in horses treated or not treated with morphine. Am. J. Vet. Res. 67 (6): 998–1004.

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14 Complications of Loco-Regional Anesthesia Eva Rioja Garcia DVM, DVSc, PhD, DACVAA, DECVAA, MRCVS Optivet Referrals, Havant, Hampshire, UK

O ­ verview

●● ●●

All pain management techniques and drugs have the potential to produce complications related to the technique itself or due to the drugs’ side effects; however, the benefits related to the pain relief that they provide usually outweigh the risks. When performing loco-regional blocks the anatomy (landmarks) of the region as well as the technique should be well known to avoid puncture and potential damage of structures or organs. This chapter will cover some of the most important and relevant complications related to loco-regional blocks. Complications related to loco-regional blocks performed for lameness examination are included in Chapter  44: Complications of Diagnostic Tests for Lameness.

­General Complications Vascular Puncture Definition  When performing a loco-reginal block, significant bleeding due to puncture of a blood vessel or inadvertent intravascular injection of the local anesthetic, either in a vein or an artery, can occur. Risk Factors ●● ●● ●●

­ ist of Complications Associated L with Loco-Regional Anesthesia ●●

●●

●● ●●

●●

●●

General complications ○○ Vascular puncture ○○ Nerve injury ○○ Myotoxicity ○○ Chondrotoxicity ○○ Allergic reactions Complications related to specific loco-regional blocks ○○ Epidural Analgesia –– Ataxia/Recumbency Infection inside the spinal canal Pruritus ○○ Retrobulbar Blocks Brainstem Anesthesia ○○ Inferior Alveolar Nerve Block Self-Inflicted Lingual Trauma ○○ Intravenous regional anesthesia (IVRA)

Tourniquet failure Local and systemic effects of tourniquet ischemia

●●

Use of blind techniques Lack of knowledge of anatomy of the region Injecting the local anesthetic with no previous aspiration Significant bleeding may occur in horses with coagulopathies

Pathogenesis  When a nerve is targeted to perform a block, there is always an associated vein and artery nearby; therefore, there is always the potential to puncture a blood vessel and consequently to induce bleeding and hematoma formation in the area. Similarly, there is the potential to inadvertently inject intravenously or intra-arterially. This can lead to systemic toxicity, which could be even lethal, depending on the dose of local anesthetic administered intravascularly. In the spinal canal, there are many blood vessels that could be punctured when performing an epidural injection, the most prominent being two venous plexuses at the floor of the canal, that run parallel to the spinal cord on each side. When performing a proximal paravertebral block with the needle inserted paramedially (parallel to the sagittal plane, separated a few centimeters from the spinal

Complications in Equine Surgery, First Edition. Edited by Luis M. Rubio-Martinez and Dean A. Hendrickson. © 2021 John Wiley & Sons, Inc. Published 2021 by John Wiley & Sons, Inc.

­General Complication 

canal), there is also risk of arterial or venous puncture, especially if the needle is advanced too far as it could reach the abdominal aorta (left side) or caudal vena cava (right side). A recent retrospective study in horses looked at the complications associated with loco-regional anesthesia for dental procedures, and found that hematoma occurred in 5 out of 270 blocks performed, giving a 1.8% incidence rate [1]. There is a report of retrobulbar hematoma formation in a dog following inadvertent puncture of a blood vessel during a maxillary block, which led to exophthalmos, periorbital swelling, extensive scleral  hemorrhage and ecchymosis [2]. In humans, bleeding or intravascular cannulation occurred in 0.67% of cases where an epidural technique was performed [3]; however, this article did not report the consequences of this complication. Systemic toxicity related to local anesthetics injected intravascularly inadvertently usually starts with the development of neurological signs and it is followed by signs of cardiovascular toxicity. There are no published reports of systemic toxicity in horses following regional anesthetic blocks, most likely because the toxic dose is normally higher than the dose administered locally. In small animals, seizures occurred in two medetomidinesedated dogs following subcutaneous administration of lidocaine for skin biopsies, although in these animals a very high dose was used and most likely this caused the systemic toxicity and not an inadvertent intravascular injection  [4]. Severe cardiovascular depression was reported in an anesthetized cat immediately following mandibular nerve block with bupivacaine and seizurelike activity upon recovery, which could have been due to inadvertent intravascular injection as the dose administered was low  [5]. In the human literature, there are reports of inadvertent intravascular injection during different types of blocks, leading to seizures and/or cardiac arrest; however, the overall incidence of major complications is very low [6]. Prevention  Knowledge of the anatomy, careful needle insertion and avoiding passing the needle repeated times should decrease the risk of puncturing a blood vessel. Aspiration before injection should be done to ensure no intravascular injection. Once it has been ascertained that the needle is not in a vessel it should not be moved and injection performed. Whenever the needle is repositioned aspiration should be done again before injecting. Ultrasound-guided needle insertion can prevent puncturing undesired structures such as blood vessels [7, 8]. The toxic dose of the local anesthetic should be calculated for the individual horse, and the total administered dose should be below this toxic dose.

When performing epidural injections, the risk of puncturing a venous plexus is lower when the needle is in midline and is not advanced to the floor of the canal, which is where the venous sinuses run, on both sides of the spinal cord. When performing paravertebral blocks, the needle should be advanced carefully until it reaches the transverse process of a vertebra and then “walked off” the process and advanced only one or two more centimeters to avoid reaching the abdomen. Loco-regional blocks, especially epidural or paravertebral injections, should be avoided in animals with coagulation defects. Diagnosis  If blood is observed in the hub of the needle

while it is being advanced, it is advisable to reposition the needle until blood flow stops or to abort the procedure and repeat it using a new needle in a slightly different location. Inadvertent intravascular injection may just lead to block failure if the total dose was low. But it could also lead to systemic signs of toxicity. The first signs are neurological due to central nervous system toxicity, starting with rapid eye blinking, ataxia, progressing to sedation, muscle twitching, seizures and unconsciousness  [9]. When the intravascular dose of local anesthetic is high enough to cause cardiovascular toxicity, the signs may include ventricular premature beats, ventricular tachycardia and/or fibrillation followed by cardiovascular collapse and arrest [10]. The clinical signs of local anesthetic toxicity are different in conscious and anesthetized animals. Anesthetized animals are more resistant to the central nervous system toxicity and no seizures are observed, while cardiovascular depression might occur at lower doses than in conscious animals [10].

Treatment  Normally no specific treatment is necessary for hemorrhage/hematoma if the horse’s coagulation is normal. If there is a clotting problem or the bleeding is significant, administration of an antifibrinolytic agent could be considered such as tranexamic acid or epsilonaminocaproic acid. If the hematoma is big, drainage of the blood may be attempted, as well as application of local cold treatment and local and/or systemic administration of non-steroidal anti-inflammatory agents. When systemic toxicity is noticed, the administration of local anesthetic should be halted. Treatment of systemic toxicity is supportive as there is no reversal agent. If seizures are observed, an anticonvulsant drug such as a benzodiazepine (i.e. diazepam) can be administered, although it may be safer to induce general anesthesia with

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a barbiturate (i.e. thiopental). Supportive treatment consists of endotracheal intubation, oxygen administration and controlled respiration  [11]. Signs of cardiovascular toxicity induced by lidocaine or mepivacaine are usually mild and reversible with positive inotropic drugs such as dobutamine and fluid therapy. Longer acting local anesthetics such as bupivacaine, levobupivacaine or ropivacaine are more cardiotoxic and the cardiac arrhythmias that they produce are usually malignant and refractory to routine treatment (i.e. ventricular tachycardia or fibrillation). In these cases, administration of a low dose of epinephrine (for cardiac arrest), amiodarone (for ventricular tachycardia) or defibrillation (for ventricular fibrillation) are the recommended treatments. An intravenous infusion of a 20% lipid emulsion (“lipid rescue”) is recommended to treat refractory arrhythmias induced by highly lipophilic local anesthetics (i.e. bupivacaine), as it has been shown to be the only effective treatment in different experimental models [12, 13] and in human clinical reports [14. 15]. Expected outcome  The consequences and the prognosis

of hemorrhage/hematoma could be serious depending on the location and amount of blood lost. It is likely that this complication occurs commonly in practice but that it does not carry any serious consequence for the animal. An immediate consequence to this complication could be a less effective or an ineffective block, due to the dilution and entrapment of the local anesthetic within the blood/ clots. If significant bleeding occurs within the spinal canal following an epidural injection, this could lead to spinal cord compression, which depending at what level it occurs, it could lead to ataxia and/or recumbency of the animal. Puncture of the caudal vena cava or the aorta when performing a proximal paravertebral block could lead to significant intra-abdominal bleeding; however, no reports of such complication could be found by the author. The outcome of local anesthetic systemic toxicity is generally good when only mild central nervous system signs are observed (i.e. muscle fasciculations); however, it could be fatal if seizures occur as the horse may injure itself. When cardiovascular toxicity occurs, this could lead to irreversible cardiac arrest, particularly when using the longer acting local anesthetics (i.e. bupivacaine).

Nerve Injury Definition  Direct needle puncture of a nerve and/or injecting the local anesthetic into a nerve may lead to nerve damage.

Risk Factors ●●

●● ●●

●●

The neurotoxicity of local anesthetic is greater as concentrations increase. Blind injection techniques Several passages of the needle and movements of the needle The type of bevel of the needle can also influence the degree of damage as well as the orientation that the needle has with respect to the nerve fibers.

Pathogenesis  Local anesthetic agents have cytotoxic effects and therefore can produce direct neurotoxicity. Small fiber neurons such as C and Aδ (responsible for pain and temperature transmission) are more sensitive to chemical damage than the larger fibers Aα and Aβ (responsible for motor function, proprioception, pressure and touch)  [16]. These neurotoxic effects will manifest clinically as persisting sensory and/or motor deficits in the area innervated by the nerve. The degree of damage depends where within the nerve the local anesthetic solution is injected. The nerves are surrounded externally by a layer of connective tissue, the epineurium. Inside the nerve the neuronal axons are bundled together forming fascicles, and several fascicles form a nerve. Between the fascicles there is connective tissue and intrinsic blood vessels. Fascicles are surrounded by another layer of connective tissue, the perineurium. Finally, each individual axon is surrounded by another layer of connective tissue called the endoneurium. The perineurium is a barrier that regulates the entry of substances from adjacent tissues and the blood vessel endothelium regulates the entry from the vascular compartment, both maintaining the internal milieu of the nerve fascicle. When a local anesthetic is deposited inside the nerve but outside the perineurium, the regulatory function of the perineurial and endothelial blood–nerve barriers is only marginally compromised and little or no nerve damage occurs  [17].  However, when the local anesthetic is injected inside the nerve fascicle (intrafascicular injection) axonal degeneration and blood– nerve barrier changes occur, which become progressively worse when the concentration increases [18, 19]. Mechanical damage due to needle-tip penetration of the nerve can also lead to injury, but this seems not to be the main cause of clinical complications [20]. Nerve damage is more likely to occur when the solution is injected intrafascicularly due to interruption of the perineural tissue around the nerve fascicles, causing a breach of the blood–nerve barrier leading to edema and herniation of the endoneural contents [17]. Nonetheless, intrafascicular injection of saline solution that caused pressures transiently exceeding the nerve capillary perfusion pressure did not

­General Complication 

induce any changes in the microscopic anatomy or diffusion barriers within the nerve  [19], which indicates that the main source of peripheral nerve injury is injection of the local anesthetic into a fascicle. Based on data in dogs, when lidocaine 2% is injected intrafascicularly with a low injection pressure ( 11 psi), normal motor function will return in 3 hours  [21]. In another study in dogs where lidocaine 2% was also administered, neurological function returned to baseline 3 hours after perineural injections and within 24 hours after intraneural injections with injection pressures below 12 psi [22]. Long-beveled needles (14-degree angle) are more likely to cause nerve damage if they impale a nerve than shortbeveled ones (45 degrees) [23]. Also, if the needle pierces a fascicle with the bevel transverse to the nerve fibers, the damage is greater than if the bevel is parallel to them [23]. Application of tourniquets at high occlusion pressures may cause mechanical deformation of the portion of the nerve under the tourniquet leading to damage. The most sensitive neurons to this type of insult are the fast conducting, large diameter myelinated fibers (Aα and Aβ)  [24]. Ischemic damage of nerves due to long tourniquet application times may also occur, but these changes seem not to be permanent following ischemic periods of less than 6 hours [25]. Neurological deficits can also occur secondary to an expanding hematoma that causes nerve compression. To the best of the author’s knowledge there are no reports of neurotoxicity associated with clinical local/regional anesthesia in horses, which indicates that this complication is probably very rare considering the vast number of local blocks performed in equine clinical practice. In humans, serious nerve injury resulting in permanent nerve damage is rare, with a 1.5/10,000 incidence reported  [26]. Most reported injuries are transient and often subclinical, with a reported incidence of transient paresthesia as high as 8–10% in the immediate days after the block [27]. Prevention  The lowest dose and concentration that will be effective to produce a block should be used to minimize the risk of chemical nerve damage. Puncturing a nerve with a needle is associated with a burning or prickling sensation (paresthesia) as described in human medicine. Injection of a local anesthetic into a nerve will cause pain. Therefore, if the horse reacts during the advancement of the needle or during the injection of the solution, this could indicate intraneural placement and the injection should be halted. If the patient is anesthetized or heavily sedated these warning signs will be obtunded and therefore there is an increased risk of intraneural injection. Ultrasound-guided needle insertion decreases the incidence of paresthesias compared with other techniques in humans [8]. The use of a nerve stimulator, which delivers

an electrical current to stimulate a motor response associated with a specific nerve, in theory would decrease the risk of intraneural injections; however, studies show that this is not the case and even the absence of motor response to nerve stimulation does not exclude intraneural needle placement [28]. Careful technique, gentle needle movements and using short-beveled needles with the bevel parallel to the nerve could reduce the risk of nerve damage. Also, stopping the injection if high pressure is felt may help to decrease the risk of nerve injury, as it was shown that intrafascicular injections associated with high pressures ( 25 psi) caused persistent motor deficits with destruction of neural structure and axonal degeneration, while lower pressures ( 11 psi) did not cause any permanent motor dysfunction or histological abnormality [21]. Diagnosis  The clinical manifestations of nerve damage

caused by local anesthetics are reported in humans to include spontaneous paresthesias and deficits in pain and temperature perception, and not so frequently loss of motor, touch or proprioceptive function [16]. Clinical signs associated with tourniquet-induced neuropathy are mainly motor and proprioception loss and diminished touch sense [29].

Treatment  There is no specific treatment for nerve damage, only supportive. Treatment of the hematoma or the ischemic area may help to regain normal nerve function faster. Expected outcome  In humans, symptoms of nerve injury following regional blocks resolved in 4–6 weeks in 92–97% of cases and by 1 year in 99% of cases [30].

Myotoxicity Definition  The occurrence of myositis and/or myonecrosis following the injection of a local anaesthetic solution into a muscle Risk factors  Local anesthetic-induced myotoxicity is

concentration-dependent, but it is observed at clinically relevant concentrations of all commonly used local anesthetics (e.g. bupivacaine 0.5%, mepivacaine 2%, lidocaine 2%) [31–33].

●●

The greatest risk of clinically relevant myopathy and myonecrosis is when local anesthetics are administered intramuscularly and repeatedly (either serially or continuously) [34].

Pathogenesis  Experimentally, all local anesthetics can cause toxicity to skeletal muscle with the most toxic being

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bupivacaine and the least being procaine [34]. Bupivacaine causes the most severe changes characterized by calcific myonecrosis, formation of scar tissue and a marked rate of fiber regeneration, which were observed 7 and 28 days after a continuous femoral nerve block in a study in pigs [32]. Injury mechanisms seem to involve early and late aberrations to cytoplasmic calcium (Ca2+) homeostasis by the sarcoplasmic reticulum Ca2+ ATPase [35]. Clinically, myotoxocity may cause muscular pain and dysfunction, although in most cases these changes seem to be regenerative and clinically imperceptible. Clinically relevant myotoxicity is very rare and only described in the human literature. In humans, clinical cases of myotoxicity caused by local anesthetics have been described mostly following continuous peripheral blocks and peri- and retrobulbar blocks.  [36–38]. A recently published systematic review of the literature in humans showed that the incidence of myotoxicity in ophthalmic studies was 0.77% [35]. Prevention  Using low concentrations of local anesthetics, especially of bupivacaine (70 mmHg) was a negative predictor of survival to hospital discharge (though anesthetic survival was unchanged) [80]. In another study, intraoperative hypocapnia (arterial carbon dioxide 95%) improves arterial oxygen tensions in anesthetized horses. Although using a low fraction of inspired oxygen during anesthesia has the theoretical benefit of reducing pulmonary shunts created by adsorption atelectasis, horses anesthetized using low inspired oxygen fractions are at greater risk of hypoxemia and arterial oxygen tensions increase dramatically with oxygen supplementation, even though shunt fraction does increase [90, 91]. Application of recruitment maneuvers consists of creating high peak inspiratory pressures (60–80 mH2O) for a prolonged inspiratory hold during several breaths. This in combination with the use of positive end expiratory pressure (PEEP) can be successful in improving arterial oxygen tensions in horses  [92–94]. These techniques, however, have detrimental effects on cardiac output. When cardiac output is significantly decreased, oxygen delivery to tissues is reduced and thus the benefits of having higher oxygen tensions may be negated. Bronchodilators have been used with mixed results to improve oxygenation. Early studies used intravenous clenbuterol, which was successful but had undesirable systemic side effects such as sweating and tachycardia [95]. Inhaled salbutamol has been used more recently with success, improving arterial oxygen tensions without causing tachycardia, though sweating was still noted and a small percentage of horses failed to respond to treatment. In order to deliver the drug, an inhaler and endotracheal tube adapter are used [96]. Horses should routinely be provided with high flow oxygen insufflation (15 liters per minute) in the recovery stall  [97]. Horses entering the recovery stall already hypoxemic, despite high fractions of inspired oxygen during anesthesia, may benefit from the use of a demand valve as described earlier. Expected Outcome  Despite the fact that oxygen is essential for cellular processes and it would seem that hypoxemia should influence survival, there are few data on the effect of hypoxemia on clinical outcome in horses. Two studies in

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horses undergoing colic surgery failed to link intraoperative hypoxemia and negative outcome  [80, 81]. Regardless, studies reflect that serum biochemical changes do occur in experimental horses when arterial oxygen is low over a period of several hours [98]. Additionally, horses with suboptimal oxygenation on high fractions of inspired oxygen during anesthesia have the potential to become severely hypoxemic when moved to the recovery stall and provided a lower oxygen fraction in addition to drugs that depress ventilation (e.g. postanesthetic sedation). Severe hypoxemia in experimentally apneic horses is associated with rapid progression to cardiovascular collapse [99], and this scenario in a clinical case is certainly possible. Horses undergoing colic surgery, in which recruitment maneuvers and positive end expiratory pressure were used to maintain arterial oxygen tensions over 400 mmHg, had fewer attempts to stand and shorter recoveries with a higher (though statistically insignificant) median recovery quality score compared to controls that were ventilated conventionally  [94], which would suggest that aggressive attempts to correct arterial oxygen are of benefit at least to recovery from anesthesia. However, as stated earlier, the cardiovascular effects of these ventilation strategies are not benign. In a horse presenting with hemodynamic instability, efforts should be made to augment cardiovascular function prior to and during attempts to improve arterial oxygen tensions.

Aberrations in Body Temperature Definition  Larger patients are less likely to lose the same degree of body heat under anesthesia as a smaller patient due to the smaller surface area to body weight ratio, but it is not uncommon for body temperature to decrease substantially, even in the adult horse during general anesthesia  [100–102]. Although hypothermia is most common, the opposite extreme in body temperature may also occur. Malignant hyperthermia, which is an extreme situation, has only been sporadically reported in the horses exposed to inhalation anesthetics [103–105]. Risk factors for hypothermia  General anesthesia ●● ●● ●● ●● ●● ●●

Cool intravenous fluids Cold operating room and recovery stall surfaces Uncovered limbs Open body cavities (e.g. abdominal surgery) Lack of ability to keep the horse dry Lack of active warming devices

Risk factors for  hyperthermia  Genetic predisposition to

malignant hyperthermia

Pathogenesis  Normal body temperature is controlled by thermoregulatory centers in the brain and reflects the balance of heat generated from metabolic processes and heat dissipated. Anesthesia affects thermoregulatory centers in the brain and also influences generation and dissipation of heat. Due to a decrease in metabolic rate induced by the sleep state of anesthesia, heat generation is decreased. However, in general, heat loss is increased by a number of mechanisms related both to anesthesia and surgery. Cool intravenous fluids and inspired gases, cold tables, surgically clipped and prepped areas, and open body cavities all contribute to this loss of heat. Therefore, in general, most patients regardless of body size tend to lose heat during anesthesia. In addition, horses lose heat when placed on the floor of the recovery stall [100]. Monitoring  Temperature monitoring, though valuable and

very simple to perform, is often ignored in clinical practice. Temperature can be measured either intermittently using a thermometer placed in either the rectum or auricular canal or continually using a thermistor probe placed in the esophagus or rectum.

Prevention  In human medicine, hypothermia is prevented largely through the use of pre-warming techniques. This would be practically difficult to implement and has not been studied in horses. However, other risk factors for hypothermia can be mitigated. Ambient operating room temperatures can be adjusted to the warmest possible, taking into account the comfort of the surgeons. The immediate area around the patient can also be kept warm using heat lamps, though careful attention should be given to the fact that heat lamps can cause burns to both the patient and nearby equipment. Horses can be placed on thoroughly dried and warmed surgical surfaces such as a water bed or heating pad rather than a surgical mat alone. Intravenous fluids can be warmed prior to use via storage in an incubator. Protecting the patient from becoming wet from surgical fluids or flush will mitigate evaporative heat loss. Active warming devices (e.g. forced air warmers) can be used whenever possible, depending on the surgical procedure, with particular attention to covering the extremities. Treatment  Treatment of hypothermia via the use of active warming devices is possible in horses, but is more likely to be successful in small patients and if initiated at the beginning of the surgical procedure. It is especially important for foals and perhaps practically easier to provide active warming. Attention should be given not only to the surgical period but also to the recovery period, where

­Complications During Anesthetic Recover 

warming should continue if possible. In addition, drying wet patients will help prevent continued evaporative heat loss in recovery. Expected Outcome  Under extreme conditions, hypothermia

alters blood viscosity and coagulation pathways and will increase the likelihood of myocardial fibrillation. Smaller decreases in body temperature as likely to be observed in the horse will affect anesthetic dose requirements (MAC is reduced 5–8% per degree centigrade decrease in body temperature) and rate of clearance of anesthetic drugs [106, 107]. This has clinical relevance in that an individual may unknowingly over-anesthetize a patient and likely prolong recovery from anesthesia. Much attention is given to inadvertent perioperative hypothermia in human medicine as it is associated with increased morbidity (e.g. wound infection, coagulopathy) and prolonged hospital stay [108]. It is also associated with shivering in the recovery period, which not only increases metabolic oxygen demand but is also reported to be extremely uncomfortable 109. Although not much work has been done with respect to the complications associated with hypothermia in horses, hypothermia does occur routinely in anesthetized horses and is correlated with both increasing number of attempts and time it takes for a horse to stand in recovery [102].

­ omplications During Anesthetic C Recovery Poor Recovery Quality Definition  Poor recovery quality could be defined in a number of ways, from simply uncoordinated to involving minor or even serious injury. While historically presumed cardiovascular events during the anesthesia period contributed to the mortality rate, recent information suggests that injury in the recovery period is the primary reason for peri-anesthetic mortality in adult horses  [59, 110, 111]. Risk Factors ●● ●● ●●

●● ●● ●● ●● ●●

Length of procedure Temperament of the horse Physiologic status (e.g. systemically compromised colic, lactating mare) Painful procedure Pre-existing long bone fracture Placement of heavy bandages, splints, or casts Slippery or uneven recovery surfaces Light plane of anesthesia on transport to recovery stall

Pathogenesis  It is often said that if an animal has a poor induction, the recovery too will be poor. In the authors’ experience, neither a good nor poor induction has been a consistent predictor of recovery quality. Poor recovery quality or catastrophic injury in recovery likely does not have a single causative factor, and in some cases catastrophic injury can occur in the absence of an otherwise poor recovery (e.g. a horse stands in one relatively quiet attempt but suffers a long bone fracture upon standing). Clearly the temperament of the horse may play a role [112] and learning with repeated anesthesia may play a role in improving recovery [113], but other factors, such as the general well-being of the animal, nature of the procedure, use of analgesic and supportive medications, drainage of the urinary bladder, placement of a cast or heavy bandage, the environment and footing, assistance provided in recovery, etc. may all influence the recovery from anesthesia. Prevention  Risk of catastrophic injury in recovery has resulted in the increasing prevalence, perhaps even routine, use of providing a sedative or tranquilizer to horses recovering from inhalation anesthesia. Studies have compared doses of injectable agents, different injectable agents [114, 115], transitioning from inhaled to injectable agents  [116, 117], and more recently reducing inhaled anesthesia dose during procedures by concurrent use of injectable agents [23, 118. 119]. While largely favorable results support the use of these techniques, poor recoveries sometimes with disastrous consequences to the horse and injury to personnel still occur. Assistance in recovery can take many forms, ranging from basic assistance on the tail to stabilize the animal and helping it rise during attempts to stand to recovery using a pool, air pillow, or sling. While much has been written on these techniques  [120–124], there are no comprehensive studies to support use of any one method when other factors surrounding anesthesia management and logistical considerations (e.g. experience of personnel with the system) are applied. In the authors’ experience, the most broadly applied system and one that can be learned fairly quickly seems to be the use of head and tail ropes to help support and assist the horse to standing. Treatment  The anesthetist should always be prepared for the catastrophic injury in recovery. A dose of sedation and anesthetic induction drugs should be readily available until the horse is safely standing, as treatment might include re-sedating or anesthetizing the horse to facilitate diagnostic testing (e.g. radiographs) and intervention to manage the condition. Humane euthanasia may be necessary, depending on the situation.

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Expected Outcome  Many horses can experience poor recovery quality, such as stumbling, flipping over, or making multiple attempts to stand without apparent harm or only minor injuries. There is obviously potential for long bone fractures to occur and outcome thus depends on the nature and location of the fracture as well as the owner’s willingness to pursue treatment. Numerous studies have described complication rates during equine recovery, which are generally considered better following injectable medications than after inhalation anesthesia [40, 125, 126]. However, the overall reporting of mortality does not seem to have changed significantly, despite newer medications and advances in other aspects of anesthesia management [48]. The reader is referred to Chapter  16: Complications During Recovery from General Anesthesia.

­ ther Complications Associated O with Sedative and Anesthetic Drugs Increased Urine Output Definition  Not necessarily considered a complication in its own right but one that might influence management of standing sedation and anesthesia is the notable increase in urine production following administration of alpha-2 agonist medications to horses. Risk factors  Use of alpha-2 adrenergic agonists Pathogenesis  Xylazine and detomidine have both been shown to increase urine production multi-fold over normal in standing horses  [127–129]. The mechanism by which alpha-2 agonists increase urine production is primarily related to inhibition of anti-diuretic hormone [37]. General anesthesia tends to reduce production  [130] but it still remains above normal values of approximately 0.5 ml/kg/ hour, even in water deprived animals [127]. Monitoring  Urine production can be assessed via the

placement of a urinary catheter and measurement of urine output over the anesthetic period.

Treatment  There is no specific treatment, but diuresis of this magnitude may contribute to dehydration and should be considered when calculating intravenous fluid administration rates during sedation and anesthesia. In addition, horses sedated for standing procedures with alpha-2 adrenergic agonist drugs will often shift body position or attempt to posture to void. Therefore, catheterization of the urinary bladder can be helpful for

longer procedures and is especially recommended in female horses when procedures involve rectal or vaginal manipulation or when constant rate infusions of alpha-2 agonists are used.

Blood Glucose Abnormalities Definition  Hyperglycemia is an effect of alpha-2 adrenergic agonist drugs, which increase blood glucose concentrations for variable durations following administration [128, 131]. On the other hand, hypoglycemia is also possible, especially in foals who are fasted or medically compromised. Risk factors for  hyperglycemia  Use of alpha-2 adrenergic

agonists

Risk factors for hypoglycemia  Neonatal or pediatric patients

(especially fasted)

Pathogenesis  Alpha-2 agonists cause hyperglycemia as a result of decreased insulin release from pancreatic beta cells [37]. Monitoring  Blood

glucose concentrations are often provided by bench top blood gas analyzers. However, glucose can also be easily measured via the use of a handheld glucometer. Although specific brands of glucometers are not necessarily designed for use in equines, some glucometers have been evaluated in studies against bench top analyzers and laboratory standards using both equine whole blood and plasma [132, 133].

Treatment  While no untoward consequences of an alpha-2 agonist related increase in blood glucose have been documented in horses, the anesthetist should be aware of its occurrence. While in other species hyperglycemia may result in diuresis, to date urine glucose data suggests that this is not the routine situation in the horse in this circumstance of drug induced hyperglycemia. Blood glucose concentrations should be carefully monitored in foals during anesthesia, and hypoglycemia should be treated. Depending on the fluid administration rate, 1–5% dextrose in a balanced electrolyte solution will help correct hypoglycemia.

Decreased Gastrointestinal Motility Definition  Many drugs used for management of sedation and anesthesia in the horse negatively influence gastrointestinal motility and may lead to post-anesthesia colic. The reported incidence of post-anesthetic gastrointestinal dysfunction in healthy horses undergoing

­Other Complications Associated with Sedative and Anesthetic Drug  147

elective procedures varies based on whether reduced fecal output, clinical signs of abdominal discomfort, or treatment for abdominal discomfort are used as case definitions but is estimated to be between 2.5% and 10.5% [134]. Risk Factors ●● ●● ●● ●● ●●

Use of anticholinergics Use of opioids Use of alpha-2 adrenergic agonists Pre-anesthetic fasting Post-operative pain

Pathogenesis  Opioids have most notably been associated with decreased gastrointestinal motility, which is a direct effect of stimulation of opioid receptors found throughout the gastrointestinal tract (including the myenteric plexus)  [135, 136]. Alpha-2 adrenergic agonist drugs also play a role in decreasing gastrointestinal motility  [137, 138]. Similar to opioids, their effect is at alpha-2 receptors at the level of the myenteric plexus [139]. Anticholinergic drugs reduce gastrointestinal motility like opioids and alpha-2 agonists by inhibiting contractile neural activity in all segments of the gastrointestinal tract [37]. Pre-operative fasting, while generally considered beneficial to anesthesia management (to reduce gastrointestinal volume and improve both ventilation and oxygenation), may further reduce gastrointestinal motility via decreased colonic myoelectric activity [139]. Much of the information published about risk factors for post-anesthetic colic in horses is conflicting, which may be a result of the retrospective nature of most studies, the lack of large numbers of horses in each study, and the variety of anesthetic and management protocols horses are subjected to. Combining information from several studies, factors found to be associated with the development of postoperative gastrointestinal dysfunction include being an Arabian horse  [140] or racing Thoroughbred  [141], orthopedic surgery [142], orthopedic surgery lasting longer than an hour  [143], out-of-hours orthopedic surgery, administration of morphine  [144], use of sodium penicillin  [141, 145], use of ceftiofur, inhalant anesthesia with isoflurane, having a surgical procedure (vs. MRI) [145], increased arterial lactate, positioning in right lateral recumbency, and post-anesthetic hypothermia [140]. At the same time, these studies also determined that certain factors (some the same as above) were not associated with or were even protective for the development of postoperative gastrointestinal dysfunction, including the use of butorphanol [142], the use of no opioid or butorphanol [144], administration of morphine  [145, 146], the use of any specific anesthetic or peri-anesthetic drugs  [140]. longer

versus shorter anesthetic duration, use of romifidine as a premedication, being sedated before anesthesia on two or more occasions, and the use of procaine penicillin [145]. These differing results indicate that understanding risk factors for post-anesthetic colic is challenging, and further studies are required with larger numbers of horses to fully elucidate causative factors. Prevention  No specific strategy has been proven unequivocally useful in the prevention of post-anesthesia colic, but suggestions are outlined below. To date, studies are not conclusive with respect to the link between the use of opioids and post-anesthetic colic  [134, 141, 143, 145, 146]. However, gastrointestinal stasis is a known complication of opioid use and risk of relevant gastrointestinal dysfunction grows when opioids are used systemically at high doses over long periods of time. Therefore, these drugs should be used judiciously and in regional routes (e.g. intra-articular) whenever possible. Similarly, excessive doses of long-acting alpha-2 agonists given over several hours (e.g. for standing sedation) should be avoided if possible (i.e. long procedures could be staged into two shorter procedures separated by a return to feeding). Anticholinergics, as discussed previously, are recommended to be used with care and only when low heart rate is detrimental, reversal of agents causing bradycardia is not possible, and other methods used to improve hemodynamics have failed. They should be titrated carefully such that the lowest effective dose is used. Use of local anesthetic techniques may be helpful from the standpoint of prevention of post-operative pain (thus aiding a quicker return to normal feeding behavior) as well as to reduce the dose of sedative and systemic analgesic drugs required to complete the procedure. There is also no conclusive recommendation as to the most appropriate pre-operative fasting or post-operative refeeding regimen to prevent post-operative colic, though as mentioned earlier fasting does contribute to decreases in gastrointestinal motility. Monitoring  In many hospitals, it is routine to monitor and

record fecal output in addition to both subjective and physiological indicators of abdominal discomfort in the post-anesthetic period. Early signs of discomfort may be subtle or masked by systemic use of analgesic drugs (e.g. phenylbutazone) in the peri-operative period. Since the consequences of impaired gastrointestinal motility in the horse are potentially dire, observation of behavior and normal fecal production in the recovery period are essential.

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Treatment  In-depth discussion of the treatment of postanesthesia gastrointestinal dysfunction is beyond the scope of this chapter, and management strategies for postoperative ileus have been reviewed elsewhere [147, 148]. Outcome  Post-anesthetic gastrointestinal dysfunction may respond well to medical management or, depending on the severity, could necessitate exploratory abdominal surgery or euthanasia.

Expected

­Summary Complications are associated with sedation and general anesthesia in all species. Some of these are further magnified in the horse as a result of their size, unique associated physiology, and temperament. However, anticipation and management of the same can go a long way toward alleviating significant untoward outcomes.

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16 Complications During Recovery from General Anesthesia Alexander Valverde DVM, DVSc, DACVAA Ontario Veterinary College, University of Guelph, Guelph, Ontario, Canada

O ­ verview Horses have the highest anesthetic mortality risk among veterinary patients. A significant proportion of complications occur during the recovery period. This review summarizes the pre- and intraoperative factors that predispose to higher risk, their pathogenesis, prevention, and/or treatment. These factors include idiosyncratic characteristics of the horse (breed, behavior), cardiorespiratory function, muscle blood flow, and logistic aspects such as proper positioning on the surgery table, anesthetic time, type of surgery, and infrastructure available to facilitate the recovery.

­ ist of Complications Associated L with Recovery from General Anesthesia ●● ●● ●●

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Morbidity and mortality of general anesthesia Risk factors in general Complications associated with recovery from general anesthesia General measures for prevention Pathogenesis in general Musculoskeletal/nervous system –– Myopathy Additional actions Central and peripheral neuropathies –– Central –– Peripheral nerve damage –– Cardiovascular system Respiratory system

bidity risk are often considered in the first 24–48 hours related to the anesthetic/surgery event; therefore, anesthetic mishaps can occur from the time of anesthetic drug administration to the intra- and postoperative period. In horses, all anesthetic periods are considered high-risk and in the immediate recovery period, risk of anesthetic mortality is significantly higher than for other species. ●●

–– 100 times higher than in people (0.01%, 1 in 10,000) –– 9 times higher than in cats (0.11%, 1 in 909) –– 5 times higher than in dogs (0.05%, 1 in 500) –– Similar to rabbits (0.73%, 1 in 137) ●●

The risk increases in critical cases (ASA >3) to 2–10% (1 in 10 to 1 in 50), in horses undergoing emergency laparotomy [1, 4, 6, 7].

­Risk Factors in General A list of risk factors is presented in Box 16.1. These risks are all related to alterations in cardiorespiratory function and muscle blood flow during anesthesia, which may be influenced by the type of procedure performed, the time to complete it, positioning and padding of the horse on the surgery table, and behavior of the horse during the recovery phase. ●●

­Morbidity and Mortality of General Anesthesia ●●

Equine anesthesia has the highest reported risk of mortality among domestic veterinary species. Mortality and mor-

Mortality risk in horses is around 1% (1 case in 100) for ASA 1–2 cases, and significantly higher than in other species [1–9]:

Cardiorespiratory depression during anesthesia impacts the horse systemically and if these changes are not properly addressed during anesthesia, they can directly affect the recovery phase because it also impairs muscle perfusion. Orthopedic surgery to repair fractures is associated with an increased risk of anesthetic-related death when compared to soft tissue surgeries [7. 9].

Complications in Equine Surgery, First Edition. Edited by Luis M. Rubio-Martinez and Dean A. Hendrickson. © 2021 John Wiley & Sons, Inc. Published 2021 by John Wiley & Sons, Inc.

­Pathogenesis in Genera  155

Box 16.1  Factors that contribute to increased risk of complications in recovery. Being a horse Prolonged anesthesia time [8, 11, 13]

­ omplications Associated C with Recovery from General Anesthesia

Lateral versus dorsal for myopathy [20]

Complications can occur at any time during anesthesia and impact the recovery period, directly or indirectly. These complications can lead to immediate outcomes that compromise the horse’s life to different degrees and may result in accidental death or require of humane euthanasia. Complications can also take place in a more delayed fashion (e.g. gastrointestinal disorders) and contribute to morbidity and eventually anesthetic-related deaths. Anesthetic complications mostly affect the following systems:

Dorsal versus lateral for myelomalacia [20, 25]

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Too young (5 years of age) [9] Excitable temperament [11] Inexperience of horse with recovery [12] Higher ASA classification [7] Fracture repair [7. 9] Hypotension (