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Edited by Doherty Second Edition Valverde Reed
A fully updated new edition of this practical guide to managing
Manual of anesthesia in horses and other equids, providing updated and Equine Anesthesia
Equine Anesthesia and Analgesia
expanded information in a concise, easy-to-read format
and Analgesia Manual of Equine Anesthesia and Analgesia provides practitioners and veterinary students with concise, highly practical guidance to anesthetizing horses, donkeys, and mules. Using a bulleted quick-reference format, this popular resource covers the basic physiological and pharmacological principles of anesthesia, patient preparation and monitoring, and the management of sedation and anesthesia. Chapters written by leading veterinary anesthesiologists contain numerous clinical images and illustrations, case examples, tables, diagrams, and boxed summaries of important points.
Now in full color, the second edition features extensively revised and updated information throughout. New sections cover chronic pain, management of horses undergoing MRI, ventilators, nerve blocks for Edited by reproductive surgery, muscle relaxants, various new drugs, paravertebral anesthesia, treatment of pain
Manual of using acupuncture and physical rehabilitation techniques, and more. Up-to-date appendices contain Tom Doherty • Alex Valverde • Rachel A. Reed drug lists and dosages as well as equations related to equine cardiovascular and respiratory systems. This concise, easy-to-follow guide:
• Provides practical, clinically oriented information on anesthetizing equids
• Uses a bulleted format designed for fast access of key information • Offers step-by-step instructions and diagrams of nerve blocks of the limbs, head, and ophthalmic structures • Includes new coverage of topics including regulation of extracellular fluid and blood pressure, acid-base disorders, and hemodynamic effects of autonomic drugs
Manual of Equine Anesthesia and Analgesia, Second Edition, remains a must-have resource for all equine practitioners and veterinary students involved with anesthetizing horses.
The editors
Tom Doherty, MVB, MSc, DACVAA, is Professor (retired) at the College of Veterinary Medicine, University of Tennessee in Knoxville, TN, USA.
Alex Valverde, DVM, DVSc, DACVAA, is Professor at Ontario Veterinary College, University of Guelph in Guelph, Ontario, Canada.
Edition History Blackwell Publishers Ltd (1e, 2006)
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The right of Tom Doherty, Alex Valverde, and Rachel A. Reed to be identified as the authors of the editorial material in this work has been asserted in accordance with law.
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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: Doherty, T. J. (Tom J.), editor. | Valverde, Alex, editor. | Reed, Rachel A., editor. Title: Manual of equine anesthesia and analgesia / edited by Tom Doherty, Alex Valverde, Rachel A. Reed. Description: Second edition. | Hoboken, NJ : Wiley-Blackwell, 2022. | Includes bibliographical references. Identifiers: LCCN 2021034858 (print) | LCCN 2021034859 (ebook) | ISBN 9781119631286 (paperback) | ISBN 9781119631293 (Adobe PDF) | ISBN 9781119631323 (epub) Subjects: MESH: Equidae–surgery | Horses–surgery | Anesthesia–veterinary | Analgesia–veterinary | Handbook Classification: LCC SF951 (print) | LCC SF951 (ebook) | NLM SF 951 | DDC 636.10897–dc23 LC record available at https://lccn.loc.gov/2021034858 LC ebook record available at https://lccn.loc.gov/2021034859
Set in 9.5/12.5pt STIXTwoText by Straive, Pondicherry, India
10 9 8 7 6 5 4 3 2 1 v
Contents
List of Contributors xi Preface xv Acknowledgments xvi
1 Preoperative Evaluation and Patient Preparation 1
The Risk of Equine Anesthesia 1 Tanya Duke-Novakovski Patient Preparation 5 Tanya Duke-Novakovski
2 Serum Chemistry and Hematology 8
Carla Sommardahl
3 The Cardiovascular System 19
Physiology of the Cardiovascular System 19 Tamara Grubb Evaluation of the Cardiovascular System 36 Daniel G. Kenney
4 The Respiratory System 50
Anatomy of the Equine Respiratory System 50 Robert Reed Physiology of the Respiratory System 55 Carolyn Kerr Evaluation of the Respiratory System 67 Tom Doherty Airway Management 68 Tom Doherty Tracheostomy 78 Tanner Snowden and Jim Schumacher vi Contents
5 The Renal System 86
Natalie S. Chow
6 Neurophysiology and Neuroanesthesia 98
Tanya Duke-Novakovski
7 The Autonomic Nervous System 110
Christine Egger
8 Electrolyte and Fluid Therapy 119
Electrolytes 119 Rachel A. Reed Fluid Therapy 125 Christopher K. Smith
9 Acid-Base Physiology 137
Traditional Approach 137 Alex Valverde and Tom Doherty Physicochemical Approach 147 Diego E. Gomez and Alex Valverde
10 Hemostasis and Hemotherapy 155
Hemostasis 155 Kira L. Epstein emotherapy 162 H Kira L. Epstein
11 Thermoregulation 173 Chiara E. Hampton
12 Pharmacology of Drugs Used in Equine Anesthesia 184
Guaifenesin 209 Alicia Skelding Ketamine 210 Alicia Skelding Tiletamine and Zolazepam (TZ) 213 Alicia Skelding Alfaxalone 214 Alicia Skelding Propofol 216 Alicia Skelding Barbiturates 218 Alicia Skelding Intravenous lidocaine 219 Patricia Queiroz-Williams Horse-related drug Regulations in Europe 222 Regula Bettschart-Wolfensberger and Simone K. Ringer
13 Inhalational Anesthetics 223
Rachel A. Reed
14 Local Anesthetics 232
Catherine M. Creighton and Leigh Lamont
15 Neuromuscular Blocking Agents in Horses 244
Manuel Martin-Flores and Daniel M. Sakai
16 Non-steroidal Anti-Inflammatory Drugs and Corticosteroids 250
Non-steroidal Anti-Inflammatory Drugs 250 Stephanie Kleine Corticosteroids 259 Stephanie Kleine
17 Anesthetic Machines and Equipment 266
Rachel A. Reed
18 Positioning the Anesthetized Horse 287
Hui Chu Lin
19 Monitoring the Anesthetized Horse 294
Monitoring the Central Nervous System 294 Joanna C. Murrell Cardiovascular Monitoring 300 Alanna N. Johnson viii Contents
Respiratory Monitoring 310
Alanna N. Johnson Anesthetic Agent Monitoring 323 Alanna N. Johnson Monitoring Temperature 324 Chiara E. Hampton onitoring Neuromuscular Function 328 M Manuel Martin-Flores and Daniel M. Sakai
20 Standing Sedation 333
Catherine M. Creighton
21 General Anesthesia Techniques 339
Regula Bettschart-Wolfensberger and Simone K. Ringer
22 Anesthesia of the Head and Neck 352
Anesthesia of the Head 352 Jim Schumacher, John Schumacher, and Ray Wilhite axillary Nerve Block in Donkeys M 358 Usama Hagag Cervical Plexus Block 363 Luis Campoy
23 Anesthesia of the Eye 369
Daniel S. Ward
24 Anesthesia of the Limbs 376
Jim Schumacher, John Schumacher, and Ray Wilhite
25 Anesthesia of the Perineum and Testicle 396
Pudendal Nerve Block – Electrostimulation Technique 396 Kirsty Gallacher and Luiz Santos udendal Nerve Block – Blind Approach P 399 Jim Schumacher Local Anesthesia for Castration 400 Philip D. Jones
26 Anesthesia of the Abdominal Wall 404
Thoracolumbar Paravertebral Block (TPVB) – Electrostimulation Technique 404 Luiz Santos and Kirsty Gallacher Paravertebral Nerve Block – Blind Technique 406 Alex Valverde Transversus Abdominis Plane Block 409 Alex Valverde and Flavio SA. Freitag Contents ix
Caudal Intercostal Block for Abdominal Surgery (CIBAS) 413
Benjamin Gingold
27 Epidural Analgesia and Anesthesia 416
Alex Valverde
28 Pathophysiology of Pain 425
Rachel A. Reed
29 Pain Recognition in Horses 431
Karina B. Gleerup, Casper Lindegaard, and Pia Haubro Andersen
30 Management of Pain 450
The Pharmacologic Approach to Pain Management 450 Rachel A. Reed ehabilitation Modalities for Acute and Chronic Pain in Horses 456 R Tena L. Ursini Equine Acupuncture 462 Neal Valk
31 Anesthesia of Foals 472
Tom Doherty and Alex Valverde
32 Anesthesia of Horses with Intestinal Emergencies (Colic) 494
Tom Doherty
33 Anesthesia of the Geriatric Horse 501
Reza M. Seddighi
34 Anesthesia and Pregnancy 511
Lydia Donaldson
35 Anesthesia for Equine Imaging 522
Carrie A. Davis
36 Anesthesia of Donkeys and Mules 543
Anatomic, Physiologic, and Behavioral Differences 543 Suzanne L. Burnham Sedation and Anesthesia of Donkeys and Mules 548 Tom Doherty Donkey Pain Assessment Scales 552 Machteld van Dierendonck and Thijs van Loon
37 Remote Capture of Equids 565
Nigel Caulkett x Contents
38 Complications 573 Intraoperative Hypotension 573 Christopher K. Smith and Tom Doherty I ntraoperative Hypertension 580 Tom Doherty ypoxia and Hypoxemia H 582 Rachel A. Reed ypercarbia 588 H Tom Doherty Pulmonary Edema as a Consequence of Airway Obstruction 590 Tom Doherty Endotoxemia 592 Tom Doherty Postanesthetic Myopathy 594 Krista B. Mitchell Neuropathy 599 Rachel A. Reed yperkalemic Periodic Paralysis (HYPP) H 604 Alanna N. Johnson and Rachel A. Reed Malignant Hyperthermia 609 Alanna N. Johnson and Rachel A. Reed Delayed Awakening and Recovery 611 Tom Doherty Paraphimosis and Priaprism 614 Meggan Graves and Jim Schumacher Anaphylactic and Anaphylactoid Reactions 621 Rachel A. Reed Intra-carotid and Perivascular Injections 624 Rachel A. Reed Equine Cardiopulmonary Resuscitation 627 Genevieve Bussieres
39 Recovery from Anesthesia 633
Bernd Driessen
40 Euthanasia 653 Ron Jones and Tom Doherty
Index 661 xi
List of Contributors
Dr. Pia Haubro Andersen, DVM, PhD Dr. Nigel Caulkett, DVM, MVSc, DACVAA Department of Veterinary Clinical Sciences Veterinary Clinical & Diagnostic Sciences Section of Medicine & Surgery University of Calgary, University of Copenhagen Calgary Denmark Alberta, Canada
Dr. Regula Bettschart-Wolfensberger, Dr. med. Dr. Natalie S. Chow, DVM
vet. PhD, DECVAA Department of Small Animal Clinical Sciences Vetsuisse Faculty The University of Tennessee Department of Diagnostics and College of Veterinary Medicine Clinical Services Knoxville Section of Anaesthesiology TN 37996-4545, USA University of Zurich Zurich 8057 Dr. Catherine M. Creighton, DVM, MS, DACVAA Switzerland Department of Companion Animals University of Prince Edward Island Dr. Suzanne L. Burnham, DVM Charlottetown Department of Veterinary Pathobiology Prince Edward Island College of Veterinary Medicine C1A 4P3, Canada Texas A&M University College Station Dr. Carrie A. Davis, DVM, DACVAA TX 77843-4474, USA Irving TX, USA Dr. Genevieve Bussieres, DVM, MSc Department of Small Animal Dr. Machteld van Dierendonck, PhD Clinical Sciences Equine Behaviour Clinic The University of Tennessee Department of Equine Sciences College of Veterinary Medicine Faculty of Veterinary Medicine Knoxville Utrecht University, the Netherlands TN 37996-4545, USA Dr. Tom Doherty, MVB, MSc, DACVAA Dr. Luis Campoy, LV, Cert VA, DECVAA, MRCVS Knoxville Department of Clinical Sciences TN, USA Cornell University College of Veterinary Medicine Dr. Lydia Donaldson, DVM, PhD, DACVAA Ithaca Middleburg NY 14853, USA VA 20118, USA xii List of Contributors
Dr. Bernd Driessen, DVM, DrMedVet., DACVAA, Dr. Karina B. Gleerup, DVM, PhD DECVPT Elleorevej 9 University of Pennsylvania 4000 Roskilde New Bolton Center Denmark Kennett Square PA 19348, USA Dr. Diego E. Gomez, MV, MSc, MVSc, PhD, DACVIM Department of Clinical Studies Dr. Tanya Duke-Novakovski, B VetMed, DACVAA Ontario Veterinary College Department of Veterinary Anesthesia The University of Guelph Radiology and Surgery Ontario, Canada Western College of Veterinary Medicine University of Saskatchewan Dr. Meggan Graves, DVM Saskatoon Department of Large Animal Clinical Sciences Saskatchewan The University of Tennessee S7N 5B4, Canada College of Veterinary Medicine Knoxville Dr. Christine Egger, DVM, MVSc, DACVAA TN 37996-4545, USA Department of Veterinary Anesthesia, Radiology and Surgery Dr. Tamara Grubb, DVM, PhD, DACVAA Western College of Veterinary Medicine Uniontown University of Saskatchewan WA 99179, USA Saskatoon Saskatchewan Dr. Usama Hagag, Dr. med. vet, PhD S7N 5B4, Canada Faculty of Veterinary Medicine Department of Surgery, Anesthesiology and Dr. Kira L. Epstein, DVM, DACVS-LA, DACVECC Radiology University of Georgia Beni-Suef University College of Veterinary Medicine Beni-Suef 62511, Egypt Athens GA 30602, USA Dr. Chiara E. Hampton, DVM, MS, DACVAA Dr. Flavio SA. Freitag, DVM, MSc School of Veterinary Medicine Department of Clinical Studies Baton Rouge Ontario Veterinary College LA 70803, USA The University of Guelph Ontario, Canada Dr. Allana N. Johnson, DVM, DACVAA Department of Comparative, Diagnostic & Dr. Kirsty Gallacher Population Medicine School of Animal and Veterinary Sciences University of Florida Roseworthy Campus Gainesville The University of Adelaide FL 32608, USA Adelaide 5371 Australia Dr. Philip D. Jones, DVM, MS, DACVS-LA Department of Large Animal Clinical Sciences Dr. Benjamin Gingold, DVM, DACVAA The University of Tennessee Turner College of Veterinary Medicine ACT Knoxville Australia, 2612 TN 37996-4545, USA List of Contributors xiii
Dr. Ron Jones, MVSc, FRCVS, DVA, DrMedVet, Dr. Manuel Martin-Flores, MV, DACVAA DECVAA, DACVAA (Hon) Department of Clinical Sciences Oxton, Prenton Cornell University College of Veterinary Merseyside CH43 5UF Medicine England Ithaca NY 14853, USA Dr. Daniel G. Kenney, VMD, DACVIM Health Sciences Centre Dr. Krista B. Mitchell, DVM, DACVAA Ontario Veterinary College Department of Clinical Studies The University of Guelph Ontario Veterinary College Ontario, Canada The University of Guelph Dr. Carolyn Kerr, DVM, DVSc, PhD, DACVAA Ontario, Canada Department of Clinical Studies Ontario Veterinary College Dr. Joanna C. Murrell, BVSc, PhD, DECVAA The University of Guelph Highcroft Veterinary Referrals Ontario, Canada Whitchurch Bristol, UK Dr. Stephanie Kleine, DVM, PhD, DACVAA Department of Small Animal Clinical Sciences Dr. Patricia Queiroz-Williams, DVM, MS The University of Tennessee School of Veterinary Medicine College of Veterinary Medicine Baton Rouge Knoxville LA 70803, USA TN 37996-4545, USA
Dr. Leigh Lamont, DVM, MS, DACVAA Dr. Rachel A. Reed, DVM, DACVAA Department of Companion Animals University of Georgia University of Prince Edward Island College of Veterinary Medicine Charlottetown Athens Prince Edward Island GA 30602, USA Canada Dr. Robert Reed, DVM, PhD Dr. Hui Chu Lin, DVM, MS, DACVAA Department of Biomedical and Diagnostic Department of Clinical Sciences Sciences College of Veterinary Medicine The University of Tennessee Auburn University College of Veterinary Medicine AL 36849, USA Knoxville TN 37996-4545, USA Dr. Casper Lindegaard, DVM, PhD, DECVS Department of Veterinary Clinical Sciences Section of Medicine & Surgery Dr. Simone K. Ringer, PD, Dr. med. vet. University of Copenhagen PhD, DECVAA Denmark Department of Clinical Diagnostics and Services Dr. Thijs van Loon, DVM, PhD, DACVAA Section of Anaesthesiology Division of Anaesthesia and Intensive Care Vetsuisse Faculty Department of Equine Sciences University of Zurich Faculty of Veterinary Medicine Zurich Utrecht University, The Netherlands Switzerland xiv List of Contributors
Dr. Daniel M. Sakai, MV, DACVAA Dr. Tanner Snowden, DVM
University of Georgia Oklahoma Equine Hospital College of Veterinary Medicine Washington Athens OK 73093, USA GA 30602, USA Dr. Carla Sommardahl, DVM, PhD, DACVIM Dr. Luiz Santos, DVM, MS, MANZCVS, DACVAA Department of Large Animal Clinical Sciences School of Animal and Veterinary Sciences The University of Tennessee Roseworthy Campus College of Veterinary Medicine The University of Adelaide Knoxville Adelaide 5371 TN 37996-4545, USA Australia Dr. Tena L. Ursini, DVM, DDACVSMR Dr. Jim Schumacher, DVM, MS, DACVS Department of Large Animal Clinical Sciences Department of Large Animal Clinical The University of Tennessee Sciences College of Veterinary Medicine The University of Tennessee Knoxville College of Veterinary Medicine TN 37996-4545, USA Knoxville TN 37996-4545, USA Dr. Neal Valk, DVM, DACVS Department of Large Animal Clinical Dr. John Schumacher, DVM, MS, DACVIM Sciences Department of Clinical Sciences The University of Tennessee College of Veterinary Medicine College of Veterinary Medicine Auburn University Knoxville AL 36849, USA TN 37996-4545, USA
Dr. Reza M. Seddighi, DVM, PhD, DACVAA Dr. Alex Valverde, DVM, DVSc, DACVAA Department of Large Animal Clinical Sciences Department of Clinical Studies The University of Tennessee Ontario Veterinary College College of Veterinary Medicine The University of Guelph Knoxville Guelph TN 37996-4545, USA Ontario NIG 2W1, Canada
Dr. Alicia Skelding, DVM, MSc, DVSc, DACVAA Dr. Daniel S. Ward, DVM, PhD, DACVO Toronto Animal Health Partners Emergency Department of Small Animal Clinical Sciences and Specialty Hospital The University of Tennessee North York, Ontario College of Veterinary Medicine Canada Knoxville TN 37996-4545, USA Dr. Christopher K. Smith, DVM, DACVAA Department of Small Animal Clinical Dr. Ray Wilhite, MS, PhD Sciences Department of Anatomy, Physiology and The University of Tennessee Pharmacology College of Veterinary Medicine College of Veterinary Medicine Knoxville Auburn University TN 37996-4545, USA AL 36849, USA xv
Preface
The second edition of the Manual of Equine Anesthesia & Analgesia has been updated and rearranged. Most topics have been expanded and new chapters added. Chapters devoted to the sedation and anesthesia of horses undergoing imaging procedures, anesthesia of donkeys and mules, and recognition of pain in horses and donkeys are now included. Case examples of the pharmacologic control of pain are provided, and information on non-pharmacologic treatment of acute and chronic pain using acupuncture and physical rehabilitation techniques have also been added. In addition, a suggested reading list is included for the reader who wishes to seek further information on the topic. This edition of the Manual of Equine Anesthesia & Analgesia strives to deliver relevant informa- tion on the physiologic and pharmacologic principles underpinning the anesthesia of equids, in addition to providing useful information on the clinical practice of anesthesia. The Manual has retained the same easily accessible format of the first edition, and we believe that it will be a useful guide to all those involved in the anesthesia of equids. Tom Doherty Alex Valverde Rachel A. Reed xvi
Acknowledgments
We wish to acknowledge our contributors for providing their expertise, and we greatly appreciate the time and effort they expended on this project. A special word of thanks to the staff at John Wiley & Sons, especially Ms. Erica Judisch, Ms. Susan Engelken, and Ms. Merryl Le Roux, for making this project possible. 1
Preoperative Evaluation and Patient Preparation
The Risk of Equine Anesthesia
Tanya Duke-Novakovski
●● Risks of equine anesthesia have been linked with various conditions and situations and are reviewed in detail elsewhere and summarized in this chapter.
I Risk of equine anesthesia
●● Anesthesia of the horse always involves an assessment of risk.
●● Potential complications range from the less serious (e.g. skin wounds) to the more serious (e.g. long bone fractures, myopathies, and peripheral neuropathies), and to death in some cases. ●● There is also risk of injury to personnel and safe handling should be practiced. ●● The goal of the anesthetist is to minimize the adverse effects (ideally at minimum cost) by: ⚪⚪ Identifying and defining the risk(s).
⚪⚪ Selecting the best strategy for controlling or minimizing the risk(s).
●● Data from single clinics have cited mortality rates of 0.24–1.8% in healthy horses. ●● Data from multicenter studies cite the death rate for healthy horses undergoing anesthesia at around 0.9% (approximately 1 : 100). ●● The overall death rate, when sick horses undergoing emergency colic surgery are included, has been reported to be 0.12% when fatalities were directly related to anesthesia in one study, and 1.9% in another study.
II Classification of physical status (see Box 1.1)
●● Classification of health status is generally based on the American Society of Anesthesiologists
(ASA) system. ●● This system uses information from the history, physical examination, and laboratory find- ings to place horses into one of five categories. ●● The classification allows for standardization of physical status only. ●● The ASA system does not classify risk, although increased risk of complication is associated with a high ASA status. ●● These classifications are not always useful for horses: nevertheless, the system serves as a guide to case management.
ASA 1 Healthy horse does not require intervention (e.g. castration). ASA 2 Horse with mild systemic disease (e.g. mild anemia, mild recurrent airway obstruction) or localized injury (e.g. wound repair). ASA 3 Horse with moderate systemic disease (e.g. stable colic, infected joint). ASA 4 Horse with severe systemic disease (e.g. recent ruptured bladder, endotoxemia). ASA 5 A moribund horse not expected to survive longer than 24 hours (e.g. unstable colic, ruptured bladder of several days duration). E The letter E is added to status 2–5 under emergency conditions.
III Risk factors
A Age and physical status
⚪⚪ The risk increases with age, and horses aged 12 years or older are at an increased risk of mortality. ⚪⚪ Older horses may be more prone to fracture of a long bone in the recovery period, which could result in euthanasia. ⚪⚪ Foals have an increased risk of fatality and this is probably associated with unfamiliarity with neonatal anesthesia, an immature cardiovascular system, and presence of systemic illness. ⚪⚪ Pregnant mares have increased risk of mortality in the last trimester of pregnancy and this is probably associated with a need for emergency surgery. Otherwise, there is no dif- ference between sexes. ⚪⚪ Horses with a high ASA physical status have increased risk of mortality.
B Type of surgery and recovery
⚪⚪ In otherwise healthy horses, the risk of mortality (euthanasia) following fracture repair is highest from repair failure or from fracture of another bone. ⚪⚪ However, long periods of anesthesia typical of fracture repair have also been associated with
increased mortality, and horses presented for fracture repair may be dehydrated and stressed. Emergency surgery (non-colic) carries a 4.25 times higher risk of mortality compared with elective surgery, and for emergency abdominal surgery the risk of fatality is 11.7%. Colic surgery is associated with increased mortality because of a higher ASA physical sta- tus, emergency procedure with less time for stabilization, and use of dorsal recum- bency possibly with episodes of hypotension. Eye surgery, in one institution, resulted in longer recovery times and risk of complications and were associated with long anesthesia time compared to non-ophthalmic procedures. Fluconazole (microsomal P450 enzyme inhibitor) use was associated with increased risk of postoperative colic and longer recovery time. The use of the lowest effective volume of local anesthetic for a retrobulbar block was also recommended (10 ml/500 kg horse). Ophthalmic procedures have been associated with unsatisfactory recovery quality. ⚪⚪ Assisted recovery with ropes can decrease the risk of fracture and dislocation, although
the benefit of assisted-recovery is still debatable.
Preoperative Evaluation and Patient Preparation 3
C Time of day ⚪⚪ Performing anesthesia outside of normal working hours carries an increased risk for horses. This increase in risk is separate from the fact that most of these cases are emergency in nature. ⚪⚪ Surgeries performed between midnight and 6 a.m. carry the highest risk of mortality. This may be due to the nature of the emergency, as well as to staff shortages and personnel fatigue.
D Body position ⚪⚪ Dorsal recumbency was found to increase risk compared to either lateral recumbency, but most “colic” surgeries are performed with the horse in dorsal recumbency. ⚪⚪ An increased risk of postanesthetic myelopathy has mostly been associated with draft breeds between 6 and 24 months of age and dorsal recumbency.
E Drug choice ⚪⚪ Using total inhalational anesthesia regimen in foals (<12 months of age) without pre- medication carries the highest risk. ⚪⚪ Halothane sensitizes the myocardium to circulating catecholamines. Fewer cardiac arrests occurred when isoflurane was substituted for halothane, although overall mortal- ity did not differ between groups because limb fracture in recovery was prevalent for the isoflurane group. ⚪⚪ Isoflurane and sevoflurane may be associated with unsatisfactory recovery, and sedation is often used following anesthesia to reduce the risk of excitable recovery. ⚪⚪ Use of isoflurane and sevoflurane was linked with increased mortality, but this was because these drugs are more likely to be selected for sick horses. ⚪⚪ Not using any premedication is associated with the highest risk, probably owing to increased circulating catecholamines from stress. It may be prudent to premedicate foals before induction of anesthesia, especially when using halothane. ⚪⚪ Acepromazine lowers the risk of mortality when used alone as a premedicant, because it reduces the incidence of ventricular arrhythmias in the presence of halothane. ⚪⚪ No particular injectable induction regimen is associated with greater risk when used with inhalational anesthesia. ⚪⚪ Total intravenous anesthesia (TIVA) is associated with the lowest risk of all, but TIVA is often used for short procedures. TIVA has been associated with reduced stress response.
F Duration and management of anesthesia
⚪⚪ Long periods of anesthesia (>2 hours) with volatile anesthetics are often associated with cardiovascular depression and poor tissue perfusion, leading to problems such as cardiac arrest or postanesthetic myopathy. ⚪⚪ Intraoperative hypotension during anesthesia has clearly been associated with postanes- thetic myopathy, and can still occur with short anesthetic periods. Direct arterial pressure monitoring should be used during lengthy anesthetic periods. ⚪⚪ Postanesthetic myopathy may lead to bone fracture or dislocation. ⚪⚪ Postanesthetic airway obstruction and pulmonary edema may be prevented by keeping the head in a normal position thereby reducing the risk of laryngeal nerve paralysis, and with good airway management in the recovery period. 4 Manual of Equine Anesthesia and Analgesia
Suggested Reading
Arndt, S., Hopster, K., Sill, V. et al. (2020). Comparison between head-tail-rope assisted and unassisted recoveries in healthy horses undergoing general anesthesia for surgeries. Vet. Surg. 49: 329–338. Bidwell, L.A., Bramlage, L.R., and Rood, W.A. (2007). Equine perioperative fatalities associated with general anaesthesia. Vet. Anaesth. Analg. 34: 23–30. Niimura del Barrio, M.C., David, F., Hughes, J.M.L. et al. (2018). A retrospective report (2003–2013) of the complications associated with the use of a one-man (head and tail) rope recovery system in horses following general anaesthesia. Ir. Vet. J. 71: 1–9. Curto, E.M., Griffith, E.H., Posner, L.P. et al. (2018). Factors associated with postoperative complications in healthy horses after general anesthesia for ophthalmic versus non-ophthalmic procedures: 556 cases (2012–2014). J. Am. Vet. Med. Assoc. 252: 1113–1119. Donaldson, L.J., Dunlop, C.S., Holland, M.S., and Burton, B.A. (2000). The recovery of horses from inhalant anesthesia: a comparison of halothane and isoflurane. Vet. Surg. 29: 92–101. Dugdale, A.H.A. and Taylor, P.M. (2016). Equine anaesthesia-associated mortality: where are we now? Vet. Anaesth. Analg. 43: 242–255. Dugdale, A.H.A., Obhrai, J., and Cripps, P.J. (2016). Twenty years later: a single-centre, repeat retrospective analysis of equine perioperative mortality and investigation of recovery quality. Vet. Anaesth. Analg. 43: 171–178. Duke, T., Filsek, U., and Read, M.R. (2006). Clinical observations surrounding an increased incidence of post-anesthetic myopathy in halothane-anesthetized horses. Vet. Anaesth. Analg. 33: 122–127. Grandy, J.L., Steffey, E.P., Hodgson, D.S., and Woliner, M.J. (1987). Arterial hypotension and the development of postanesthetic myopathy in halothane-anesthetized horses. Am. J. Vet. Res. 48: 192–197. Johnston, G.M., Taylor, P.M., Holmes, M.A., and Wood, J.L.N. (1995). Confidential enquiry of perioperative equine fatalities (CEPEF-1): preliminary results. Equine. Vet. J. 27: 193–200. Johnston, G.M., Eastment, J.K., Wood, J.L.N., and Taylor, P.M. (2002). The confidential enquiry into perioperative equine fatalities (CEPEF): mortality results of phases 1 and 2. Vet. Anaesth. Analg. 29: 159–170. Johnston, G.M., Eastment, J.K., Taylor, P.M. et al. (2004). Is isoflurane safer than halothane in equine anaesthesia? Results from a prospective multicenter randomized controlled trial. Equine. Vet. J. 36: 64–71. Leece, L., Corletto, F., and Brearley, J.C. (2008). A comparison of recovery times and characteristics with sevoflurane and isoflurane anaesthesia in horse undergoing magnetic resonance imaging. Vet. Anaesth. Analg. 35: 383–391. Parviainen, A.K.J. and Trim, C.M. (2000). Complications associated with anaesthesia for ocular surgery: a retrospective study 1989-1996. Equine. Vet. J. 32: 555–559. Ragle, C., Baetge, C., Yiannikouris, S. et al. (2011). Development of equine post anesthetic myelopathy: thirty cases (1979-2010). Equine. Vet. Educ. 23: 630–635. Santos, M., Fuente, M., Garcia-Iturralde, P. et al. (2003). Effects of alpha2 adrenoceptor agonists during recovery from isoflurane anaesthesia in horses. Equine. Vet. J. 35: 170–175. Senior, M. (2005). Post-anesthetic pulmonary oedema in horses: a review. Vet. Anaesth. Analg. 32: 193–200. Young, S.S. and Taylor, P.M. (1990). Factors leading to serious anaesthetic related problems in equine anaesthesia. J. Ass. Vet. Anaesth. 17: 59. (abstr). Young, S.S. and Taylor, P.M. (1993). Factors influencing the outcome of equine anaesthesia: a review of 1,314 cases. Equine. Vet. J. 25: 147–151. Preoperative Evaluation and Patient Preparation 5
Patient Preparation Tanya Duke-Novakovski
I Preparation of the horse
A Evaluation ⚪⚪ History and physical examination findings help with evaluation of health. ⚪⚪ Many emergency cases, especially intestinal emergencies, are in cardiovascular shock and must be stabilized as much as possible prior to induction of anesthesia.
B Laboratory tests ⚪⚪ In normal horses undergoing elective surgery, there is generally no value in performing extensive laboratory tests. ⚪⚪ In emergency cases, performing laboratory tests such as electrolyte and metabolic acid- base status may be vital to the management of the case (e.g. a foal with uroabdomen).
C Physical examination ⚪⚪ During the examination, attention should be directed to the neurological, cardiovascular, and respiratory systems. ⚪⚪ Musculoskeletal problems, which may affect recovery, should be considered, and a plan should be made to assist recovery if deemed necessary.
D History ⚪⚪ May reveal information that affects case management. ⚪⚪ A recent history of coughing may indicate a viral infection of the airway, in which case elective surgeries should be postponed until one month following resolution of clini- cal signs. ⚪⚪ Owners might report that the horse previously had a “bad” or “over” reaction to an anes- thetic or sedative drug. These concerns should be investigated.
E Fasting ⚪⚪ Fasting (~12 hours) was previously advised because of the potential benefits for lung function and the reduced risk of stomach rupture from trauma at induction or recovery. ⚪⚪ Many equine hospitals do not fast horses prior to elective surgery. In one study, the PaO2 values during anesthesia were not significantly better in fasted versus non-fasted horses, and not fasting might reduce the incidence of postanesthetic colic due to changes in gas- trointestinal motility. ⚪⚪ However, it is generally the case that grain is removed. ⚪⚪ Water should be made available up to the time of surgery. 6 Manual of Equine Anesthesia and Analgesia
F Medications ⚪⚪ It is best to administer all ancillary drugs (e.g. antimicrobials, anti-inflammatories) prior to sedation. Sodium penicillin can reduce systolic arterial pressure by 8–15 mmHg in anes- thetized horses. If antimicrobials are administered during the anesthetic event, this effect can be minimized by administering the drug slowly.
G Jugular catheter ⚪⚪ An intravenous (IV) catheter should always be placed prior to anesthesia. ⚪⚪ This reduces the likelihood of perivascular injection and provides ready access for further IV anesthetic or emergency drugs.
H Flushing the oral cavity
⚪⚪ It is important to flush food debris from the oral cavity, especially if the airway is to be intubated (see Figure 1.1).
I Removal of shoes ⚪⚪ Removal of shoes prevents damage to the horse and hospital flooring. –– However, removal of shoes is not popular with owners. An alternative is to apply band- age material or tape to improve grip and to cover metal points. ⚪⚪ Certainly, loose shoes and nails should be removed. ⚪⚪ Removal of shoes and metallic debris is necessary when an MRI is to be performed.
Figure 1.1 Rinsing of the mouth with water prior to induction
of anesthesia using a large dosing syringe. Preoperative Evaluation and Patient Preparation 7
Suggested Reading
Bailey, P.A., Hague, B.A., Davis, M. et al. (2016). Incidence of post-anesthetic colic in non-fasted adult equine patients. Can. Vet. J. 57: 1263–1266. Dobromylskyj, P., Taylor, P.M., Brearley, J.C. et al. (1996). Effect of pre-operative starvation on intra- operative arterial oxygen status in horses. J. Vet. Anaesth. 23: 75–77. Hubbell, J.A.E., Muir, W.W., Robertson, J.T., and Sams, R.A. (1987). Cardiovascular effects of intravenous sodium penicillin, sodium cefazolin, and sodium citrate in awake and anesthetized horses. Vet. Surg. 16: 245–250. Toews, A.R. and Campbell, J.R. (1997). Influence of preoperative complete blood cell counts on surgical outcomes in healthy horses: 102 cases (1986-1996). J. Am. Vet. Med. Assoc. 211: 887–888. 8
Serum Chemistry and Hematology
Carla Sommardahl
●● As previously mentioned, there is little value in performing laboratory tests for healthy horses undergoing elective procedures. ●● However, when indicated, the appropriate tests should, ideally, be performed before general anesthesia is induced. Nevertheless, this may not always be feasible in emergency situations.
I Complete blood count (CBC)
A Erythrocytes ○○ Evaluation of erythrocyte numbers can begin with a determination of the packed cell volume (PCV) or hematocrit (HCT), which measure the percentage of the volume of whole blood that the red blood cells (RBCs) occupy. ○○ Erythrocyte numbers are 6.9–10.7 x 1012/l, which represent a normal PCV of 35–45% and a normal hemoglobin of 12–15 g/dl. ○○ A stained blood smear can be used to evaluate RBC morphology and the presence of infectious organisms on the RBCs. ○○ Increased RBC numbers (erythrocytosis) is most commonly associated with hemoconcen- tration – this is called a relative erythrocytosis as there is no increase in RBC mass. –– Splenic contraction can cause a transient increase in circulating RBC mass. ○○ In rare cases, there is an increase in numbers due to an increase in RBC production, abso- lute erythrocytosis. –– Absolute erythrocytosis is further categorized as primary, as in polycythemia vera, and secondary, as results from chronic hypoxemia. ○○ Decreased RBC numbers (anemia) can be caused by increased removal from the circula- tion by blood loss or destruction (hemolysis); or by decreased production by the bone marrow. –– Intravascular hemolysis is accompanied by a decrease in hemoglobin concentration; however, extravascular hemolysis is harder to confirm. –– Decreased production with iron deficiency secondary to chronic inflammation is a common cause of nonregenerative anemia in the horse, and is characterized by micro- cytic hypochromic RBCs and decreased RBC indices.
–– Red cell distribution width (RDW) – a measure of RBC variation in size and volume -is used to detect RBC regeneration and is interpreted in conjunction with other values on the complete blood count (CBC).
B Leukocytes ○○ Granulocytes (neutrophils, eosinophils, basophils, and mast cells), monocytes, mac- rophages, and lymphocytes are important for immune function, and changes in their numbers reflect a response to a disease process. ○○ Total leukocyte count is 5.1–11.0 x 109/l. ○○ Neoplasia, bone marrow disease, or functional defects can cause a decrease or increase in leukocyte numbers.
Neutrophils –– Changes in numbers and morphology are important in evaluating the response to systemic inflammation, infection, and stress. –– However, the neutrophil count can be normal in the presence of inflammation or infection. –– Reference values include 2.8–7.7 x 109/l segmented neutrophils and 0.0–0.2 × 109/l bands. –– Neutrophilia is often associated with chronic bacterial infections. –– Neutropenia in adult horses is most often associated with endotoxemia (and other bacterial by-products). –– Neutropenia in foals is most commonly associated with sepsis and systemic inflammation.
Eosinophils –– Reference values are 0.0–0.7 × 109/l. –– Eosinophilia is rare in horses. Conditions to rule out include: ▪▪ Parasitism with cyathastomes. ▪▪ Eosinophilic colitis, enteritis, or multisystemic disease.
Lymphocytes –– Reference values are 1.3–4.7 × 109/l. –– Lymphopenia: Glucocorticoid release or administration, viral infection, old age, and immunodeficiency in foals (e.g. combined immunodeficiency disease in Arabian or Arabian crossbred foals). –– Lymphocytosis: epinephrine release or administration, exercise, equine herpesvirus 2 (foals), leukemia.
Monocytes and Basophils
–– Reference values for monocytes are 0.1–0.8 × 109/l. –– Monocytosis: Chronic inflammation, use of corticosteroids. –– Reference values for basophils are 0.0–0.1 × 109/l.
C Platelets ○○ The normal platelet count for horses is 75 000–300 000/μl. ○○ Platelets function in hemostasis, inflammatory responses, immunity, tissue regeneration, and disease pathology. 10 Manual of Equine Anesthesia and Analgesia
Thrombocytosis (platelet count >400 000/μl)
Reactive or Secondary: –– Age < 3 years, intact males, pyrexia, infectious, or inflammatory conditions. –– Platelet count: 400 000–850 000/μl. Primary or Clonal: –– A rare chronic myeloproliferative disorder. –– Platelet count >1 000 000/μl.
●● Point of care (POC) analyzers have made the evaluation of chemistry, electrolyte, and blood gas values available rapidly as stall-side or immediate vicinity testing (see Figures 2.1 and 2.2).
Figure 2.1 Bench top point-of-care blood analyzer, Source: NOVA Biomedical. Serum Chemistry and Hematology 11
●● Specific reference ranges from the laboratory or analyzer conducting the analysis should be utilized. ○○ Reference ranges for foals should be used based on age.
○○ Reference ranges for donkeys (asses, burros), mules, and hinnies should be used accordingly.
A Creatine kinase (CK)
○○ Also called creatine phosphokinase (CPK). ○○ The reference range for the horse is 108–430 U/l. ○○ CK is a specific indicator of muscle damage. –– It is a “leakage” enzyme released secondary to myocyte damage or death. ○ Serum concentrations increase quickly following myocyte damage. –– In contrast to aspartate aminotransferase (AST) concentrations which increase more slowly and persist for longer (see below). ○○ CK has a short half-life (hours); thus, serum concentrations decrease quickly after an episode. ○○ Urine will be positive for blood on test strips if myoglobin is present. –– Myoglobin and free hemoglobin have peroxidase-like activity, which results in oxygen liberation from organic peroxide in the reagent strip, causing a color change in the strip. –– The urine may be “coffee” colored.
Mild increases in CK (1000–5000 U/l) may result from:
–– Recumbency, trailer ride, recent exercise, or intramuscular injections. –– Consider a diagnosis of mild exertional rhabdomyolysis (ER) and/or polysaccharide storage myopathy (PSSM) if the above conditions are not applicable.
Moderate (~5000 U/l) to severe increases in CK (>10 000 U/l):
–– Severe cases of ER may have associated CK values >100 000 U/l. 12 Manual of Equine Anesthesia and Analgesia
–– These high values may be associated with a traumatic event, but may occur following general anesthesia. Note: Because myoglobin may cause renal tubular damage, treatment may be indicated.
B Aspartate aminotransferase (AST)
○○ AST is a “leakage” enzyme released secondary to myocyte or hepatocyte damage or death. –– Small amounts are also present in myocardial cells. ○○ Increased AST values in horses are most commonly associated with skeletal mus-
cle damage. –– The reference range for the horse is 160–400 U/l. ○○ Serum AST may also increase significantly in horses in early training.
○○ AST values in foals may be greater than adult values for many months.
–– This increase may be related to muscle growth.
○○ Small amounts are present in RBCs.
–– Thus, hemolysis can cause small increases in serum AST.
○○ AST in serum increases more slowly (peak 6–12 hours) than does CK after muscle injury.
○○ It has a long half-life (~seven days) in horses compared to other domestic species, and
serum concentrations fall slowly (three to four days to return to normal) after an episode. Note: AST activity will remain increased after CK activity has returned to normal. ○○ AST values should be interpreted in association with CK and other liver enzymes (Sorbitol
○○ Serum AST activity can also increase with in vivo or in vitro hemolysis.
C Gamma glutamyl transferase (GGT)
○○ GGT resides in the cell membranes of all somatic cells, but its greatest activity is in biliary epithelial cells, pancreatic acinar cells, and renal tubular epithelial cells. ○○ GGT is a cell surface glycoprotein and is a liver canalicular enzyme, and it is induced by dilation of the biliary tree. ○○ It has multiple functions including the regulation of the anti-oxidant glutathione. ○○ Increased GGT activity in serum is usually an indication of hepatobiliary toxicity, espe- cially cholestasis. ○○ Bile accumulation (cholestasis), biliary hyperplasia, and some drugs (e.g. phenobarbital, furosemide, phenytoin, and cimetidine) increase serum GGT activity. ○○ GGT has a long half-life (approximately three days), thus serum concentrations fall slowly after an episode. ○○ Chronic liver disease associated with hepatocyte destruction, fibrosis, and biliary hyper- plasia are associated with severe increases in GGT. ○○ Right dorsal displacement of the colon causes an increase in serum GGT activity by impeding the outflow of bile. ○○ Proximal enteritis causes increases in AST and GGT activity secondary to ascending infection of the biliary tract and/or liver damage from systemic effects such as endotox- emia and hypovolemia. ○○ Reference range: Adult horses 6–30 U/l. ○○ The normal range for burros, donkeys and asses may be 2–3 times higher, and mules and hinnies may be two times higher than values for horses. Serum Chemistry and Hematology 13
○○Foals have a higher reference range than adults for the first one to two months of life. –– Unlike in ruminant neonates, this is not due to ingestion of colostrum as GGT activity is low in mare’s colostrum. –– The increased serum GGT activity in foals in the first month of life seems to be due to endogenous sources. Note: Idiopathic increases in GGT occasionally occur in young, apparently healthy Thoroughbred horses. The cause is unknown. These horses may exhibit poor performance.
Urinary GGT ○○ GGT is not excreted by glomerular filtration; thus, its presence in urine indicates acute damage to tubular epithelial cells. ○○ GGT appears early in the urine when there is acute tubular damage, and this occurs prior to the development of azotemia. ○○ However, urinary GGT activity decreases quickly after an acute episode of tubular injury, even in the presence of ongoing tubular impairment. ○○ To allow for the effect of urine flow, GGT concentrations in the urine are generally expressed as a ratio to urinary creatinine concentrations.
D Alkaline phosphatase (ALP)
○○ ALP is present in biliary epithelial cells, hepatocytes, bone, placenta, and intestine. ○○ The reference range for the horse is 119–329 U/l. ○○ Activity originates from induction similar to GGT, but it is not liver specific. –– However, most serum ALP is derived from the liver, and the remainder is from bone, and a small amount from intestine. ○○ Increase in ALP activity indicates cholestasis from intra or extrahepatic causes. –– But increases are more likely if the obstruction is extrahepatic. ○○ Intestinal lesions can also increase ALP activity. ○○ Bone growth causes an increase in serum ALP activity. ○○ ALP in serum is highest at birth and decreases over the first month to adult range by two to four years. –– The increased ALP activity in neonatal foals may be of placental origin.
E Sorbitol (Iditol) dehydrogenase (SDH)
○○ SDH is a cytoplasmic enzyme, and it acts as a catalyst in the conversion of sorbitol to fructose. ○○ SDH activity is low, and the majority comes from the hepatocyte. ○○ SDH is a “leakage” enzyme released when hepatocytes are damaged. ○○ Thus, SDH is considered a specific indicator of liver damage, especially acute damage. ○○ SDH has a short half-life (hours), so serum concentrations fall quickly. –– It is generally not increased in chronic liver disease. ○○ It is a labile enzyme, and its activity decreases with time. –– However, it is stable in serum for up to five hours when refrigerated. ○○ Reference range: 1–8 U/l.
F Total bilirubin (TBIL)
○○ Increased TBIL in serum is an indicator of hepatic dysfunction, hemolysis, or reduced feed intake. 14 Manual of Equine Anesthesia and Analgesia
○○ TBIL may be subdivided into unconjugated (indirect) bilirubin, and conjugated (direct) bilirubin. ○○ The reference range for the horse is 21–57 μmol/l for TBIL; 2–10 μmol/l for conjugated bilirubin, and 18–52 μmol/l for unconjugated bilirubin. ○○ Hepatic dysfunction causes both indirect and direct concentrations to rise. –– If direct is greater than 8% of total, liver disease should be suspected as a contributor to the increase. ○○ Biliary obstruction (e.g. cholelithiasis) increases the direct to indirect ratio. ○○ Hemolysis raises the serum indirect concentration. ○○ Reduced feed intake raises the serum indirect concentration as a result of slowed clear- ance of bilirubin from the blood rather than from its overproduction. However, the cause is uncertain. –– Ligandin, a protein responsible for bilirubin uptake into the liver may be decreased in the fasting horse, as has been demonstrated in rats. –– Free fatty acids may play a role in fasting hyperbilirubinemia, and horses develop sig- nificant hyperlipidemia during fasting. This may result in competition for carrier proteins. –– Increases in unconjugated bilirubin occur after 12 hours of fasting. ○○ Neonates have higher bilirubin values due to immaturity of liver processing. –– This can lead to kernicterus, resulting from unconjugated bilirubin causing neurologic damage. However, this condition is extremely rare in foals, and may be more likely to occur in a foal with neonatal isoerythrolysis.
G Serum bile acids (SBA)
○○ Bile acids are synthesized and secreted by the liver. ○○ Bile acids are removed from the portal blood by hepatocytes, and SBA concentrations increase as hepatic function decreases. ○○ Increase in SBA concentration is an indicator of hepatic dysfunction. ○○ Reference range: 0–20 μmol/l. ○○ Bile acids are not affected by fasting. ○○ Only a single blood sample is required instead of pre-and post-feeding samples, as bile is released continuously because the horse lacks a gallbladder.
H Blood urea nitrogen (BUN) and creatinine (Cr)
○○ Increased BUN and or Cr indicates that the horse suffers from either pre-renal, renal, or post-renal azotemia. ○○ Reference range for BUN is 4.2–8.9 mmol/l and for Cr is 80–130 μmol/l. ○○ In contrast to urea nitrogen, Cr is not reabsorbed within the tubules, so serum Cr concen- trations provide a more accurate measurement of glomerular filtration rate (GFR) than does BUN. ○○ Neonates have higher Cr values, and the value declines over the first week of life.
Pre-renal azotemia ○○ Occurs when the increases in BUN and Cr results from a decrease in renal blood flow and the associated decrease in GFR. Serum Chemistry and Hematology 15
○○ Significant (>75%) decreases in GFR are required before the BUN is increased, especially early in disease. –– Most commonly results from dehydration and circulatory shock. ○○ When renal function is adequate (pre-renal), azotemia is accompanied by a urine specific gravity (USG) > 1.025. –– This indicates that the kidney has the ability to concentrate the urine. ○○ Uroperitoneum secondary to bladder rupture in foals also causes pre-renal azotemia.
Renal azotemia ○○ Occurs when the GFR is low due to acute or chronic kidney injury. ○○ BUN may be low because less of the filtered urea is re-absorbed in the proximal tubule. ○○ Serum Cr increases as filtration decreases. ○○ Diagnosed by concurrently measuring the USG. –– The presence of azotemia in a patient that cannot concentrate their urine (USG < 1.020) indicates kidney injury.
Post-renal azotemia ○○ Is associated with mechanical (e.g. uroliths) or functional (e.g. neurogenic bladder dys- function) obstruction of the urinary tract. ○○ It is uncommon in horses.
III Plasma proteins
●● Blood consists of plasma and solid components.
●● Plasma comprises about 55% of the blood volume. ●● Plasma contains about 90% water, and the remaining 10% consists of ions, proteins, dis- solved gases (primarily nitrogen, oxygen, and carbon dioxide), nutrients, and wastes. ●● Total protein reference range for adult horse: 6.5–7.5 g/dl. ○○ Plasma protein value is approximately 0.3–0.5 g/dl greater than serum protein.
●● The proteins in plasma include the globulins, albumin, fibrinogen, and coagulation factors. ●● A hand-held refractometer can be used to measure total solids, which are an estimate of total protein; however, the readings can be affected by other substances in the plasma. ○○ This is because refractometer scales are calibrated against normal serum, and values of
many non-protein solutes (e.g. electrolytes) vary in the population.
○○ Thus, it may be prudent to evaluate albumin and globulin concentrations separately in
some disease states.
A Albumin ○○ Albumin is the main protein present in plasma. ○○ The reference range is 2.7–3.7 g/dl. ○○ Its main function is the regulation of the colloidal osmotic pressure (COP) of blood. ○○ It accounts for 75–80% of the COP of normal plasma, although it only comprises 50–60% of the total protein content of plasma. ○○ The oncotic effect of albumin is enhanced by its ability, due to its negative charge, to attract cations, particularly Na+. –– This is termed the Gibbs-Donnan effect. 16 Manual of Equine Anesthesia and Analgesia
○○ Albumin is the smallest plasma protein in molecular weight (~66 kDa).
○○ Albumin binds water, ions, fatty acids, hormones, bilirubin, and therapeutic compounds. ○○ It is synthetized by the liver and has a plasma half-life of approximately 19 days in the horse. ○○ Albumin is classified as a negative acute phase reactant because its production is down- regulated during inflammation.
Hypoalbuminemia can result from:
○○ Increased loss (most common cause). –– Gastrointestinal (GI) (e.g., bacterial-induced colitis). –– Vasculitis, peritonitis, and pleuritis. –– Renal – due to glomerular disease. ○○ Reduced synthesis. –– End-stage or diffuse liver disease. –– Chronic inflammation. ○○ Excessive catabolism –– Most likely due to starvation. –– Plasma proteins are a rapid source of replacement for tissue proteins. ○○ Low dietary protein intake. ○○ Hypoalbuminemia may result in edema depending on the severity of albumin loss and rapidity of onset.
B Globulins ○○ The reference range is 2.1–3.2 g/dl. ○○ The globulin fraction of plasma proteins comprises dozens of proteins including: –– Carrier proteins. –– Complement. –– Immunoglobulins (IgGs). –– Enzymes. ○○ Includes α, β, and γ globulins, from smallest to largest. ○○ Globulins are large molecules (~90–150 kDa) in comparison to albumin. ○○ Reference range for α1 is 0.1–0.2 g/dl and for α2 is 0.6–0.8 g/dl. ○○ Reference range for β1 is 0.3–0.8 g/dl and for β2 is 0.2–0.9 g/dl. ○○ Reference range for γ is 0.5–1.3 g/dl. ○○ α and β globulins are synthetized in the liver. ○○ γ globulins are synthetized in lymphoid tissue by plasma cells. ○○ γ globulins are a major class of IgG.
Hyperglobulinemia ○○ Is associated with chronic disease, such as the presence of as an abscess, intestinal para- sites, or a tumor.
Hypoglobulinemia ○○ Malnutrition can result in a decrease in total globulins due to decreased synthesis. ○○ In rare cases, a congenital immune deficiency might be the cause of hypoglobulinemia. Serum Chemistry and Hematology 17
C Fibrinogen ○○ Fibrinogen is an important soluble glycoprotein that is synthetized by the liver. ○○ It is a plasma clotting factor precursor which is converted to fibrin on contact with a sticky surface. –– The fibrin threads formed in this way trap platelets to form the primary platelet clot on which a stable blood clot is formed by the process of coagulation. ○○ Fibrinogen is a positive acute phase reactant, and it can be used to diagnose and monitor inflammatory conditions. ○○ Reference range is 2–4 g/l. ○○ Plasma fibrinogen concentrations can increase up to 10-fold in an inflammatory process. –– The half-life of fibrinogen is ~three days. ○○ Foals may have increased concentrations up to six months of age. ○○ Pregnant mares may have increases of up to 40%, and fibrinogen may further increase in the immediate postpartum period, before returning to normal in about two weeks post-foaling.
IV Lactate
●● Hyperlactatemia (>2 mmol/l)
Type A –– Is due to inadequate tissue perfusion and oxygen depletion. ◾◾ e.g. hypovolemia, septic shock, anemia. Type B –– Is associated with increased lactate production in patients with underlying diseases, but with normal tissue perfusion. Type B1 –– Is associated with sepsis, neoplasia, endocrine disease, hepatic disease, and renal failure. Type B2 –– Is associated with a number of toxins and pharmaceuticals. ◾◾ e.g. salicylates, epinephrine, norepinephrine, bicarbonate. Type B3 –– Results from genetic metabolic abnormalities. ◾◾ e.g. glycogen storage disease. ●● L-lactate ○○ It is produced by mammalian cells, and can be used as a marker of hypoxia or decreased
tissue perfusion. ○○ It is the form of lactate measured by POC analyzers.
○○ In colic cases, a high lactate concentration in blood and peritoneal fluid is indicative of a
surgical lesion. ○○ In horses with colic, increases in L-lactate concentrations in the peritoneal fluid and
plasma are associated with intestinal ischemia and increased mortality.
○○ L-lactate measurement has potential application for diagnosis, monitoring, and
prognostication. 18 Manual of Equine Anesthesia and Analgesia
●● D-lactate (not routinely measured)
○○ It is a stereoisomer of mammalian L-lactate.
○○ It is not produced by mammalian cells.
○○ Rather, it is product of bacterial fermentation.
○○ D-lactate is not metabolized in mammals.
–– D-lactate produced in the gut can be measured unchanged in peripheral blood.
○○ D-lactate concentrations in the blood may increase in patients with intestinal ischemia.
○○ In colic cases, plasma D-lactate is poorly correlated with plasma L-lactate.
○○ On the other hand, peritoneal D-lactate concentration has a strong correlation with
peritoneal L-lactate. ○○ Furthermore, peritoneal fluid D-lactate is highly sensitive in detecting horses with
strangulating obstructions of the intestine.
Suggested Reading
DeNotta, S. and Divers, T. (2020). Clinical pathology in the adult sick horse: the gastrointestinal system and liver. Vet. Clin. North Am. Equine. Pract. 36: 105–120. Lester, S., Mollat, W., and Bryant, J. (2015). Overview of clinical pathology and the horse. Vet. Clin. North Am. Equine. Pract. 31: 247–268. Newman, A. (2020). Practical tips on sample handling for hematology, chemistry, and cytology testing for equine patients: getting more bang for your buck. Vet. Clin. North Am. Equine. Pract. 36: 1–14. Tennet-Brown, B. (2012). Interpreting lactate measurement in critically ill horses: diagnosis, treatment, and prognosis. Compend. Contin. Educ. Vet. 34: E2. 19
The Cardiovascular System
Physiology of the Cardiovascular System Tamara Grubb
●● The cardiovascular system consists of three components (heart, vessels, blood/plasma) whose ultimate goal is to work in concert with the respiratory system to deliver oxygen to the work- ing cells. ●● Tissue oxygen delivery (DO2) is determined by both the volume of blood pumped to the cells (cardiac output or “Q”) and the oxygen content of the blood (CaO2). ●● Anesthetic drugs can drastically alter cardiovascular function and have a global impact on organ function via decreased DO2.
I Anatomy
A Chambers ○○ The equine heart is a typical mammalian heart with four chambers: two atria and two ventricles.
Atria ○○ Primary function is to receive and store blood that will empty into the ventricles dur- ing early diastole. ○○ Oxygen depleted blood from the body is delivered to the right atrium via the cranial and caudal vena cavae and from the myocardium via the coronary sinus and car- diac veins. ○○ Oxygen rich blood from the lungs is delivered to the left atrium via pulmonary veins.
Ventricles ○○ The primary function is to pump blood into the high-pressure systemic (left ventricle) and low-pressure pulmonary (right ventricle) circulations. ○○ As described by the Law of LaPlace (see Table 3.1), the thick-walled, conical left ven- tricle is better suited for high-pressure pumping than the thin-walled, flattened right ventricle.
Name of Law Formula Formula components Application
LaPlace T=PxR ●● T = Tension For any given pressure, the tension developed ●● P = pressure by the wall of the ventricle increases as the ●● R = radius radius of the cylinder increases. RV ●● The left ventricle has a much greater radius than the right ventricle and thus is able to develop greater tension (or force). LV ●● (LV = left ventricle; RV = right ventricle)
Ohm’s Q=∆P/R ●● Q = blood flow Blood flow is directly proportional to pressure
●● ∆P = the pressure difference difference and inversely proportional to (P1-P2) between the two ends resistance. of the vessel. ●● R = resistance P = 100 mmHg Q = 0% R = 100mmHg ●● Thus, the difference in pressure between the two ends of the vessel determines the rate Q = 50% R = 50mmHg of flow and not the absolute pressure in the P = 100 mmHg vessel. Poiseuille’s Q=π∆Pr4 / ●● Q = blood flow ●● Blood flow is directly proportional to the 8ηl ●● ∆P = the pressure gradient 4th power of the radius of the vessel as long ●● r = the radius of the vessel as the flow is laminar. ●● η = the viscosity of the blood ●● Slight changes in the diameter of a vessel cause tremendous changes in flow because ●● l = the length of the vessel blood flowing in the middle of the vessel ●● π relates to the vessel radius flows freely, whereas blood at the periphery flows slowly because of friction caused by the endothelium of the vessel wall. In a small vessel, a large percentage of the blood is in contact with the vessel wall so the rapidly flowing central stream of blood is absent. r=1 ●● Changes in vessel diameter greatly r4 (Q) = 1 influence blood flow (Q). Perfusion pressure r=2 r4 (Q) = 16 (P) is constant r=4 r4 (Q) = 256
Starling’s None None ●● Within physiological limits, stretched cardiac
muscle (and other forms of striated muscle like skeletal muscle) will contract with greater force. Positive inotrope effect ●● The force of contraction of the cardiac muscle is proportional to its initial length. ●● When the diastolic filling of the heart is Stroke Volume
increased or decreased with a given
Normal curve volume, the displacement of the heart increases or decreases with this volume. ●● Excessive stretch can result in decreased contractility. Negative inotrope effect
Right Atrial Pressure or
Ventricular End-Diastolic Volume (Pressure) The Cardiovascular System 21
Atrio-ventricular valves ○○ They connect atria and ventricles. ○○ Tricuspid valve is between the right atrium and right ventricle. ○○ Mitral valve is between the left atrium and left ventricle.
Semilunar valves ○○ They connect ventricles to the outflow tracts. ○○ Aortic valve is between the left ventricle and aorta. ○○ Pulmonary valve is between the right ventricle and pulmonary artery.
B Structural or “skeletal” components of the heart
○○ Myocardium – muscle layer (striated muscle) of atria and ventricles. ○○ Endocardium – internal lining of the heart chambers, valves and blood vessels. ○○ Epicardium – external lining of the myocardium, continuous with pericardium; secretes pericardial fluid.
C Neural input to the heart
○○ Atria are highly innervated by sympathetic and parasympathetic fibers. –– Controls heart rate (HR) and contractility. –– Parasympathetic fibers – decrease rate and contractility. –– Sympathetic fibers – increase HR and contractility. ○○ Ventricles are primarily innervated by sympathetic fibers. –– They continually discharge to maintain a strength of ventricular contraction 20–25% greater than what would occur with no sympathetic input.
II Cardiac contractions
A Initiation ○○ Unlike most physiologic systems, neither the autonomic nor motor neurons are nec- essary for initiating cardiac contractions. ○○ The heart can continue beating in the absence of outside neural control because the cells of the specialized electrical conducting system of the heart are capable of auto- matic rhythmical depolarization or “self-excitation.” This is due to: –– Cell membranes that are “leaky” or permeable to sodium ions. –– Increased permeability to potassium and calcium ions also plays a role in the sponta- neous depolarization of the pacemaker cells. –– A resting cell membrane potential that is not adequately negative to keep sodium channels closed. –– The resting membrane potential of cardiac conducting cells is −60 to −70 millivolts (mV) and that of the SA node is −55 to −60 mV (compared to −90 mV for other cell membranes). 22 Manual of Equine Anesthesia and Analgesia
B Components of the specialized electrical conducting system
○○ Sinoatrial (SA node) –– Has the fastest rate of spontaneous depolarization and is the pacemaker. –– Located at the junction of the cranial vena cava and the right auricle. ○○ Atrioventricular (AV) node –– Slows the rate of impulse transmission as it conducts impulses from the atria to the ventricles. ○○ Internodal pathways – conduct impulses through the atria to the AV node. ○○ Right and left bundle branches and His-Purkinje system. –– Conduct impulses throughout ventricles and ventricular septum.
III Unique features of the equine heart
●● Large SA node. ○○ A “wandering pacemaker” is common.
–– Seen as variably shaped P waves on electrocardiogram (ECG).
●● Large atria that may depolarize slightly asynchronously. ○○ Result in biphasic P or bifid waves on the ECG.
●● Deeply penetrating His-Purkinje system.
○○ Facilitates movement of electrical impulses throughout the large ventricular muscle.
Often called Type II Purkinje system.
●● Ossa cordi. ○○ In all species there is a connective tissue “skeleton” that separates the atria from the ventricles.
○○ In cattle and in older horses, these structures may ossify and create two bones, the
“ossa cordi.”
IV Circulatory systems
●● The systemic (high pressure) and pulmonary (low pressure) circulatory systems are separate but coupled (in series) and interdependent so that dysfunction of one will lead to dysfunc- tion of the other. ●● The circulatory systems are not just mere conduits, but are active and, through dilation and constriction, control distribution of blood throughout the body and in localized tissue beds. ●● The lymphatic system is often included as a component of the circulatory system.
A Components of the systemic circulation
Aorta → Arteries → Arterioles → Capillaries → Venules → Great veins → Right atrium
○○ The elastic wall of the aorta recoils following ventricular contraction, creating a force that maintains blood flow throughout systole and diastole. The Cardiovascular System 23
○○ Arterioles provide the greatest resistance to circulation and, via dilation or constric- tion, control blood flow to each tissue capillary bed. ○○ Capillaries are the site of exchange of nutrients and waste products. ○○ The majority of the circulating blood volume (approximately 80%) is generally “stored” in the venules and great veins.
B Components of the pulmonary circulation
Pulmonary artery → Arterioles → Capillaries → Pulmonary vein → Left atrium ○○ The pulmonary artery is the only artery in the body that carries deoxygenated blood, and the pulmonary vein is the only vein that carries oxygenated blood. ○○ Although the pulmonary circulation receives the same cardiac output as the systemic circulation, the pulmonary system remains a low-pressure system due to the: –– Tremendous dispensability of the thin-walled vessels. –– The large number of vessels that are not normally perfused but that can be recruited in times of increased output. ○○ Distribution of pulmonary blood vessels is an important component of ventilation/ perfusion (V/Q) distribution and gas exchange. ○○ Unlike most tissues in the body, pulmonary tissues constrict when hypoxic (hypoxic pulmonary vasoconstriction) in an attempt to divert blood away from poorly ventilated alveoli. This phenomenon can contribute to V/Q mismatch, especially during anes- thesia since atelectasis is common in anesthetized horses. ○○ The lung also receives blood flow through the bronchial circulation, a branch of the systemic circulation that perfuses the tissues of the respiratory system.
C Blood ○○ Consists of plasma and cellular components. ○○ Normal equine hematocrit or packed cell volume (PCV) is approximately 35–45% and normal hemoglobin is approximately 15 g/dl. –– Most oxygen is transported bound to hemoglobin (see section on DO2) –– When saturated, equine hemoglobin binds 1.36–1.39 ml of oxygen per gram of hemo- globin (Hüfner’s constant).
V Cardiovascular physiology
●● The cardiac cycle can be described as a period of ventricular contraction (systole) followed by ventricular relaxation (diastole). ●● The electrical, mechanical and audible events that occur during the cardiac cycle are depicted in the Wigger’s diagram (see Figure 3.1) and described below. 24 Manual of Equine Anesthesia and Analgesia
Isovolumetric Isovolumetric
relaxation 120
contraction SLV opens
SLV Aortic pressure
closes Pressure (mmHg)
MV closes MV opens a c v Atrial pressure 0 Ventricular pressure
1300
Ventricular volume Volume (mL)
300 P QRS T Electrocardiogram
4th 1st 2nd 3rd
Phonogram
Figure 3.1 The Wigger’s diagram depicts the electrical, mechanical and audible events of the cardiac cycle. SLV, semilunar valve; MV, mitral valve; a, atrial contraction; c, tricuspid bulge; v, atrial filling.
A Events occurring during late diastole
○○ The cardiac cycle begins with the spontaneous discharge of the pacemaker, the SA node. ○○ Discharge is followed quickly by electrical activation of the right atrial muscle and then the left atrial muscle. –– This results in the P wave on the ECG. The Cardiovascular System 25
–– Passive filling of the ventricles occurs during this period.
–– Because electrical activation always precedes mechanical activity (termed the electrome- chanical delay), the actual atrial contraction occurs shortly after the P wave is generated. ○○ The rapid flow of blood from atrium to ventricle following atrial contraction gener- ates the atrial or fourth heart sound (S4) and adds blood to the ventricles so that end- diastolic blood volume (or preload) is reached. –– The atrial contribution to the ventricular blood volume is generally minimal and not affected by atrial arrhythmias such as atrial fibrillation. –– However, during high HRs when the diastolic filling time is shortened and in patients with impaired contractility and decreased stroke volume (SV) the atrial contribution becomes a significant percentage of the total ventricular volume and subsequent ejec- tion fraction. ○○ Atrial contraction causes a rise in atrial pressure (“a” wave) which is transmitted up the systemic venous system and often produces a normal jugular pulse. ○○ The atrial excitation wave reaches the medial wall of the right atrium and is con- ducted slowly through the AV node. –– This results in the PR interval on the ECG. –– AV block occurs when the impulse from the atria is not conducted through the AV node to the ventricles. ▪▪ This is reflected on the ECG as a P wave that is not followed by a QRS. ▪▪ In the horse, AV block is generally normal due to inherently high vagal tone, and is considered benign if the block is abolished by exercise or excitement.
B Events occurring during systole
○○ The impulse exits the AV node and electrical activation of the ventricles occurs. –– This results in the QRS complex on the ECG. ○○ Ventricular contraction begins shortly after electrical activation. –– Ventricular pressure quickly exceeds atrial pressure. ○○ The AV valves are forced closed, producing the high-frequency first heart sound (S1). –– Following closure of the AV valves and prior to the onset of ventricular ejection, the ventricle contracts on a constant volume of blood (isovolumetric contraction). ○○ When left ventricular pressure exceeds aortic and pulmonary artery pressure the sem- ilunar valves open and ventricular ejection (the ejection period) begins. –– The time between the onset of the QRS and the opening of the semilunar valves (the pre-ejection period) can be measured by echocardiography and is an index of ventricu- lar myocardial contractility. –– Normal functional systolic “flow” or ejection murmurs may occur during the early part of the ejection period. –– The arterial pulse can be palpated during the ejection period, but the actual timing of the pulse depends on the proximity of the palpation site relative to the heart. 26 Manual of Equine Anesthesia and Analgesia
○○ The audible “cardiac impulse” or “apex beat” occurs during early systole when the contracting heart twists slightly, causing the left ventricle to strike the chest wall just caudal to the left olecranon. –– A “c” wave will be observed during early systole due to bulging of the tricuspid valve into the right atrium or possibly due to pulsations from the carotid artery. –– Ventricular contraction causes the atria to collapse toward the ventricles (ventricular “suction”), which causes a brief collapse of the jugular vein and a decrease in atrial pressure (the “x” descent). ○○ Following this event, atrial filling begins. –– This generates the positive “v” wave.
C Events occurring at the end of the ejection period (late systole/early diastole) Ventricular pressure rapidly drops below the pressure in the aorta and pulmonary artery, ○○
causing a reversal of the direction of blood flow and closure of the semilunar valves. –– This produces the high-frequency second heart sound (S2). –– In horses, the pulmonary valve may close either slightly after or slightly before the aortic valve, resulting in an audible “splitting” of S2. This splitting is normal but can be dramatic in horses with pulmonary disease. –– Along with aortic recoil, valve closure produces the incisura of the arterial pres- sure curve. Comment: The volume of blood ejected during systole is called SV, and the ratio of the SV to the end-diastolic volume is the ejection fraction, which is a commonly used measure of systolic function.
D Events occurring during early diastole
○○ Ventricular pressure continues to fall with no change in ventricular volume (isovolu- metric relaxation). ○○ This proceeds until the ventricular pressure drops below atrial pressure, when the AV valves open and the phase of rapid ventricular filling begins. –– Ventricular pressure rises slowly but ventricular volume increases rapidly as blood that accumulated in the atria during ventricular systole flows rapidly into the ventricle. –– Rapid filling may be associated with a functional protodiastolic murmur and the termi- nation of rapid filling results in the low-frequency third heart sound (S3). –– The rapid decline in both atrial volume and pressure results in the “y” descent on the atrial pressure curve and may be visualized as a collapse of the jugular vein. ○○ The period of rapid ventricular filling is followed by a period of low velocity filling (diastasis) which extends until the next atrial systole. –– In the resting horse with a normal HR, diastasis is the longest period of diastole. –– During diastasis, jugular vein filling may occur, especially during periods of bradycardia. ○○ SA node firing followed by atrial contraction occur during the last phase of ventricu- lar diastole and start the cardiac cycle again. The Cardiovascular System 27
VI Cardiovascular function and clinical applications
●● Clinically, cardiovascular function is determined by measurable components such as HR,
blood pressure (BP) and cardiac output (see Table 3.2). ●● Anesthetic drugs, surgical positioning, surgical events (e.g. hemorrhage) and pathology prior to surgery (e.g. sepsis) can have a profound effect on cardiovascular function.
A Cardiac output
Cardiac output ( Q ) = HR × SV
○○ Defined as the volume of blood ejected by the ventricles per minute (l/min). ○○ Equals the product of HR (beats/min) and SV (l/beat). ○○ In a normally functioning heart, cardiac output equals venous return. ○○ Cardiac output in the conscious resting horse (400–500 kg) is 32–40 l/min. ○○ To standardize cardiac output among individuals, it is often normalized for body sur- face area or body weight and reported as cardiac index. –– Cardiac index in the conscious, resting horse is 70–90 ml/kg/min.
B Heart rate ○○ Horses have a wide HR range. –– A resting rate of 24–50 beats/min to a high of 220–240 beats/min at exercise. ○○ Increased HR will generally result in increased cardiac output if SV is constant. –– In horses, the greatest changes in cardiac output generally occur due to a change in HR (rather than in SV).
Table 3.2 Summary of formulas for cardiovascular variables.
Name Formula
Cardiac output (Q) Heart rate × Stroke volume
Mean arterial blood pressure Cardiac output × Systemic vascular resistance Systemic vascular Mean arterial pressure - Mean right atrial pressure resistance (SVR) Cardiac Ouutput Pulmonary vascular Mean pulmonary arterial pressure − Mean pulmonary wedge pressure resistance (PVR) Cardiac output
Arterial oxygen content (CaO2) CaO2 = ([Hb] × SaO2% × 1.36) + (PaO2 × 0.003) Oxygen delivery (DO2) Cardiac output × arterial oxygen content Another random document with no related content on Scribd: The other version current in Usagara, in the north of the Colony, says nothing of the serpent or the hot water, but states that the sorcerers began by ordering large beer-drinkings in every village. When the pombe had produced its effect, the villagers were initiated into the conspiracy, and received their dawa, of whose composition no details are given, but which, in this case also, was supposed to possess the power of making them invulnerable, so that the bullets of the Germans would simply be changed into water as soon as they left the rifle-barrel. The Majimaji soon discovered, in the course of numerous battles that this was not the case, but nevertheless, the fanaticism of these natives, who, under a murderous fire, charged up to within a spear’s length of the machine-guns—the bumbum, as they call them—is truly astonishing. From the coast to a little beyond Nyangao the character of the vegetation is essentially different from that which we find farther west. The greater part of the road (the barabara, in the carriers’ jargon, that is to say, the path cut to the regulation width on which all the long-distance traffic takes place) runs as far as Nyangao through thick scrub from 10 to 15 feet high, from which rise here and there single trees of twice or three times that height. Several times in the course of the day’s march the traveller comes across large open spaces in the bush on either side of the path. It is clear from the absence of underwood and the presence of charred stumps that this is old cultivated ground—no doubt the sites of former villages. But where are the huts and where the people who once hoed their gardens here? Here we find a typical touch of African history, more especially in recent times, when its primitive conditions have been modified by the modern plantation system with its demand for labour and the necessity for a native military force. Originally and in himself the African is by no means shy, on the contrary, he is inquisitive and fully alive to the attractions of town life and social intercourse. But he cannot stand having his private affairs interfered with. Every caravan of inland natives on their way to the coast, whether to sell their supplies of wax, tobacco or what not, or to engage themselves as labourers to some European, considered that they had a natural right to expect food and drink from the villagers along their route. Even the caravan of a white man is apt to make the same sort of demands on the villagers. How often have I seen my men scatter at every halt, to ask for some service or other—perhaps merely the loan of a gourd dipper—at one or other of the straggling huts, which may be half-a-mile apart. However good-natured and obliging the native may be, he cannot put up with an indefinite continuance of such disturbances to the quiet of his home life, and therefore prefers to pull down his huts and build new ones in the bush at a distance from the main road, where they can only be reached by narrow side paths. Anthropologically speaking, one might take the Wamwera for Indians, such is the lustrous copper tone of their skins. At first I thought that this marked redness of tint was a peculiarity of the tribe, but have since met with many individuals of exactly the same shade among the Makua of Hatia’s, Nangoo and Chikugwe, and a few among the Yaos at this place and those at Mtua, and Mtama. In fact, it seems to me very difficult to do any really satisfactory anthropological work here—the types are too much mixed, and it is impossible to tell from any man’s features the tribe to which he belongs. Probably, indeed, there is no distinction of race at all, for Wamwera, Wangindo, Wayao, Makonde, Matambwe and Makua alike belong to the great sub-group of the East African Bantu. This is one additional reason, when time is so precious, for giving to anthropology even less attention than I had originally planned. Let the gentlemen come out here themselves with their measuring instruments, compasses and poles—we ethnographers have more urgent work to attend to. The Wamwera are just now in a deplorable condition. The whole of this tribe was concerned in the rising, and though refusing to acknowledge defeat in battle after battle, were ultimately forced to take refuge in the bush. The mere fact of living for months without shelter in the rainy season would of itself cause suffering enough; and when we add that they have had no harvest, being unable to sow their crops at the beginning of the rains, it can readily be understood that numbers must have perished. Now that most of the ringleaders have been secured and sent down to the coast, the survivors are gradually coming forth from their hiding-places. But what a spectacle do the poor creatures present! encrusted more thickly than usual with dirt, emaciated to skeletons, suffering from skin-diseases of various kinds, with inflamed eyes—and exhaling a nauseous effluvium. But at least they are willing to face the white man—a sign of newly-established confidence in our rule which must not be undervalued. Several hours’ hard marching from Nyangao bring us to the residence of “Sultan” Hatia. He is the fourth of his name on this tiny throne of the Makua. The grave of his predecessor, Hatia III, lies in a deep cave on the Unguruwe mountain. This mountain is really a promontory of the Makonde plateau projecting far into the Lukuledi plain. It is visible from the road for several days before we reach it, with its gleaming red cliff-face, which might fitly be described as the emblem of the whole Central Lukuledi region. It also plays a great part in the myths and legends of the local tribes. The traditions of the past had already gathered round it before the burial of Hatia III; but now that the dead chief rests in a dark ravine forbidden to every profane footstep, from the toil and turmoil of his life, the Unguruwe has become in popular belief a sanctuary where, on moonlight nights, Hatia rises from his grave, and assembles the ghosts of his subjects round him for the dance. Hatia IV had returned to his capital just before our arrival, having had some months’ leisure on the coast, in which to think over the consequences of the rising. He impressed me as a broken man, physically in no better case than his subjects; moreover he was no better lodged, and certainly no better provided with food than they. On the day of our halt at his village, he was more than ordinarily depressed. A few hours previously a lion, whose impudence has made him famous throughout the country, had in broad daylight dragged a woman out of a hut, not far from the chief’s dwelling. The prints of the enormous paws were still quite clear in the sand, so that we could track the robber right round the hut in which a man with his wife and child had been sitting at their ease. The great brute had suddenly sprung on the woman who was sitting next the door. Her husband tried to hold her, but was weak from illness, and could offer no effectual resistance. Though for some time the poor creature’s shrieks, “Nna kufa! Nna kufa!”—“I die! I die!”—could be heard in the bush, growing fainter and fainter, no one could come to her help, for the people have been deprived of their guns since the rising, and even if they had had them, there was no ammunition, the importation of this having been stopped some time ago. The nephew and heir of Hatia IV is to take the part of avenger. He is a handsome, jet-black youth with a small frizzled moustache on his upper lip, and an enviably thick growth of woolly hair on his scalp. Armed with a rifle, of which he is unconscionably proud, he has come with us from Lindi in order to deliver his people from the plague of lions. Such an expression is, in truth, no exaggeration as far as this place is concerned. It is said that the whole length of the road from Nyangao to Masasi has been divided between four pairs of lions, each of which patrols its own section, on the look-out for human victims. Even the three missionaries at Nyangao are not safe; Father Clement, when out for a walk, not long ago, suddenly found himself face to face with a huge lion, who, however, seemed quite as much startled by the incident as the good Father himself. After examining the architecture of the present Wamwera huts, I can easily understand how the lion at Hatia’s could drag the woman out from the interior. Anyone desirous of studying the evolution of the human dwelling-house could very well see its beginnings here. Most of these dwellings are nothing more or less than two walls, consisting of bundles of grass roughly tied together, and leaning against each other in a slanting position. The addition of gable-ends marks quite a superior class of house. Besides this, the Wamwera have been compelled to build their huts, such as they are, in the untouched jungle, since they have lost all they had, even the necessary implements for tillage and for clearing the bush. Their villages, containing their only possessions of any value, were of course levelled with the ground by our troops. The lion is shy of open spaces, but feels at home in the pori, which he looks upon as his natural hunting-ground, and where he can creep unseen close up to a hut before making his deadly spring. One point I must not forget. Even before leaving Lindi, my mouth had watered at the descriptions I heard of the extraordinary appearance presented by the Wamwera women. But I find that these descriptions come far short of the reality. The famous Botocudos of Brazil with their labrets are nothing to the southern tribes of German East Africa. I had long known that the Makonde plateau and the whole surrounding country belong to the region of the pelele, or lip ring, but I have never come across a good illustration of earlier date than my own. The accompanying reproductions of photographs will show the nature of this extraordinary decoration more clearly than any description. The pelele, or, as it is called in Kimwera, itona, is only worn by the women, but among them it is universal. It is a peg, in older persons even an actual disc, of ebony, or else of some light-coloured wood bleached snow-white with argillaceous earth, inserted in the upper lip, which is perforated and stretched to receive it. Of course, a disc the size of a two-shilling piece is not inserted all at once: the operation is very gradual and begins by piercing the lip, between a girl’s seventh and ninth year, with the end of a razor which is ground into the shape of an awl.[8] The hole is kept open by inserting a foreign body of small size, such as a thin stalk of grass, or the like. It is then enlarged by adding another stalk at regular intervals; and after a time, a strip of palm-leaf rolled up into a spiral is substituted. This, being elastic, presses against the sides of the opening, and so, in due course renders it large enough to receive the first solid plug. Among the Wamwera the diameter of this varies from the thickness of a finger to the size of a florin; the older Makonde women, however, are said to have them twice as large. Naturally I am all impatience to see these people, whose country, moreover, is as yet a complete terra incognita, as far as science is concerned. Not content with the itona, the old women sometimes wear a pin or peg in the lower lip, called nigulila. It is long and slender, ending in a round knob, and is intended to divert the eye from the withered skin and A MWERA WOMAN faded charms of the wearer.[9] Discs or plugs inserted in the lobe of the ear are also very general. Furthermore, the YOUNG MAN OF THE countenance of these fair ones are covered MWERA TRIBE with extraordinary scars which, at a distance, suggest that they must have passed their youth at a German university. On a close inspection it will be found that these are not scars, left by straight cuts, but consist of a multitude of small keloids arranged in various patterns. The patterns are made by parallel rows of small cuts (usually vertical), which have been prevented from healing by repeatedly opening them during the process of cicatrization. Thus in the course of weeks and months they take the form of conspicuous swellings which, in their totality, give a distinctive character to the whole physiognomy. Even this is not enough to satisfy the craving of the Wamwera women for adornment. If the cloth draping chest and back slips aside for a moment, either through an incautious movement on the part of the wearer or through the inseparable baby being shifted from its usual place on its mother’s back to her hip—the astonished eye discovers that the surfaces thus revealed are adorned with markings similar to those on the face. Even the hips and upper part of the thighs are said to be covered with them. The ethnographer, reflecting on these and other queer manifestations of human vanity, may be tempted, perhaps, to indulge in a comfortable sense of superiority. But, after all, the fashion of wearing earrings is not quite extinct in Europe; and the advantages of the corset, considered as an aid to beauty, might be quite as much open to discussion as the African MWERA WOMAN ornaments we have just been describing. I am WITH PIN IN LOWER alluding, of course, to those women who think LIP that tight lacing improves the figure. Otherwise I am inclined to agree with Max Buchner of Munich, who thinks that some form of this article would be of great service to the women of all the less-clothed races among whom appliances for supporting the bust are unknown. Up to the present, I have been able to see but little of the real life of the inland tribes, yet that little has been very interesting. On the march to Masasi I noticed that wherever the natives had taken an active part in the rebellion, the roads were in perfect order, while in the territory of the friendly tribes they were nearly impassable with high grass, and sometimes bushes. These allies of ours are now, secure in the consciousness of their past services, saying to themselves that they may take things easy for a time, as the “Mdachi” will surely consider their loyalty and make no very severe demands on them. Captain Ewerbeck, however, has been laying down the law with great precision and energy to the Akidas and Jumbes, the district chiefs and village headmen, who are responsible for order within their own districts. One can enjoy magnificent spectacles by night in Africa. Sitting in front of my tent on the way here, or now, when I step out in front of the Baraza—the rest-house in which I have taken up my abode—I see, wherever I turn my eyes, the red glow of flames on the horizon. This is the burning of the grass—a custom practised by the Africans for thousands of years. It may be remembered that when Hanno, on his voyage from Carthage, sailed down the West coast of Africa, nothing produced such a deep and lasting impression of terror on himself and his crew as the streams of fire seen to flow down from the coast-ranges at night. In my opinion, which, of course, I do not consider decisive, these streams of fire were certainly not, as has so often been maintained, connected with any volcanic phenomena, but resulted from the processes still put into operation by the inhabitants of the Dark Continent every night during the dry season. ROAD THROUGH THE BUSH IN THE NEIGHBOURHOOD OF CHINGULUNGULU
Much has been written in our Colonial publications with regard to
the benefit or injury to be derived from this grass-burning. Some condemn it as deleterious to the growth of trees, while others take the part of the natives and say that only by burning off the high grass and brushwood of the African forest at regular intervals can they possibly get the upper hand of the vermin, which would otherwise increase by myriads. Besides, it is said, the ashes are for the present the only manure that can be applied on a large scale. I do not feel justified in attempting a decision, but confine myself to admiring the magnificent effect of the near and distant fires, reflected in the most varied gradations of light and colour in the misty atmosphere. None of these fires, moreover, is dangerous to the traveller; where the flames seize a patch of completely dry grass, they rush along, it is true, with a noise like the crackling of musketry-fire; but otherwise, and indeed in general, the people have to keep up the conflagration by systematic kindling of the grass in fresh places. In any case they have the direction and extent of the fire fully under control. This burning is, so far as I am enabled to judge, only possible where the remarkable form of vegetation prevails which characterizes the greater part of Africa, and covers the whole extent of the great plain on the west and north-west of the Makonde plateau. This is the “open bush and grass steppe” (lichte Baumgras- steppe) as it has been very appropriately named by the geologist Bornhardt. In fact, this form of vegetation is neither exclusively forest nor altogether steppe; it unites the characters of the two. Imagine a particularly neglected orchard, in some rural part of Germany (where I am sorry to say the farmers still pay far too little attention to this branch of cultivation), and fill up the spaces between the scattered apple, pear or plum trees, not with our modest German grass but with the African variety, two or three yards high and more like canes, mix this with underwood—thorny, but not very close—and finally bind together the tops of the trees (which are not very high— certainly none of them over forty feet—and all varieties having a sort of general resemblance to our maple) by means of a system of airy lianas. Having done all this, you have, without any further strain on the imagination, a fairly correct picture of what is here generally called pori, though in the North the name of “myombo forest” is more usually applied to it. During the rains, and just after them, this pori must undeniably have its charms,—in fact, Ewerbeck and his companion Knudsen are indefatigable in singing its praises as it appears in that season. Now, on the other hand, in July, it is anything but beautiful: it neither impresses us by the number and size of its trees, nor refreshes us with any shade whatever, nor presents the slightest variation in the eternal monotony which greets the traveller as soon as he leaves Nyangao and crosses to the right bank of the Lukuledi and from which he only escapes after a march of several weeks, high up on the Upper Rovuma. “So this is the exuberant fertility of the tropics, and this is what an evergreen primeval forest looks like!” I thought, after enjoying this spectacle for the space of a whole day. Just as with regard to the alleged want of appetite experienced by Europeans in the tropics, we ought to see that the general public is more correctly informed as to the supposed fertility of Equatorial Africa, and so saved from forming extravagant notions of the brilliant future in store for our colonies. The pori becomes downright unpleasant wherever the owners of the country have just been burning it. To right and left of the road extends a thick layer of black or grey ashes, on which, here and there, lies a dead tree, steadily smouldering away. Now that there is no grass to obstruct the view, the eye ranges unhindered through what at other times is impenetrable bush. For the sportsman this state of things is a pleasure, as he can now see game at almost any distance; but for the traveller, especially if encumbered with a large caravan, it is nothing less than torture. This is not so much the case in the early morning, when the fine particles of dust are laid by the heavy dews; but, when the sun rises higher, marked differences of temperature are produced within a comparatively small area. Tramping on through the glowing heat of noon, suspecting no harm and intending none, the traveller suddenly sees something whirling in front of his feet—a black snake spinning round in a raging vortex, rises straight up, dances round him in coquettish curves, and then vanishes sideways behind the trees, with a low chuckle, as if in derision of the stranger and his immaculately clean khaki suit. The native followers have not suffered, being of the same colour as the insidious foe. But what is the aspect presented by the leader of the expedition! Though not guaranteed to wash, he presents a sufficiently close resemblance to a blackamoor, and under the circumstances, the faithful Moritz and Kibwana, as soon as we have reached camp, will have no more pressing task than to prepare the bath for their master and thoroughly soap him down from the crown of his head to the sole of his foot. And all this is the work of the pori whirlwind. In these small distresses of life on the march, the imperturbable cheerfulness of the natives is always a comfort. Among the Wamwera on the scene of the late rising, there was little inclination for dancing and merriment—the prevailing misery was too great; but everywhere else, before our camp was even half arranged, the inhabitants of the place had assembled in crowds, and the scene which ensued was always the same in its general features, though varying in detail. The negro has to dance. As the German, whenever anything lifts him out of the dead level of the workaday mood, feels irresistibly impelled to sing, so the African misses no opportunity of assembling for a ngoma. The word ngoma, in its original signification means nothing more than a drum; in an extended sense it denotes all festivities carried on to the sound of the drum. These festivities have an indisputable advantage over ours, in that the instrumental music, dancing, and singing are all simultaneous. The band drums, but also occasionally improvises songs, the audience standing round in a circle form the chorus and at the same time march round the band to the rhythm of the song. This is the usual picture, with all its strangeness so fascinating that the oldest residents in the coast towns do not think it beneath their dignity to honour this expression of aboriginal life by attending from time to time, if only for a few minutes. Other and less sophisticated whites are regular habitués at these festivals, and never let a Saturday evening pass—this being the day when ngomas are allowed by law—without standing for hours among the panting and perspiring crowd. One of these dances, executed by the women of every place I have so far visited, on every possible occasion, is peculiarly pleasing. It is called likwata (“clapping of hands”). A number of women and girls stand in a circle, facing inwards. Suddenly arms rise into the air, mouths open, feet twitch in unison, and all goes on in exact step and time; hand- clapping, singing and dancing. With the peculiar grace which characterizes all movements of native women, the whole circle moves to the right, first one long step, then three much shorter. The hand- clapping, in time and force, accurately follows the above rhythm, as does the song, which I shall presently reproduce. Suddenly, at a certain beat, two figures step out of the line of dancers—they trip in the centre of the circle, moving round one another in definite figures, the movements in which, unfortunately, are too rapid for the eye to follow—and then return to their fixed places in the circle to make way for two more solo artists. So the game goes on, without interruption or diminution of intensity, hour after hour, regardless of the babies who, tied in the inevitable cloth on their mothers’ backs, have gone through the whole performance along with them. In this confined, hot, and often enough dirty receptacle, they sleep, wake or dream, while the mother wields the heavy pestle, pounding the maize in the mortar, or grinds the meal on the stone, while she breaks the ground for sowing, hoes up the weeds or gathers in the crops, while she carries the heavy earthen water-jar on her head from the distant spring, and while, as now, she sways to and fro in the dance. No wonder if, under such circumstances, the native baby is thoroughly familiar with the national step and rhythm even before he has left the carrying-cloth and the maternal breast. The sight of tiny shrimps of three and four moving with absolute certainty through the mazes of the grown people’s dance, would almost of itself be worth the journey to East Africa. And now come the very profound words accompanying this dance which seems so full of meaning and poetry. The spectator standing by and watching the varied and graceful movements of the women— perhaps working the cinematograph at the same time—is apt, in spite of all previous resolutions, to pay too little heed to the words sung. When, the dance over, he arranges the performers before the phonograph, he is tempted to believe that his ears have deceived him, so utterly inane are these words. I have made records of the likwata at a number of different places, but never succeeded in getting any other result than the following—
[10]
The reader will agree that no undue amount of intellect has been lavished on this ditty, but this is a trait common to all native songs here in the South. Even those acknowledged virtuosi, my Wanyamwezi, cannot do very much better in this respect. Here we have really every right to say, “We Wazungu are better singers after all!” MOUNTAINS NEAR MASASI. DRAWN BY SALIM MATOLA CHAPTER V LOOKING ROUND
Masasi, July 25, 1906.
I have been here at Masasi quite a week. My abode is a hut in the
purest Yao style, built by the natives under the orders of the Imperial District Commissioner, expressly for the benefit of passing European travellers. This hut—or, I suppose I ought to say, this house, for it is a sizeable building of some forty feet by twenty—lies outside the boma which shelters the local police force. It is an oval structure whose roof is exactly like an overturned boat. The material of the walls is, as everywhere in this country, bamboo, and wood, plastered inside and out with dark grey clay. My palace is superior to the abodes of the natives in the matter of windows, though they are not glazed. At night, before I creep under my mosquito-net into the camp bed, the openings are closed with shutters constructed of strong pieces of bamboo. The floor, as in all native huts, is of beaten earth, which can in general be kept quite clean, but is not calculated for the sharp edges of European boot-heels, which soon play havoc with its surface. The interior forms an undivided whole, only interrupted by the two posts standing as it were in the foci of the ellipse, and supporting the heavy thatched roof. This projects outward and downward far beyond the wall of the house, its outer edge being carried by a further ellipse of shorter posts, and so makes a broad shady passage round the whole house, such as, under the name of baraza is an essential part of every East African residence. The natives give the name of Masasi to a whole district alike interesting from the point of view of geography, geology, botany or geography. Almost immediately after passing Nyangao, as one comes from the coast, begins the “open bush and grass steppe” already mentioned, while at the same time the edges of the Makonde plateau on the south and of the high ground to the north of the Lukuledi retreat further and further. As one walks on, day after day, across a perfectly horizontal plain covered with the same monotonous vegetation, the journey is by no means exciting. Then, suddenly, at a turn of the path, we see a huge cliff of glittering grey. We draw a long breath and forget all our fatigue in presence of this new charm in the landscape. Even the heavy-laden carriers step more lightly. Suddenly the bush, which has become fresher and greener as we approach the rock, ceases, and instead of the one cliff we now see a whole long range of rocky peaks, which seem to stand as a barrier right across our path. This, however, is not the case, for close to the foot of the first mountain the road turns sharply to S.S.E., running parallel and close to the range. When the range ends, the road ends too, for there, embosomed in a circle of “hill-children,”—as the native would say in his own language, i.e., low hills of a few thousand feet or under,—lies the military station of Masasi. The dome-shaped gneiss peaks of Masasi are celebrated in geological literature: they are, in fact, unique, not in their petrographic constituents, but in the regularity of their serried ranks. Orographically this whole region of East Africa which I am now traversing is characterized by insular mountains (Inselberge), as they are called by the geologist Bornhardt. The name is very appropriate, for, if the land were to sink some three hundred feet, or the Indian Ocean to rise in the same degree, the valleys of the Lukuledi, Umbekuru and Rovuma, as well as, in all probability, several rivers in Portuguese East Africa, and also the whole vast plain west of the Mwera and Makonde plateaus would form one great lake. Here in the west, only these lumpy, heavy gneiss peaks would rise as tiny islands above the waters, while towards the coast the plateaus just mentioned would so to speak represent the continents of this piece of the earth’s surface. THE INSULAR MOUNTAIN OF MASASI
In general these peaks are scattered irregularly over the whole
wide area of the country. If I climb one of the smaller hills immediately behind my house, I can overlook an almost illimitable number of these remarkable formations to north, west and south. They are mostly single or in small clusters, but several days’ journey further west a large number are gathered into a close cluster in the Majeje country. The Masasi range in our immediate neighbourhood is the other exception. Corresponding to their irregular distribution is a great variety in height. Many are only small hillocks, while others rise to a sheer height of 1,600 feet and over from the plain, which here at Masasi is fully 1,300 feet above sea-level. The highest of these hills thus attain about the middle height among our German mountains. As to the origin of these strange mountain shapes, not being a geologist, I am in no position to form an opinion. According to Bornhardt, who in his magnificent work on the earth-sculpture and geology of German East Africa[11] has described the geological features of this landscape with admirable vividness, all these insular peaks testify to a primeval and never interrupted struggle between the constructive activity of the sea and the denuding, eroding, digging and levelling action of flowing water and of atmospheric influences. He sees this tract in primordial times as an immense unbroken plain of primitive gneiss. In this, in course of time, streams and rivers excavated their valleys, all more or less in the same direction. At the end of this long-continued process, long hill ridges were left standing between the different valleys. Then came another epoch, when stratification took the place of destruction. Whereas formerly, rain, springs, brooks and rivers carried the comminuted and disintegrated rock down to the sea, now, the sea itself overflowed the land, filled the valleys, and probably covered the whole former scene of action with its sediment. This sediment, again, in the course of further ages became hardened into rock. Once more the scene changed; again the land was left dry; and wind, rain and running water could once more begin their work of destruction. But this time their activity took a different direction. They had formerly carried the detritus north or south, but now they swept it eastward, at right angles to their former course, and so gradually ground and filed away the whole of the later deposit, and also eroded the long ridges which had survived from the first period of destruction. Finally, when even this primitive rock had been worn away down to the bottom level of the first valleys, nothing remained of the old sheet of gneiss except in the angles formed by the crossing of the two lines of abrasion and erosion. The superincumbent strata being swept away, the hard gneiss cores of these angles of ground form the very insular peaks I have been describing. Bornhardt’s theory is a bold one and assumes quite immeasurable periods of time, but it has been generally accepted as the most plausible of all attempts to explain the facts. In any case it is a brilliant proof of the capacity for inductive reasoning possessed by German scholars. These mighty masses of rock, springing with an unusually steep slope, direct from the plain, dominate their surroundings wherever one comes across them, but where they appear in such a wonderfully regular series as they do here—Mkwera, Masasi, Mtandi, Chironji, Kitututu, Mkomahindo, and the rest of the lesser and greater elevations within my horizon,—they present an incomparable and quite unforgettable spectacle. When once the projected railway across the Umbekuru basin is completed, the tourist agencies will have no more popular excursion than that to the Masasi Range. From a botanical point of view, also, the visitor finds himself well repaid for his trouble. Once in the shadow of these hills, the desolation of the pori is forgotten as if by magic; one plantation succeeds another, and patches of all the different varieties of millet bow their heavy cobs and plumes in the fresh morning breeze, which is a real refreshment after the stifling heat of the long day’s march through the bush. Beans of all kinds, gourds and melons, rejoice the eye with their fresh green, on either side of the path the mhogo (manioc) spreads its branches with their pale-green leaves and pink stalks. Wherever there is an interval between these various crops, the bazi pea rattles in its pod. This fertility (astonishing for the southern part of German East Africa) is only rendered possible by the geological constitution of the soil. Wherever we have set foot on the main road, and north and south of the same, as far as the eye can reach, the principal constituents of the upper stratum have been loamy sand and sandy loam. In places where the action of water has been more marked, we find an outcrop of bare, smooth gneiss rocks; or the ground is covered with hard quartzite, crunching under foot. Only where these mighty gneiss ranges break the monotony does anyone examining the country with an eye to its economic value find full satisfaction. Gneiss weathers easily and forms excellent soil, as the natives have long ago discovered; and, though they by no means despise the less fertile tracts, yet the most favoured sites for settlements have always been those in the immediate vicinity of the gneiss islands. Masasi, with its enormous extent, taking many hours to traverse, is the typical example of such economic insight. Since this would naturally attract people from all directions, it is not to be wondered at if a question as to the tribal affinities of the Masasi people should land one in a very chaos of tribes. Makua, Wayao, Wangindo, a few Makonde, and, in addition a large percentage of Coast men:—such are the voluntary immigrants to this little centre of social evolution. To these we must add a miscellaneous collection of people belonging to various tribes of the far interior, who are here included under the comprehensive designation of Wanyasa. These Wanyasa are the living testimony to an experiment devised in the spirit of the highest philanthropy, which, unfortunately, has not met with the success hoped for and expected by its promoters. This very region was some decades ago the scene of an extremely active slave-traffic; the trade, kept up by the Zanzibar and Coast Arabs, preferred the route through this easily-traversed and at that time thickly-populated country. The situation of Kilwa Kivinje on a bay so shallow that Arab slave-dhows, but not the patrolling gun-boats of rigidly moral Powers, can anchor there, is to this day a speaking testimony to that dark period in the not excessively sunny history of Africa. In order to get at the root of the evil, English philanthropists have for many years been in the habit of causing the unhappy victims driven down this road in the slave-stick, to be ransomed by the missionaries and settled on their stations as free men. The principal settlement of this kind is that among the gneiss peaks of Masasi. The Christian world cherished the hope that these liberated slaves might be trained into grateful fellow-believers and capable men. But when one hears the opinion of experienced residents in the country, it is not possible without a strong dose of preconceived opinion to see in these liberated converts anything better than their compatriots. The fact remains and cannot by any process of reasoning be explained away, that Christianity does not suit the native; far less, in any case than Islam, which unhesitatingly allows him all his cherished freedom. Personally, however, I must say I have not so far noticed any discreditable points in the character of the Masasi people; all who have come in contact with me have treated me in the same friendly fashion as the rest of those I have come across in this country. Such contact has by no means been wanting in spite of the shortness of my stay here, since I have thrown myself into my work with all the energy of which I am capable, and am convinced that I have already seen with my own eyes and heard with my own ears a large and important part of the people’s life. The very beginning of my studies was remarkably promising. The Mission station of Masasi lies a short hour’s walk north north- eastward from us, immediately under the precipitous side of Mtandi Mountain. This Mtandi is the most imposing peak of the whole range; it rises in an almost vertical cliff directly behind the straw huts of the Mission, ending, at a height of nearly 3,100 feet in a flat dome. District Commissioner Ewerbeck and I had already, when riding past it on the day of our arrival, determined to visit this mountain; and we carried out our project a day or two later. The trip was not without a certain fascination. At 4.30 a.m. in a pitch-dark tropical night, we were ready to march, the party consisting of two Europeans and half- a-dozen carriers and boys, with Ewerbeck’s Muscat donkey and my old mule. As quickly as the darkness allowed, the procession passed along the barabara, turning off to the left as we approached Mtandi. The animals with their attendants were left behind at the foot of the mountain, while the rest of us, making a circuit of the Mission grounds, began our climbing practice. I had equipped myself for my African expedition with the laced boots supplied by Tippelskirch expressly for the tropics. When I showed these to “old Africans” at Lindi, they simply laughed at me and asked what I expected to do in this country with one wretched row of nails on the edge of the sole. They advised me to send the things at once to Brother William at the Benedictine Mission, who earns the gratitude of all Europeans by executing repairs on shoes and boots. Brother William, in fact, very kindly armed my boots with a double row of heavy Alpine hobnails, and I wore a pair the first day out from Lindi, but never again on the march. They weighed down my feet like lead, and it soon appeared that the heavy nails were absolutely unnecessary on the fine sand of the barabara. After that first day, I wore my light laced shoes from Leipzig, which make walking a pleasure. Here, on the other hand, on the sharp ridges of Mtandi, the despised mountain boots rendered me excellent service. I prefer to omit the description of my feelings during this ascent. It grew lighter, and we went steadily upwards, but this climbing, in single file, from rock to rock and from tree to tree was, at any rate for us two well-nourished and comfortable Europeans, by no means a pleasure. In fact, we relinquished the ambition of reaching the highest peak and contented ourselves with a somewhat lower projection. This was sensible of us, for there was no question of the magnificent view we had expected; the heights and the distant landscape were alike veiled in thick mist, so that even the longest exposure produced no effect to speak of on my photographic plates.
Psychonauts Psychedelics A Systematic Multilingual Web Crawling Exercise Valeria Catalani John Martin Corkery Amira Guirguis Flavia Napoletano Davide Arillotta Caroline Zangani All Chapter
