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EQUINE NEONATOLOGY: ACASE-BASED APPROACH ISBN-13: 978-1-4160-2353-1
ISBN-10: 1-4160-2353-4
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Notice
Companion animal practice is an ever-changing field. Standard safety precautions must be
followed, but as new research and clinical experience grow, changes in treatment and drug therapy
become necessary or appropriate. The authors and editors of this work have carefully checked the
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the contraindications for administration. This is of particular importance in regard to new or
infrequently used drugs. Recommended dosages for animals are sometimes based on adjustments
in the dosage that would be suitable for humans. Some of the drugs mentioned here have been
given experimentally by the authors. Others have been used in dosages greater than those
recommended by the manufacturer. In these kinds of cases, the authors have reported on their
own considerable experience. It is the responsibility of those administering a drug, relying on their
professional skill and experience, to determine the dosages, the best treatment for the patient, and
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ISBN-13: 978-1-4160-2353-1
ISBN-10: 1-4160-2353-4
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Dedication
This book is dedicated to the Trustees of The Dorothy Russell Havemeyer Foundation,
especially Gene Pranzo, for their contribution to the acquisition and sharing of new
knowledge in the field of Equine Neonatology.
Preface
Equine neonatology became a recognized area of those facts to is inefficient and unproductive. Telling
interest in the early 1980s. In the last 25 years, research stories or presenting examples allow the reader to use
and literature on the subject of the newborn foal have imagination to conjure up the patient and question
flourished. The purpose of this book is two-fold: to what might be happening. The reader becomes
chronicle the new developments in the field, and to an active participant in the case. As the case unravels
write a text that presents this information in a manner and the solutions are presented, the reader receives
that actually encourages people to read for a bigger insight into how the situation developed. This active
picture. participation is one of the most important factors in
The first goal is accomplished by assembling a team learning.
of authors who have worked intensely with the equine So the question becomes—How does one tell stories
neonate during their careers and are willing to share in a textbook? If you look at the table of contents for
their experiences and knowledge with others to con- this book, you will see that all the normal topics will
tinue the trend of improvement in medicine and the be covered. It is how they are covered that is impor-
outcomes of our patients. Each author approaches tant for this particular book. Each chapter will be made
a case in a slightly different manner, thus adding up of one or more cases. There might be a single case
breadth to the manner in which the reader can ap- that the author has seen or a conglomerate of different
proach a problem. cases that present the salient points of the particular
In order to accomplish the second goal, one needs to disease. Anatomy and physiology is discussed in the
see how textbooks are currently used. As a professor context of diagnosis and treatment of the disease.
teaching large animal veterinary medicine, I have Through this method, the reader will have the experi-
found that most textbooks are only used as reference ence of “seeing” all of the patients, not only “experi-
books. The only person that reads a veterinary text- encing” the cases but also actually beginning to
book from cover to cover is the resident preparing for understand basic mechanisms of disease and decisions
their specialty examination! This is certainly not a bad behind the tests and treatments.
use of a textbook but it generally limits one’s search to Of course the names of the patients have been
brief excursions into one disease and may not open changed to protect the confidentiality of the owners.
one up to other possible diagnoses or treatments. See if you can find a connection between the foal’s new
Learning a litany of facts about a certain disease name and its disease! I hope that you enjoy this format
without having a particular patient or story to tie and look forward to your comments.
vii
Acknowledgments
I would like to acknowledge all the work done by As you may see I have dedicated this book to the
the contributors to this book—not only for this book Trustees of the Dorothy Russell Havemeyer Founda-
but for the profession as a whole. I consider the con- tion, especially Gene Pranzo. I met Gene in 1990 when
tributors of this book to be not only the writers of he asked me to become a primary investigator for the
the cases but also my colleagues who have done Foundation. The foundation has given me the freedom
the research that supports the information found here. to investigate clinical diseases of the newborn foal,
I would like to thank Andy Cunningham from support clinical cases that may otherwise have been
the Educational Media division at Tufts Cummings euthanized, and gather experts in the field to exchange
School of Veterinary Medicine for the work that he the newest foal research to help develop new ideas as
did to make sure all of the pictures were clear and to what the next steps should be. I am eternally grate-
sharp. As the chapters started rolling in, Sue Corey ful for this opportunity.
was instrumental in helping me organize the drafts. A percentage of the royalties of this book will be
My editors at Elsevier—Jolynn Gower, Andrea donated to the ACVIM Foundation to support contin-
Campbell, and Ellen Kunkelmann—were always ued clinical research, and to the Travis Fund at Tufts
receptive to my ideas and vision for the book. Thank Cummings School of Veterinary Medicine in support
you. of patients who lack funds for treatment.
ix
Contributors
Michelle Henry Barton, DVM, PhD, Jill R. Johnson, DVM, MS,
DACVIM(LAIM) DACVIM(LAIM), DABVP
Professor, Large Animal Medicine Professor of Equine Medicine
College of Veterinary Medicine Veterinary Clinical Sciences
University of Georgia School of Veterinary Medicine
Athens, Georgia Louisiana State University
Baton Rouge, Louisiana
Daniela Bedenice, Dr. med. vet., Isabel Jurk, DVM, DACVO
DACVIM(LAIM) Tufts Cummings School of Veterinary Medicine
Assistant Professor, Clinical Sciences Tufts University
Tufts University School of Veterinary Medicine North Grafton, Massachusetts
North Grafton, Massachusetts
K. Gary Magdesian, DVM,
DACVIM(LAIM), DACVECC, DACVCP
Virginia Ann Buechner-Maxwell DVM,
Assistant Professor, Equine Critical Care Medicine
MS, DACVIM(LAIM) Department of Medicine and Epidemiology
Associate Professor and Section Chief University of California, Davis
Large Animal Clinical Sciences Davis, California
Virginia-Maryland Regional College of Veterinary
Medicine Melissa R. Mazan, DVM, DACVIM(LAIM)
Blacksburg, Virginia Assistant Professor, Director of Sports Medicine
Clinical Sciences
Tufts University School of Veterinary Medicine
Katherine Chope, VMD
North Grafton, Massachusetts
Large Animal Ultrasound Consultant
Hospital for Large Animals Rose Nolen-Walston, DVM,
Tufts University School of Veterinary Medicine
DACVIM(LAIM)
North Grafton, Massachusetts
Tufts Cummings School of Veterinary Medicine
Tufts University
Brett Dolente, VMD, DACVIM(LAIM) North Grafton, Massachusetts
Staff Veterinarian
Jonathan Palmer, VMD, DACVIM(LAIM)
Sections of Large Animal Internal Medicine and
Associate Professor of Medicine
Emergency, Critical Care, and Anesthesia
Department of Clinical Studies—New Bolton Center
School of Veterinary Medicine
School of Veterinary Medicine
University of Pennsylvania
University of Pennsylvania
Kennett Square, Pennsylvania
Kennett Square, Pennsylvania
Bettina Dunkel, DVM, DACVIM(LAIM) Mary Rose Paradis DVM, MS,
Department of Veterinary Basic Science DACVIM(LAIM)
Royal Veterinary College Tufts Cummings School of Veterinary Medicine
North Mymms, Hatfield Tufts University
Hertfordshire, UK North Grafton, Massachusetts
xi
CONTRIBUTORS
Patricia J. Provost, VMD, MS, DACVS Craig D. Thatcher DVM, MS, PhD,
Department of Clinical Sciences DACVN
Tufts University Cummings School of Veterinary Professor
Medicine Department of Large Animal Clinical Sciences
North Grafton, Massachusetts Virginia-Maryland Regional College of Veterinary
Medicine
Debra C. Sellon, DVM, PhD,
Blacksburg, Virginia
DACVIM(LAIM)
Professor, Equine Medicine
Pamela A. Wilkins, DVM, MS, PhD,
Department of Veterinary Clinical Sciences
DACVIM(LAIM), DACVECC
Washington State University
Pullman, Washington Chief, Section of Emergency, Critical Care and
Anesthesia
Sarah J. Stoneham, BVSc Cert, ESM,
Clinical Studies, New Bolton Center
MRCVS School of Veterinary Medicine
Rossdale and Partners University of Pennsylvania
Newmarket, United Kingdom Kennett Square, Pennsylvania
xii
1
Assessing the Newborn Foal
Case 1-1 Normal Foal Sarah J. Stoneham
maternal progestagen levels (principally pregneno-
lone:P5) during the last few weeks of pregnancy as
a result of increasing stimulation of the fetal adrenal
gland by ACTH. There are differences in maternal
progestagens levels between horses and ponies,
although the pattern of change is consistent.
This is followed by a redirection of steroidogenesis
in the last few days prior to parturition. It is thought
that increasing levels of cortisol induce 17α hydroxy-
lase. This enhances metabolism of P5 to cortisol, pro-
ducing a rise in fetal cortisol and a concomitant
decrease in maternal progestagens. This rise in cortisol
usually occurs in the last 5 days of gestation, contin-
ues for a few hours after birth,1,2and is essential to the
viability of the foal.
Fig. 1-1Labour of Love, 340 days pregnant, in foaling stall.
Normal foals have high progestagen levels at birth,
which decrease rapidly in the first few hours after birth
At 340 days of pregnancy, Labour of Love, a multiparous (Figure 1-2). Progestagen levels in abnormal and pre-
Thoroughbred mare, had been showing signs of impend- mature foals remain high, and a decrease can be asso-
ing parturition over the last 5 days. She had a well- ciated with recovery. In foals that do not survive, levels
developed udder, and “wax” was beginning to form on the may remain elevated. It is thought that this may be due
ends of her teats. The muscles around her hindquarters to blocking of an enzyme, which is necessary for pre-
appeared to be softer, and her vulva was relaxed. As with venting overproduction.3,4
her previous pregnancies, this pregnancy had been Signs of impending parturition may include relax-
uneventful. (Figure 1-1) ation of the muscles of the hindquarters and length-
ening of the vulvar lips. During pregnancy, the
mammary glands are exposed to high levels of estro-
gen and progestagens. It is thought that lactation is
HORMONAL SIGNALING OF PARTURITION
triggered by the rise in progestagens from about
310 days gestation, then the precipitous decrease 2 to
The fetal hypothalmo-pituitary-adrenal axis initiates 3 days prior to parturition, combined with increasing
fetal maturation and the cascade of hormonal events prolactin levels during the last week of pregnancy.
resulting in parturition and functional maturation of Udder enlargement usually begins 2 to 3 weeks before
fetal organ systems. During the second part of preg- parturition. As birth becomes imminent, small
nancy, progestagens are synthesised by the fetus and amounts of beaded colostrum may form on the tips of
the utero-placental unit. There is a marked rise in the teats. This is called “waxing.” Calcium content of
1
1
EQUINE NEONATAL MEDICINE
Fig. 1-2Mean ±s.d. plasma progestagen levels in the normal foal (determined
by radioimmunoassay). From Houghton E et al.: Plasma progestagen concen-
trations in the normal and dysmature foal, J Reprod Fert Suppl 44:609-617,
1991.
the mammary secretion increases over the last day of
pregnancy. Field tests are available to measure calcium
in the hopes of predicting when a mare will foal. These
tests are not 100% reliable.5 It is important to remem-
ber that each mare is an individual and that not all
“wax up.” Also, some don’t enlarge the udder until
days before the birth. Occasionally a mare will actually
produce and leak milk 1 to 5 days before the birth. This
is of grave concern because the potential loss of
colostrum for the foal and failure of passive
immunoglobulins.
The production of colostrum is a unique event. It is
a vital component that enhances the efficacy of the
foal’s naïve immune system. Maternal immunoglobu-
lins are concentrated in a nonspecific way in the
mammary gland. Colostrum provides immuno-
Fig. 1-3 ’03 Labour of Love with mare sitting in sternal recum-
globulins, complement, lysozyme, and lactoferrin and
bency 10 minutes after birth.
large numbers of B-lymphocytes. It also contains
growth factors important in maturation of the gas-
(see Figure 1-3). A few minutes later the umbilical cord
trointestinal tract. AThoroughbred mare typically pro-
broke with the filly’s first attempts to stand. The filly
duces 1 to 2 liters of colostrum. (See Chapter 4.)
was moved in front of the mare, and the umbilical rem-
nants were treated with a 0.5% chlorhexidine and surgi-
Because of her increasing restlessness, Labour of Love cal alcohol mix. The foal had a suckle reflex present, and
was placed in the foaling stall, where she appeared unin- the foal made attempts to stand as the mare licked it.
terested in hay and grain. By 10 PM, she started to sweat Forty-five minutes after birth, the foal was able to stand
and pace the stall. Her tail was bandaged, and her udder with a base-wide stance and started typical udder-
and perineum were cleaned. Just after 10:30 PM, Labour of seeking behavior (Figure 1-4).
Love “broke her water,” and she went down in lateral The mare passed an intact placenta weighing 6kg, 1
recumbency and started to strain. Gentle vaginal exami- hour after foaling. A small sample of colostrum was
nation revealed the foal to be presented normally with the taken before the foal nursed and specific gravity was
nose palpable between the extended forelimbs. The mare checked using a sugar refractometer. It measured 29%,
was observed and left to foal unassisted. which is considered to indicate good colostral quality.
Ten minutes after the beginning of second-stage labor, The foal suckled from the dam 65 minutes after foaling.
a filly was born and rapidly attained a sternal position
2
1
CHAPTER 1 ASSESSING THE NEWBORN FOAL
Table 1-1 Mean (±sem) PaO Values Following
2
100% Oxygen Administration in Foals
Ages 30 Minutes to 7 Days
Fig. 1-4Typical base-wide stance of newborn foal in early udder-
(from Stewart et al., 1984).
seeking behavior.
over the first week (Table 1-1).7,8 This results in a sig-
TRANSITION TO EXTRAUTERINE LIFE
nificant increase in respiratory reserve by day 7.
Surfactant is present in the lungs from about 300
At birth the foal is hypoxemic and hypercapnic; this days gestation; however, a recent study9 has shown
stimulates the first gasping breaths, which start to that at 2 days after birth, surfactant surface tension is
inflate the lungs. There is also a marked decrease in markedly increased (tenfold) when compared with
pulmonary vascular resistance due to expansion of the that of 5-day-old foals. Also, the sum of anionic phos-
lungs and rising PaO , which allows increased blood pholipids is decreased in normal foals when compared
2
flow through the lungs. This produces increased return with that of adults. In the Thoroughbred, bronchiolar
of blood to the left atrium and functional closure of the duct endings continue to increase in the foal until
foramen ovale. Closure is also facilitated by the about 1 year of age. This continued postnatal devel-
decrease in right atrial pressure, due to absence of opment appears to be absent in ponies.10
venous return from the umbilical vein. The ductus
arteriosus constricts and flow is reversed, producing
physiological closure within 24 hours and anatomical
STAGES OF LABOR
closure over several days after birth.
Hypoxemia, hypothermia, and acidosis can lead to
reversion to a transitional or fetal circulation with right Most Thoroughbred mares foal at night, with 86%
to left shunting, as the foramen ovale and ductus arte- occurring between 7 pm and 7 am, and maximal inci-
riosus reopen and pulmonary hypertension develops. dence between 10 pm to 11 pm.11 During first-stage
This results in a worsening of the hypoxemia and labor, coordinated uterine contractions push the
further increases in pulmonary resistance. allanto-chorion into the dilating cervix; at this stage,
Stroke volume in the neonate is limited, so cardiac the mare starts to become restless and may begin to
output is rate dependant. There are significant changes sweat and walk. First-stage labor ends with rupture of
in the proportion of blood flow to the various organs the membranes and release of the allantoic fluid (i.e.,
at birth. In utero the kidney receives 2% of blood flow, “breaking water”). During this first phase of parturi-
which increases to 8% to 10% postpartum. The lungs tion, the front half of the foal starts to rotate from a
only receive 15% in utero, which increases to 100% flexed dorsopubic position to a dorsosacral position
postpartum.6 with the forelimbs and head extending into the birth
The chest wall of the neonatal foal is very compliant, canal.12 During second-stage labor, the caudal half of
but the lungs are relatively inelastic, which limits tidal the foal rotates. Although mares can foal in a standing
volume, increases work of breathing, and lowers func- position, most go into lateral recumbency at the start
tional reserve capacity of the lungs. High respiratory of second-stage labor.
rates help to overcome this. Tidal volume increases by The passage of the foal into the birth canal stimulates
about 20% during the first week; there is a continued oxytocin release, enhancing strong uterine and abdom-
rise in PaO and an increase in alveolar ventilation. The inal contractions that result in rapid expulsion of the
2
response to 100% inspired oxygen alters significantly foal. The white translucent amniotic sac around the
3
