Intensive Care of The Neonatal Foal

Symposium on Neonatal Equine Disease
Intensive Care of the Neonatal Foal
Anne M. Koterba, D.V.M.,*

Willa H. Drummond, M.D. t, and
Phillip Kosch, D.V.M., Ph.D.+
Throughout the years, a prevailing attitude of horse owners,

breeders, and veterinarians has been that the abnormal or weak new-
born foal, regardless of the cause of its problem, had no potential to
develop into a useful adult. Therefore, many have considered in-
vestment in intensive perinatal care (support of the animal's life) to
be a waste of effort and money. Interestingly enough, this same re-
luctance to interfere with the workings of nature also profoundly
influenced the way in which sick human infants were approached
until well into the second half of the twentieth century. Physicians'
visits to the nursery were a low-priority task, often accomplished
during the lunch hour; mortality rates in the newborns were corre-
spondingly high. 31 From the experience gained in human medicine
in the past 20 years, it is obvious that dramatic improvements can
be made in the survival of sick human infants with new intensive
care technology. Veterinary medicine has lagged far behind. How-
ever, the increasing monetary value of many equine neonates, com-
bined with the precedent set in human neonatology, has led breeders
to demand improved methods of caring for sick equine neonates.
Current experience indicates that although a certain nUlnber of com-
promised equine neonates will never be useful or even viable indi-
viduals, there are many others that can make dramatic recoveries and
become normal adults with proper support and management. 2 The
purpose of this article is to present some concepts and techniques
that have been found to be useful in dealing with the abnormal new-
born foal at the University of Florida Veterinary Medical Teaching
Hospital.
Froln University of Florida, Gainesville, Florida

* Diplomate, Alnerican College of Veterinary Internal Medicine; Graduate Research As-
sistant, Deparhnent of Medical Sciences, College of Veterinary Medicine
t Associate Professor, Deparhnents of Pediatrics and Physiology, College of Medicine,
and Deparhnent of Medical Sciences, College of Veterinary Medicine
* Associate Professor, Deparhnent of Physiological Sciences
Veterinary Clinics of North America: Equine Practice-Vol. 1, No.1, April 1985 3

4 ANNE M. KOTERBA, WILLA H. DRUMMOND AND PHILLIP KOSCH
General Concepts of Neonatal Intensive Care

Before addressing specific intensive care procedures, a few
major concepts relating to intensive care in the foal need to be dis-
cussed. First, the primary aim of the veterinarian should be to min-
imize the need to employ heroic measures to revive the collapsed
foal. A substantial proportion of neonatal losses can and should be
prevented by good management techniques and very early interven-
tion, diagnosis, and treatment in situations involving the high-risk
mare or foal. Second, the level of care delivered to an abnormal foal
can range from the very basic, such as provision of a heat lamp and
shelter, to considerably more sophisticated and labor-intensive life
support measures, such as mechanical ventilation, total parenteral
nutrition, and 24-hour nursing care. The decision as to what level of
care is provided to an individual animal must take into account a
variety of factors, including the amount of manpower available to
provide the care, the wishes of the owner and often the insurance
company, the nature and prognosis of the illness, and the potential
value of the animal compared to the cost of the treatment. .
The third concept, and one that cannot be stressed strongly
enough, is that the neonatal foal, although relatively mature at birth,
is not merely a miniature version of the adult; in many ways, it more
closely resembles neonates of other species. Some of these neonatal
characteristics strongly dictate tl1e type of care that must be delivered
in order to achieve a successful outcome. One of the most important
characteristics is the tendency for the neonate's condition to change
dramatically, for better or for worse, very quickly (witbin hours),
usually with only subtle advance notice. Careful, close observation
and monitoring of the abnormal foal by trained personnel is essential
so that the early warning signs of development of a new problem or
change in a current one can be detected and acted upon promptly,
before a disaster occurs. Once a problem is identified or suspected,
there is no room at all for the "let's wait and see how he's doing
tomorrow before we do anything" philosophy so common and usually
innocuous in adult equine medicine. Time and time again, novices
at neonatal medicine express amazement at the detrimental effect
that only a few hours' delay in treatment can make in the eventual
outcome of a case.
It is characteristic of the sick foal to accumulate a bewildering
array of problems. Rarely is a foal only premature; he may also have
multiorgan dysfunction secondary to asphyxia during birth, a variety
of infections, corneal ulcers, and crooked legs. A problem-oriented
approach, in which each problelll is listed and addressed separately,
allows a better grasp of a seemingly hopelessly complicated case and
helps to prevent the tendency to ignore a potentially major, but less
obvious, problem that is not the primary diagnosis.
A third characteristic of neonates in general is that their imlllune
system is not as competent as the adult's, and they are at higher risk
of acquiring a life-threatening infection. Although little research has
been specifically perforllled in the foal, it is likely that a variety of
INTENSIVE CARE OF THE NEONATAL FOAL 5
defense mechanisms, such as neutrophil function,13 do not operate
at maximum efficiency in the newborn foal. If, in addition, the foal
fails to acquire sufficient quantity of colostral antibodies (see the sec-
tion on colostrum) from the mother or another source, the animal is
in even greater danger of becolning infected. Thus, in delivery of
intensive care to these partially immunocompetent animals, sterile
technique, sanitary conditions, and provision of adequate passive im-
munity become crucial considerations.
Identification of the High-Risk Foal

In order to achieve the most favorable results from intensive
care, the patient must be recognized early in the course of the disease
process. In many cases, predisposing conditions are present long
before the actual birth and may profoundly affect the well-being of
the fetus. A functional fetoplacental unit and a healthy uterine en-
vironment are crucial both for normal fetal development and for
smooth adaptation to independent life after birth. Acquisition of a
detailed history to identify any prenatal problems is essential to pro-
vide adequate perinatal management to both the mother and fetus
or newborn. A list of some of the more common conditions associated
with the abnormal newborn foal is presented in Table 1. Prenatal
maternal problems such as fever, vaginal discharge, and illness often
predispose to fetal stress. Infection may reach the placenta and fetus
via an ascending route through the vagina or through a hematogenous
route. Careful examination of the fetal membranes, not only for in-
tegrity, but also for discolorations, abnormal thickenings, edema, or
other lesions often provides important clues concerning the etiology
of abnormalities such as a premature birth or an asphyxiated foal. 32,49
Histologic evaluation of sections of the relatively fresh placenta
may disclose subtle abnormalities contributing to placental insuffi-
ciency and fetal hypoxia that would otherwise be overlooked.
If possible, the true gestional age, as calculated from the
breeding dates, and an estimate of gestational age from physical ex-
amination should be determined and compared..Unfortunately, at
this time, gestational age estimation in newborn foals is not nearly
as accurate as in human neonates, and normal intrauterine growth
curves for the equine fetus have not been established. Even with
these limitations, however, the information may still serve as a valu-
able aid in identifying and diagnosing the abnormal foal. The pre-
luature foal (gestational age less than 320 days) has many immature
body systems, which places it at much higher risk than the term foal
of developing a variety of respiratory, metabolic, and infectious prob-
lems. 26 The post-term foal, although potentially perfectly normal,
may have congenital abnormalities such as anencephaly or in utero
growth retardation secondary to placental insufficiency. A comparison
of true gestational age and gestational age estimated from physical
examination is a very useful parameter in identifying the foal that is
small for its gestational age (SGA). SGA implies that some type of
chronic derangelnent during gestation, such as malnutrition, pla-
Table 1. Conditions Associated with High-Risk Neonatal Foal

MATERNAL CONDITIONS
1. Purulent vaginal discharge

2. Fever
3. Hydrops allantois
4. General anesthesia
5. Colic surgery
6. Endotoxemia
7. Excessive administration of Inedication
8. Past history of foal with isoerythrolysis, neonatal InaladjustInent syndrolne,
congenital anolnalies
9. Excessive colostral leakage before parturition
10. Poor nutritional status
CONDITIONS OF LABOR OR DELIVERY
1. Premature parturition
2. Abnonnally long gestation
3. Prolonged labor
4. Induction of labor
5. Dystocia
6. Early rupture of umbilical cord
7. Caesarian section
NEONATAL CONDITIONS
1. Meconium-stained fluid or foal

2. Placental abnonnalities (such as prelllature placental separation)
3. Placentitis (fungal or bacterial)
4. Twins
5. Orphan
6. Delay in or lack of intake of adequate colostrulll
7. hnmaturity or prematurity
8. Exposure to infectious diseases
9. Trauma (birth, predators)
cental insufficiency, congenital defects, in utero infections, or twin

placentas, interrupted normal growth processes. The seA animal
often experiences difficulty in adapting to the extrauterine environ-
ment and Inay well be in need of special care during this transition
n
period. Previously, Rossdale has used the term "immature or "dys-
n
mature to describe the type of foal that has signs of prematurity but
is born after a gestation greater than 325 days.39 With the seA ter-
minology, a foal may be termed as both prelnature and seA or Ina-
ture and seA.
During the birth process, there is great potential for a foal to
become severely asphyxiated. Indeed, in Inost norlnal births, some
degree of hypoxia and respiratory acidosis is transiently present. 37
However, when severe asphyxiation takes place, almost every organ
in the body may be adversely affected, and this damage may result
in a wide range of physiologic dysfunctions, creating multiple clinical
signs. A period of severe asphyxia may be easily recognized, as in
the case of a dystocia, or may be totally inapparent. In many situa-
I TENSIVE CARE OF THE NEONATAL FOAL 7
tions, if adequate nursing care is provided during the transition pe-
riod, even severely affected foals can completely recover and become
normal adults. The effects of acute and chronic hypoxia on the neo-
natal foal are covered in more detail in a recent review. 26
Any foal that fails to absorb normal amounts of colostrum during
the first 24 hours of life should be considered at increased risk of
acquiring a bacterial infection. Whatever the initial cause of the foal's
failure to ingest adequate colostrum, whether it be premature lac-
tation, lack of production by the mare, or an abnormality in the foal
(prematurity, asphyxia, intrapartum trauma), infection frequently be-
comes the most important problem causing the eventual demise of
the foal.
Hopefully, future research will disclose better techniques, such
as ultrasound evaluation and biochemical tests, to assess fetal stress
and placental abnormalities before parturtion. Although not all foals
will be severely affected when one or more of the conditions listed
in Table 1 are present, foals with these problems warrant careful
observation, environmental support, and, possibly, prompt work-up
and intervention. Consideration of historical factors in combination
with the physical examination and laboratory and radiologic results
may also provide key information for accurate diagnosis.
Initial Work-Up of the Neonatal Foal

At first glance, one critically ill foal looks very much like the
next one. The most common early clinical signs in a variety of dif-
ferent illnesses are vague and nonlocalizing, such as weakness and
decreased appetite. If one prominent localizing sign, such as diarrhea
or seizures, is present, it may obscure the fact that other organ sys-
tems are also severely involved. Clinical diagnosis in the newborn
foal is an extremely challenging, yet essential, proposition. In order
to facilitate an efficient and thorough work-up of the foal, a standard
diagnostic protocol (Table 2) is utilized for all foal admissions to the
University of Florida Veterinary Medical Teaching Hospital. Prompt
completion of the steps outlined in the protocol allows rapid accu-
mulation of an initial data base useful for early and accurate identi-
fication, evaluation, and treatment of many of the foals;) problems; it
also guides selection of further diagnostic tests. Although the protocol
calls for some investment of tilue and money at the outset, we feel
the benefits of a complete work-up at this time outweigh the disad-
vantages. Several problems have resulted when one or more steps
have been left out of the work-up. For example, when one 3-day-old
foal with diarrhea did not "look;);) septicemic, neither blood cultures
nor chest films were taken; antibiotic therapy was delayed for 3 days,
and the foal died from pneumonia at 1 week of age. In sum, execution
and proper interpretation of these diagnostic procedures helps the
veterinarian to remain one step ahead of the foal's clinical course
rather than a few steps behind, and to provide the client with an
educated idea of the prognosis relatively early in the disease process.
Table 2. Protocol for Receiving Neonatal Foals at University of Florida

Neonatal Intensive Care Unit
1. Assess immediate needs. Evaluate breathing pattern, respiratory rate, heart
rate, and mucous membrane perfusion. Perform resuscitation procedures or
begin 02 therapy if respiratory distress is present, before proceeding with
further diagnostic evaluation.
2. If hypothermia (less than 99°F) is present, apply heat lamps and heating
blankets.
3. Perfonn whole blood glucose determination. If result is less than 40 mg per

dl, continuously infuse 10 percent glucose solution to give 8 to 12 mg per kg
per minute of glucose (.08 ml per kg per minute of 10 per cent glucose) and
recheck blood glucose frequently.
4. Assess fluid balance. Aseptically insert intravenous catheter if fluid therapy

is required.
5. Draw blood for complete blood count and differential, count fibrinogen,
electrolytes, creatinine. Run zinc sulfate turbidity test and quantitative IgG
(if foal is more than 8 hours old and has nursed).
6. Draw blood for aerobic and anaerobic blood cultures.
7. Attempt to acquire arterial blood gas sample. If pulse quality is very poor,
obtain venous sample for acid-base evaluation.
8. Cauterize umbilicus with 3 per cent iodine if newborn or stump is moist.
9. When condition is stabilized, radiograph thorax and, if indicated, abdomen.
10. Submit placenta for histologic and gross examination. Culture uterus if in
utero infection is suspected.
11. Evaluate laboratory data, physical examination results and decide on

appropriate antibiotic, plasma, fluid therapy, tetanus antitoxin.
Initial Assessment: Rule Out Need for Immediate Intervention

The degree of compromise to the integrity of all homeostatic
systems must be evaluated. Immediate resuscitative procedures may
be required. Guidelines for resuscitation are outlined in Figure 1,
and emergency drug doses are listed in Table 3. In general,-resus-
citative efforts are directed towards several goals: 20
1. Expansion of lungs by clearing airway, thereby ensuring a patent airway.
2. Increasing arterial oxygenation (P0 2) by providing adequate alveolar ven-
tilation and oxygenation.
3. Maintaining adequate cardiac output, which may necessitate blood
volume expansion (using colloid [plasma], if possible).
4. Minimizing oxygen consumption by providing heat, glucose, and quiet.
The sequence of resuscitative efforts must be determined by the
condition of the animal. Re-evaluation of efficacy of efforts should be
made frequently. One must also take care to not be too aggressive
No improvement- - - ...
~
Improvement •
z
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t!j
z
~
Initial measures: <
t!j
1. Establish patent airway
n
a. Remove amniotic remnants >
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3. Provide 02 via mask or nasal insufflation t!j
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Is breathing pattern present and adequate? ~
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Begin external cardiac Entubate trachea

Provide
massage at 60-BO/min and ventilate
supportive
and continue. with Ambu bag (02)
care (02,
or mechanical ventilator
warmth,
at 20/minute.
fluids)
I _ 1
as needed
f f I·i t"
, , ,-1 Check blood gases
I
I NaHC03
as needed.
I<a+1 T
I
Dopamine IV
Figure 1. Resuscitation of the neonatal foal. Drug dosages may be found in Table 3. '"
Table 3. Emergency Drugs and Their Doses for Neonatal Resuscitation

DRUG DOSAGE ROUTE
Epinephrine .1 mI/kg, 1: 10, 000 solution IV

Calcium gluconate 1-2InI/kg, 10% solution IV
Sodium bicarbonate 2 mEq/kg (.5 InEqhnl) IV
Atropine 0.02 mgjkg SQ,IV
Isoproterenol 0.05-1. 0 IJwg/kg/minute IV
Dopamine 2-5 IJwgjkg/minute IV
Dobutamine 2-10 IJwgjkgjlninute IV
Doxapram 0.02-0.05 lng/kgjlninute IV
in intervening when the animal is making adequate progress on his

own. Besides potentially causing iatrogenic problems such as frac-
tured ribs, inappropriate intervention can adversely affect the process
of maternal bonding as well.
Asphyxia
The natural history of asphyxia has been experimentally repro-
duced in several species and is divided into four stages. In the rhesus
monkey, rapid gasps occurring shortly after the onset of asphyxia
cease after about 1 minute, beginning the period of primary apnea.
This apnea lasts about 1 minute and is followed by a series of spon-
taneous deep gasps lasting for 4 to 5 minutes, which weaken and then
end after about 8 minutes of total anoxia. This final period, called
secondary apnea, is followed by death if no ventilatory support takes
place. 14
A major difference between primary and secondary apnea is that,
in the latter, the respiratory center is no longer responsive to sensory
or chemical stimuli. Therefore, there is no indication for use of an-
aleptic drugs such as doxapram during this final stage of apnea; they
may only be of benefit during primary apnea. Once secondary apnea
occurs, it can be reversed only by assisted ventilation and circulatory
support. As it is usually difficult to determine in a clinical setting
whether primary or secondary apnea is present, the latter should be
assumed.
Although the newborn mammal generally tolerates asphyxia
better than the adult, severe hypoxia may well overcome any pro-
tective mechanisms in operation. Acid-base parameters change dra-
matically during total asphyxia. The pH drops sharply as the PaC0 2
rises, and severe respiratory acidosis and severe hypoxia result. Blood
lactate levels also rise, reflecting a switch to anaerobic metabolism
and accumulation of excess acid. Therefore, when asphyxia is pro-
longed, metabolic acidosis as well as (the primary) respiratory acidosis
may result. The appropriate treatment for respiratory acidosis is ad-
equate ventilation. Any attempt to correct the condition with
NaHC0 3 without ample ventilation may serve to worsen the acidosis
because NaHC0 3 is converted to CO 2 and is retained.
The use of hypertonic NaHC0 3 solutions has also been associ-
ated with both severe hyperosmolarity29 and an increased incidence
of cerebral vascular accidents, especially in newborn premature
human infants. 19 ,41 Because of these potential complications,
NaHC0 3 solutions should be administered with caution.
Metabolic acidosis can often be completely corrected with ap-
propriate ventilation and by improving circulation volume, thus elim-
inating the need for alkali therapy. However, if a foal's clinical con-
dition does not improve after adequate ventilation has been insti-
tuted, and blood gas analysis is not available, NaHC0 3 may be used
empirically at a dose of 2 mEq per kg intravenously (.5 mEq per L)
for treatment of suspected metabolic acidosis.
Emergency Ventilation
In an emergency situation, adequate ventilation can usually be
achieved by mouth-to-nose resuscitation. The neck should be ex-
tended, the nostrils cleared, the down nostril occluded, and a breath
delivered to the up nostril approximately 20 to 30 times per minute.
The size of the breaths delivered should be sufficient to cause rea-
sonably prominent thoracic excursions.
Ventilation can be provided more efficiently via an endotracheal
tube, but the necessary eq~ipment-an endotracheal tube, syringe
for cuff inflation, and lubrication-must be at hand. Silicone rubber
endotracheal tubes* 8 to 10 mm in internal diameter and 45 to 55
cm in length are recommended for foals up to 1 month of age; these
may be passed into the trachea from the mouth or the nose. 46 ,47
Ventilation can be delivered with a l-'L self-inflating, nonrebreath-
ing bagt that delivers oxygen-enriched room air.
Restraint and Sedation
A major obstacle to efficiently providing care to many neonatal
foals is the foals' tendency to be totally uncooperative patients, which
can turn the simplest procedure into a trying ordeal for all involved.
Therefore, finding effective, yet nonstressful, methods of restraint
becomes extremely important. Unfortunately, because we have not
yet discovered a mechanical device that safely restrains a thrashing
foal nearly as well as the human body, we must rely heavily on human
beings to serve this function. When virtually any prolonged inter-
vention, such as placement of an intravenous catheter, is required,
lateral recumbency with the down eye protected is the position of
choice. The foal's head may be placed in the operator's lap and one
of the operator's legs can be placed over the foal's shoulder in order
to control body movements. After a period of time, even normal foals
usually relax and often fall asleep when restrained in this position.
Another person placed at the rear of the foal may be needed in the
case of the violently thrashing foaL Ideally, a foal hed or platform is
* Bivona. Surgical, Inc., Gary, Indiana.

t Ambu Bag. North American Drager, Telford, Pennsylvania.
12 A E M. KOTERBA, WILLA H. DRUMMO D AND PHILLIP KOSCH
utilized to elevate the foal from the ground and improve hygiene. In
the severely depressed foal, when sternal recumbency is desired,
heavy wedge-shaped blocks may be built and placed at the shoulders
and hips to maintain this position. For short periods of time, most
foals may be effectively immobilized in the standing position by
firmly grasping both ears and holding them upright.
In the neonatal foal, a small bleb of lidocaine (2 per cent without
epinephrine) placed subcutaneously with a 25-gauge needle prior to
placement of the catheter or arterial puncture greatly facilitates these
procedures and may be the only anesthetic intervention necessary.
In many severely ill, seizuring or thrashing foals, long-term se-
dation is essential to prevent self-inflicted injuries. A number of
drugs have been suggested for use in these situations, and additional
information concerning them may be found in other articles in this
symposium and in previous reports. 4
Diazepam* is a sedative with anticonvulsant activity. It should be
administered intravenously slowly, starting with a dose of .1 mg per
kg (5 mg per 50-kg foal). Rossdale has suggested a dose of 10 to 20
mg per foal. 39 Cardiovascular and respiratory depression may accom-
pany intravenous administration. One seizuring foal died after a total
dose of 40 mg was administered over a short period of time. Di-
azepam is usually our initial therapy for seizure control and is effec-
tive at low doses (5 to 10 mg) in some foals. In others, however,
multiple doses at frequent intervals may become necessary. In these
foals, and in the foals that are not responsive to diazepam, other,
longer-acting anticonvulsants are often required.
Phenobarbitalt acts by raising the seizure threshold, and its peak
effect is seen at approximately 30 minutes. 4 Although lower doses
have been recommended previously, a dose of 20 mg per kg given
over 25 to 30 minutes has been suggested and used successfully in
clinical patients. This initial dose is followed by a maintenance dose
of 9 mg per kg administered intravenously three times a day.42 The
major side effects of phenobarbital observed in foals have been se-
dation and transient ataxia. Interactions between phenobarbital and
other drugs usually involve induction of the hepatic microsomal en-
zyme system. 51
Phenytoin:t has also been recomInended for seizure control in the
newborn foal. Initial dose is 5 to 10 mg per kg given intravenously
followed by 1 to 5 mg per kg every 2 to 4 hours for the first 12 hours,
then with increasing frequency. 39 This dosage has resulted in effective
seizure control in several foals that were unresponsive to both di-
azepam and phenobarbital; however, it also appeared to cause
marked depression in SOlne patients at the University of Florida.
* Valiuln. Hoflinan-LaRoche Inc., Nutley, New Jersey.

t Eli Lilly & Co., Indianapolis, Indiana.
+Dilantin. Parke-Davis & Co., Detroit, Michigan.
Unfortunately, at this time, reports of the pharmacokinetics of phe-
nytoin in the foal are unavailable, and the optimal dosage and toxic
side effects and drug interactions are not known. Weaning from an-
ticonvulsant therapy should be gradual in order to avoid recurrence
of seizure activity.
Xylazine* is a potent sedative in the foal, but its side effects include
depressed cardiovascular and respiratory function. 4 In several ab-
normal neonatal foals, marked depression and blanching of the mu-
cous membranes were noted following even low doses of xylazine
(.44 mg per kg or .2 mg per lb intravenously). Recovery was pro-
longed in several foals, and two foals died after receiving a dose of
.55 mg per kg (.25 mg per lb) intravenously. It is the authors' opinion
that xylazine should not be used for sedation in the already compro-
mised newborn foal.
The drug of choice for more complete, long-term immobilization
has not yet been determined. Occasionally, a foal is in need of me-
chanical ventilation for several days but is too vigorous to passively
tolerate this procedure. Sometimes, sedatives such as phenobarbital
are sufficient when the foal is already relatively depressed. In other
cases, anesthesia is indicated. Pentobarbital given at an initial dose
of 10 mg per kg and titrated to effect was used to maintain an ade-
quate plane of anesthesia for several days in a 5-day-old foal, but the
need for repeat doses did become increasingly frequent during that
time.
Skeletal muscle paralysis has been extensively used in human
medicine for IOllg-term restraint of infants receiving ventilator
therapy. Pancuronium sulfate (0.6 mg per kg, repeated as necessary)t
has been effective for short-term immobilization in combination with
pentobarbital (15 mg per kg) in the normal neonatal foal. However,
its usefulness and safety in long-term management of clinical cases
has not been established, although it is currently under investigation.
An obvious result of muscle paralysis is that the foal becomes totally
dependent on ventilator therapy, and machine malfunction or oper-
ator error may quickly result in death.
Intensive Care of the Respiratory System: Assessing the Need
for Therapy
Diseases associated with the respiratory tract are very common
in the neonatal foal, occurring both as primary conditions and as
conditions secondary to other disease processes. In many foals, ab-
normalities result from failure of the lungs to make a complete tran-
sition from a collapsed, fluid-filled, relatively inactive organ to an
air-filled structure responsible for acquiring sufficient oxygen for the
entire body. Even if the lungs are reasonably normal at birth, lung
pathology often develops during the course of a neonate's illness and
* ROlnpun. Haver-Lockhart, Shawnee, Kansas.

t Pavulon. Organon Pharmaceuticals, West Orange, New Jersey.
is often overlooked clinically. In one report of 37 foals less than 1

week of age, only three had a completely normal respiratory system
on pathologic examination. 17
Recognition of pulmonary abnormalities in the live foal is often
a diagnostic challenge. In evaluation of the respiratory system, re-
spiratory rate, pattern and effort of breathing, and mucous membrane
color should be observed and recorded at frequent intervals. Fre-
quent vital sign charts are often useful for spotting trends, such as a
progressive rise of respiratory rate over 6 to 8 hours. The normal
respiratory rate of the neonatal foal is 30 to 40 breaths per minute. 38
Many factors that are nonrespiratory in nature, such as excitement,
pain, high environmental temperatures, fever, metabolic acidosis,
systemic hypotension, and neurologic disease, may also elevate re-
spiratory rate. -In some cases, an elevation in respiratory rate does
correspond closely with a worsening pulmonary condition, but on the
other hand, a normal respiratory rate and pattern may be present 'in
spite of severe lung pathology (Fig. 2). Although auscultation of the
lung fields is often essential in order to identify respiratory abnor-
malities, lung sounds do not always correlate well with the severity
of the disease. Foals with few or no audible thoracic abnormalities
may have severe pulmonary pathology, especially interstitial lung
involvement and atelectasis, and increasingly obvious adventitial lung
sounds may be associated with recovery rather than deterioration in
condition. Mucous membrane color is not a reliable indicator of the
adequacy of oxygenation of the neonatal foal. Cyanotic mucous mem-
branesusually were not observed until the partial pressure of arterial
bxygen reached very low levels (Pa0 2 less than 40 mm Hg). A cough
is usually not present.
Figure 2. Lateral thoracic radiograph of a 7-day-old Arabian foal with Escherichia

coli septicemia. Note severe mixed interstitial and alveolar infiltrate in the ventral por-
tions of the lung fields. At this tilne, the respiratory rate wa~ 24 per lninute, lungs
auscultated normally, and no cough or nasal discharge was present. The pneulnonia grad-
ually iInproved with long-term antibiotic therapy.
Because of the difficulty in accurately assessing the respiratory
system through physical examination alone, chest radiology and ar-
terial blood gases have become integral components of our work-up
of the abnormal neonatal foal (see Table 2).
Thoracic Radiology
Thoracic radiology is often necessary to firmly establish that a
respiratory problem exists and to determine the extent of pulmonary
involvement. Thoracic radiographs in human neonatology have be-
come very useful in identification of several specific patterns char-
acteristic of particular disease process; with time, this may be possible
in equine neonatology as well. For example, hyaline membrane dis-
ease is typically represented by a diffuse ground-glass appearance
with prominent air bronchograms in the human infant; the same
appears to be true in the horse (Fig. 3). Radiology is also useful to
monitor the progress of a respiratory condition. It must be kept in
mind that radiographic changes may follow or precede changes in
clinical condition and that major changes can occur surprisingly rap-
idly (Fig. 4). Unfortunately, at this time, large voids still exist in our
knowledge concerning even the normal radiographic appearance of
the foar s thorax at different gestational ages. In the past, thoracic
films have not been easily available to the veterinary practitjoner,
but with the development of rare earth screens, quality chest ra-
diography is possible using portable x-ray unit~.
Arterial Blood Gas Analysis
Arterial blood gas analysis has been traditionally avoided by vet-
erinarians for a variety of reasons. Blood gas analysis is often expen-
sive, and laboratories with the necessary equipment are not always
conveniently located for practitioners. Arterial blood samples can be
quite difficult to obtain, and many veterinarians feel uncertain about
interpreting the resulting values. However, it is very difficult to safely
and effectively administer respiratory support to neonates without
means to monitor Pa02 . Even the simple technique of oxygen insuf-
flation is potentially hazardous; if high oxygen partial pressures are
inadvertantly maintained, resorptive atelectasis and pulmonary ox-
ygen toxicity may result. 48 Thus, arterial blood gas data are important
to define the severity of respiratory compromise, the type of therapy
indicated, and the response to therapy.
Technique. Arterial blood gases can be obtained by direct
puncture from several sites. Although the carotid is the largest artery,
hematomas commonly form after a few samplings. More peripheral
arteries such as the brachial as it crosses the medial aspect of the
foreleg, great metatarsal, and facial are readily palpable ifblood pres-
Sure is adequate.' The brachial vein may be inadvertantly sampled
fairly easily, but the likelihood of mistakenly acquiring venous blood
in the area of the great metatarsal artery is much less, for in most
foals the vein is very small. As mentioned earlier, a small bleb of
local anesthetic (lidocaine 2 per cent, wlo epinephrine) can greatly
faCilitate proper collection ana minimize needless struggling and sub-
I,
,._.
t
Figure 3. A, Lateral thoracic radiograph of 305-day gestational age, 3-hour-old foal

in respiratory distress. A severe diffuse alveolar pattern is present throughout the lung
fields and "is suggestive of hyaline membrane disease. B, Lung from foal in part A ap-
proximately 24 hours after radiographs were taken. Many alveoli are lined by hyaline
membranes. Interstitial areas are widened by inflammatory cells, primarily neutrophils.
(Hematoxylin and eosin, X 85)
sequent hyperventilation. A small gauge needle (25 gauge, 5/8 inch)

attached to a 3-ml syringe with the· hub filled with heparin is used
for arterial sampling. Any air bubbles are removed" the syringe is
sealed with a rubber cork and placed in ice slush until analysis is
carried out. A sample handled in this manner may be stored for 6
hours without major changes in Pa0 2 . 22 Pressure should be applied
to the arterial puncture site for 1 to 2 minutes after needle withdrawal
to avoid formation of a hematoma.
Problems caused by poor patient compliance and vessel trauma
after multiple punctures can be serious limitations to adequate blood
gas monitoring. Percutaneous placement of an indwelling arterial
Figure 4. A, Chest radiograph of a 6-day-old Thoroughbred foal in respiratory

distress with severe pneumonia secondary to Staphylococcus aureus septicelnia. B, Chest
radiograph of same foal 5 days later, when clinical condition was markedly improved.
Note the almost complete resolution of the previously extensive puhnonary infiltrate.
(Froln Kosch, P. C., Koterba, A. M., Coons, T. ]., et al.: Developments in management
of the newborn foal in respiratory distress: Evaluation. Equine Vet. ]., 16:312-318, 1984;
with permission.)
catheter in the great metatarsal artery is not difficult if pulse quality

is adequate, but maintenance of catheter position and patency can
be difficult in all but the most depressed patients. The catheter must
be firmly sutured to the skin and bandaged carefully to limit motion
and maintain sterility. A slow constant saline infusion system is safer
and more effective than intermittent heparin flushes in maintaining
patency. Other options for catheter insertion include s~rgical cut-
down on the great metatarsal artery or, if the birth of a high-risk foal
is attended, insertion of an umbilical arterial catheter. In each case,
18 A NE M. KOTERBA, WILLA H. DRUMMOND AND PHILLIP KOSCH
the advantages of continuous access to an artery must be carefully

weighed against the disadvantages, including the potential for intro-
duction of serious systemic and local infection and hemorrhage.
Interpretation. Valid interpretation is dependent not only on
,correct sampling and measurement techniques but also involves rec-
ognition of the circumstances present at the time of sampling. These
include the following: (1) position of the foal; (2) degree and duration
of struggling; (3) inspired oxygen concentration; and (4) gestational
age of foal. In certain foals, particularly those with immature or dis-
eased lungs, a significant decrease in Pa0 2 was caused by reposi-
tioning from sternal to lateral recumbency.25 This observation also
tJecomes important in treatment consideration. Struggling and sub-
sequent hyperventilation will usually result in a temporary decrease
in PaC0 2. With supplemental 02' Pa0 2 will be increased variably,
depending on the amount of right to left shunting present. For ex-
ample, Pa0 2 of 85 torr would be considered very normal in a foal
breathing room air, but it would be very abnormal if the animal was
breathing 100 per cent oxygen. Finally, "normal" blood gas values
are influenced by both gestational and postnatal age of the foal. A
summary of previously reported normal blood gas is presented in
Table 4.
One of two patterns of blood gas derangements is generally en-
countered: hypoxemia (p02 less than 70 mmHg) with normal or low
PaC0 2 and hypoxemia with hypercapnia. If th~re is hypercapnia and
resulting respiratory acidosis, hypoventilation is diagnosed. Hypo-
ventilation usually results from the inability or unwillingness of the
animal to breathe hard enough to compensate for the lung pathology
present. Clinical signs must be evaluated in addition to blood gas
analysis in order to choose the appropriate therapy. Certain hypoxic
foals do not display signs of respiratory distress, whereas others with
the same blood gas picture will be markedly distressed; the reasons
for these discrepancies are not well understood but may include ra-
pidity of development of the problem, developmental or pathologic
variations in chemoreceptor function, and type of lung pathology
present.
Therapy of Hypoxia
The correction of hypoxia involves the following: (1) optimization
of breathing efforts by ensuring a patent airway and by positioning
of the foal; and (2) increasing the fractional inspired concentration of
oxygen (FI0 2) to provide adequate arterial oxygenation. The possi-
bility of inadvertent inspiration of dirt or bedding should be mini-
mized. Excessive secretions or foreign substances should be suc-
tioned from the airways with long (56 cm) 10- to 15-gauge catheters. 47
Care should be taken to avoid long periods of suction, for this can
cause dramatic falls in arterial oxygenation. 8 As previously men-
tioned, improved arterial oxygenation and decreased effort of
breathing has been noted when hypoxic foals have been repositioned
from lateral to sternal recumbency.25 Therefore, attempts are made
to maintain some semblance of sternal recumbency, and blood gases
~
z...,
trl
Z
~
tTi
n
>-
::;:J
trl
o"'I"j
...,
::c:
Table 4. Blood Gas Values Reported for Normal Term and Premature Foals* trl
Z
t!'J
FOAL Pa02 (MMHG) P a C0 2 (MMHG) PHa o
Z
>-
...,
Age post- 95% 95% 95% ~
Gestational partum Mean confidence Mean confidence Mean confidence L'
status (hours) Number ± SEM limits ± SEM limits ± SEM limits REFERENCES ~
o
>-
L'
Normal 3-168 10 80.1 ± 3.8 56-104 47.5 ± 2.6 31-62 7.354 ± 0.011 7.28-7.42 38
Normal 1-12 6 77.4 ± 3.1 60-92 42.2 ± 1.8 34-50 7.378 ± 0.015 7.34-7.41 37
Normal 12-48 6 83.2 ± 3.1 68-98 44.5 ± 1.2 38-50 7.374 ± 0.004 7.35-7.39 37
Normal 48-168 5 88.2 ± 5.9 61-114 42.4 ± 1.0 37-47 7.384 ± 0.014 7.32-7.45 37
Normal 4-11 5 83.8 ± 6.3 55-Ill 39.5 ± 1.8 31-47 7.367 ± 0.010 7.32-7.41 36
Premature 0.5-11 7 53.7 ± 1.5 45-62 55.3 ± 3.6 36-74 7.208 ± 0.048 6.95-7.46 36
* From Kosch, P. C., Koterba, A. M., Coons, T. J., et al.: Developments in lnanagement of the newborn foal in respiratory distress. Evaluation.
Equine Vet. J., 16:312-318, 1984; with permission.
~
~
20 ANNE M. KOTERBA, WILLA H. DRUMMOND AND PHILLIP KOSCII
are repeated in this position. If sternal position is not possible, foals

are turned at least hourly to try to avoid progressive atelectasis and
subsequent formation of intrapulmonary right to left shunts.
FI0 2 is most easily increased by insufflation using a bias flow of
100 per cent oxygen. 47 Nonirritating, flexible, plastic tubing is intro-
duced into the nasopharynx via the ventral meatus and sutured or
taped to the nose. Oxygen is usually initially delivered at a flow rate
between 5 to 10 L per minute. In order to prevent drying of the
airways, it is important that the gas be humidified. II The catheters,
humidifiers, and tubing are replaced daily, and the nose is examined
for erosions. Most foals tolerate the tubing very well; the major C0111-
plication has been a mucopurulent nasal discharge that spontaneously
resolved. The actual oxygen concentration delivered by this method
to the lung is not easily determined; it is dependent on several fac-
tors, including the position of the tube and depth of breathing. Rose
has reported that in healthy term foals, a flow rate of 10 L per minute
oxygen resulted in a Pa0 2 of around 300 torr. 36 Oxygen therapy
should be directed at maintaining a Pa0 2 of 70 to 100 mm Hg, and
the flow rate should be adjusted according to blood gas results. If
severe intrapulmonary or cardiac shunts are present, even high flow
rates may raise Pa0 2 very little. Weaning from oxygen therapy should
"be done gradually, with frequent blood gas reassessments to ensure
that the foal's condition remains stable. It should be kept in mind
that the exact Pa0 2 that produces tissue hypoxia in a particular neo-
natal foal cannot be predicted.
The decision on when to institute oxygen therapy is somewhat
subjective and should be based on clinical signs and blood gas anal-
ysis. An elevated respiratory rate, labored respirations with excessive
intercostal and abdominal muscle activity, cyanotic mucous melTI-
branes, and restlessness are considered indications for a trial of ox-
ygen administration. The diagnosis is often confirmed by a marked
improvement in attitude or breathing pattern concurrent with O 2
delivery. Absence of response may indicate either a nonrespiratory
origin of the clinical signs or severe lung pathology with shunting. If
blood gases are analyzed, the authors consider a Pa0 2 of less than 60
mmHg in lateral recumbency an objective indication for oxygen
therapy. 47
Therapy of Hypoventilation
In order for hypoventilation to be diagnosed, an elevated PaC0 2
must be present. The only treatluent for hypoventilation is to in-
crease ventilation, and the two most common ways to accomplish this
are by chemical stimulation or by positive pressure ventilation.
Aminophylline and theophylline are bronchodilators t~at have
been shown to improve tl1e contractibility of the fatigued diaphragm. l
They will be covered in greater depth in the article, "Respiratory
Problems in Foals." Doxapram* may be administered as a steady
* Dopram-V A. H. Robins Co., RichlTIond, Virginia.

I TENSIVE CARE OF THE NEO ATAL FOAL 21
intravenous infusion (.02 to .05 mg per kg per minute) to increase
ventilation but has the disadvantage of also increasing myocardial
work and oxygen consumption.
Signs of respiratory failure-that is, respiratory distress, hypox-
emia in spite of oxygen administration, and progressively increasing
PaC0 2-usually indicate a need for some type of mechanical venti-
lation. However, in a very small group of foals with all of those signs,
in which economic or other considerations dictated that mechanical
ventilation not be performed, the PaC0 2 finally stabilized between
60 to 75 torr, remained at that level for a few days, and then declined.
During that time, only nasal oxygen insufflation, antibiotics, and re-
spiratory support techniques were provided, yet the respiratory con-
dition responded to the therapy and the foals recovered.
Unfortunately, there are few procedures in equine neonatal in-
tensive care that are as time-consuming and involved as long-term
mechanical ventilation. Provisions must be made for nutritional sup-
port, blood gas monitoring, long-term sedation or anesthesia, as well
as continuous surveillance of the equipment and patient. At this time,
although experience with ventilating foals is still quite limited, some
neonatal foals with severely compromised lungs have been main-
tained on a ventilator from 12 hours to 5 days and then successfully
weaned from it. They are developing normally and show no clinical
evidence of residual lung damage at the present time.
It is not possible in this article to describe all the details of
ventilating a foal, and the reader is referred to other texts and articles
for further information. 44 ,47 A few generalities are presented here.
1. Candidates selected for ventilation ideally should be those
with pulmonary disorders that are potentially readily reversible, such
as hyaline membrane disease and congenital or aspiration pneu-
manias. For example, the colostrum-deprived foal in septic shock
with joint and other organ involvement would not be considered an
ideal candidate with our present state of knowledge.
2. Administration of positive pressure ventilation is most easily
achieved by use of intermittent mandatory ventilation (IMV). This
provides a certain number of mandatory breaths around which the
foal can breathe spontaneously. The suitability of high-frequency ven-
tilation for use in the foal is under current investigation.
3. In foals, administration of positive pressure ventilation is
probably best accomplished after nasal-endotracheal intubation with
extra-long (56 cm) flexible silastic endotracheal tubes, 8 to 10 mm
internal diameter. * This technique has an advantage over oral-tra-
cheal intubation in that the tube can be placed and maintained in
the awake foal with surprisingly little difficulty. 46
4. A volume-cycled ventilatort appears preferable to pressure-
cycled ventilators for delivery of IMV to the spontaneously breathing
foal, in terms of patient compliance and ease of operation. This type
* Bivona. Surgical, Inc., Gary, Indiana.

t 1M Ventilatory Model 3-AVM. J. H. Eluerson Co., Calubridge, Massachusetts.
of ventilator also has the capacity to deliver humidified and heated

gases, provide positive-end-expiratory pressure (PEEP) and contin-
uous positive airway pressure (CPAP).47
5. The optimal ventilator settings are extremely individual. In
the volume-cycled ventilator, tidal volume, frequency, and FI0 2 are
set and an inspiratory pressure (PIP) is generated. In the normal 40-
kg foal, a tidal volume of 500 ml (12 ml per kg) with a frequency of
20 breaths per minute might be expected to generate a peak inspir-
atory pressure of around 20 cm H 20 and maintain normal blood
gases. However, in the diseased lung, a higher tidal volume and PIP
(100 cm H 2 0 in one 30 kg foal with HMD) may be required to
maintain even marginally adequate blood gases. As PIP is increased,
the risk of pneumothorax and cardiovascular compromise is also in-
creased. Ideally, FI0 2 should be adjusted to maintain Pa0 2 between
70 to 100 mmHg.
6. In some foals, improved gas exchange may be achieved by
use of PEEP or CPAP, both of which maintain airway pressure above
atmospheric pressure during part or all of expiration. This acts to
prevent closure of small airways at end expiration, decreases the
inspiratory pressure necessary to reopen the closed airways, and thus
reduces the work of breathing. These techniques have been ex-
tremely useful in improving survival rates of premature human in-
fants with HMD and maybe of use in the foal as well. However, their
effects need to be more thoroughly studied in the foal.
7. «Assisted:>:> ventilation, in which the animal initiates inspiration
and then the breath is completed with positive pressure, may be
delivered with a demand valve* on a temporary basis to a foal with
respiratory distress. 47
8. A nasogastric tube should be left in place during positive-
pressure ventilation to allow evacuation of any gas that inadvertently
collects in the stomach. Oral feeding may also be done through this
tube if the gastrointestinal tract will tolerate this form of nutrition.
However, in many of these foals, gastrointestinal function is not
normal and the animals are best fed by parenteral alimentation.
9. Maintenance of hygiene is of utmost importance in any anilnal
receiving ventilatory support. Many of the normal defense mecha-
nisms of the respiratory system are bypassed or altered by endotra-
cheal intubation, increasing the risk of bacterial invasion and colo-
nization. Tubes should be kept clean and free of secretions by suction
with sterile catheters every 3 to 4 hours or as needed. If pneumonia
develops, antibiotics should be administered according to culture and
sensitivity results.
Respiratory Supportive Techniques
The topics of bronchodilator therapy and nebulization will be
covered in the article, «Respiratory Problems in Foals.:>:> In the foal
with pneumonia, the use of coupage on a routine basis is highly
* Hudson Oxygen TherCl:PY Sales Co., Orange Park, Florida.

I TENSIVE CARE OF THE NEONATAL FOAL 23
recommended. Both sides of the chest are rapped firmly and re-
peatedly with a cupped hand, and tenacious secretions are loosened
and mobilized from the lower airways.
Critical Care of the Circulatory System and Heart: Assessment of
the Need for Therapy
Abnormalities of the cardiovascular system are very common in
the neonatal foal. The cardiac problem lTIOst frequently occurs sec-
ondary to problems such as dehydration, hypoglycemia, bacterial in-
fections, toxemia, or birth asphyxia, with resulting dysfunction of
both myocardial and endothelial cells. Congenital structural malfor-
mations also occur in foals and should be considered if intractable
cyanosis or low output occurs. The most common manifestations in-
clude poor pulse quality, prolonged capillary refill time, hypotension,
tachycardia, cold extremities, peripheral edema, and cyanosis. Cy-
anotic heart disease must be differentiated from respiratory causes of
cyanosis as rapidly as possible. Diagnostic aids such as cardiac aus-
cultation, blood gases, blood pressure measurement, electrocardio-
grams, echocardiograms, radiology, and occasionally cardiac cathe-
terization may help to define a primary heart anomally.
A holosystolic grade I-Ill/VI murmur, loudest at the left heart
base, is generally considered normal in neonatal foals. Although it
gradually diminishes in intensity, the murmur is often still auscul-
table at several weeks of age. 28 A murmur auscultated on the right
side and a high intensity murmur with or without a palpable thrill
on either side, in the absence of severe anemia, are suggestive of
cardiac pathology and indicate the need for further work-up.
Adequacy of circulation can be judged on physical examination
by pulse quality, mucous membrane color (pink and moist), capillary
refill time (less than 1 second), heart rate, (normal is 60 to 120 beats
per minute), and adequate urine production (more than 2 mg per kg
per hour). The overall state of hydration and total fluid requirements
of the animal may not be easy to accurately assess from physical or
laboratory parameters. Frequently, although peripheral pulses are
very weak and other signs of circulatory collapse are present, the
typical signs of tissue dehydration (tenting skin, sunken eyeballs, and
so on) may not be present, particularly when onset of clinical signs
is quite abrupt. In general, measurement of packed cell volume and
total plasma solids have not been particularly useful parameters for
initial evaluation of fluid requirements; normal values are quite vari-
able between foals, and even in the same foal over time. 23 In addition,
if severe dehydration has developed slowly, very little change in
packed cell volume may be noted, yet large fluid deficits may still
be present. 9 These laboratory parameters become more useful in the
monitoring the response of an animal over time to therapy.
Therapy of the Compromised Cardiovascular System
Intravenous Catheterization. In many foals, the seriousness of
their illness dictates that parenteral fluid therapy be continuously
provided via an indwelling intravenous catheter. However, these
catheters can also serve as an important source of infection for the

compromised animal. Therefore, it is essential that sterile techniques
be stringently followed in placing and maintaining the catheter. A
variety of catheters are available but a few types seem to work par-
ticularly well in the equine neonate. These include the 16-gauge, 2-
inch long over-the-needle teflon catheters, which have provisions for
suture placement directly around the catheter for secure placement
without the need for tape. * This type is easy to introduce and if
sutured to the skin, tends not to pullout or kink. A longer (5lJ2 inch)
16-gauge over-the-needle type cathetert is also used but is more
difficult to introduce in the short-necked foal. After introduction of
the catheter, preferably through a bleb of local anesthetic, the area
should be covered with antibiotic ointment and sterile gauze after
the hub of the catheter is attached to a saline-filled extension tube
(to avoid repeated contamination of the skin site). The gauze is then
secured with an elastic tape.:I: The injection hub should be wiped off
with a disinfectant such as betadine before any injections or with-
drawals are made. The catheters are changed every 48 to 72 hours,
or sooner, if signs of infection develop. At the Veterinary Medical
Teaching Hospital, the catheter tips are routinely cultured, but the
value of this procedure has not been established.
The most commonly catheterized veins at the Hospital are the
jugular and the cephalic veins. Both are large veins and easily ac-
cessible even if marked hemoconcentration is present. In the down
and thrashing foal, a catheter securely sutured in the cephalic vein
has been easier to maintain than a jugular one. Because of their
potential for causing iatrogenic problems, indwelling intravenous
catheters are removed as soon as the condition of the foal permits.
Fluid Therapy: General Considerations
The choice and amount of fluids administered are dependent on
the degree of dehydration, magnitude of current losses, and renal
function, and the electrolyte and acid-base status of the patient. Ex-
cept in a few situations, the electrolyte status and requirements of a
particular neonatal horse are virtually impossible to predict from
physical examination alone. One of the exceptions is the foal with a
ruptured bladder, in which hyponatreluia, hyperkalemia, hypochlo-
remia and metabolic acidosis are typical but not pathopneumonic
findings. 5 Another fairly consistent metabolic derangement, partic-
ularly in the premature, asphyxiated or septic newborn, is hypogly-
cemia. Because serum levels are frequently life threateningly low
(less than 40 mg per dl), it is important to identify and correct the
deficiency promptly before irreversible damage to the cells has been
done. Whole blood glucose levels can be rapidly and satisfactorily
* Quick-cath. Travenol Labs, Deerfield, Illinois. .

t Abbocath 16 gauge x SlJ2 in. Abbott Hospitals Inc., North Chicago, Illinois.
:j: Elasticon. Johnson & Johnson, Inc., New Brunswick, New Jersey.
INTE SIVE CARE OF THE NEONATAL FOAL 25
determined at the farm by several types of reagent strips. * To avoid
erroneously low readings, the lids to the containers must be kept
tightly closed and outdated strips should be discarded. Severe hy-
poglycemia may be treated with a constant infusion of 5 to 10 per
cent Dextrose given at a rate of 4 to 8 mg per kg per minute. Hy-
pertonic glucose boluses may aggravate pre-existing central nervous
system insult and frequently result in rebound hypoglycemia 40 to
90 minutes after they are discontinued. 30 Blood glucose level should
be monitored frequently during therapy. For the most part, serum
electrolyte values are necessary to formulate an optimal fluid replace-
ment plan. A number of foals that show vague signs of illness during
the first few days of life have had unexpected and unusual electrolyte
values. For example, one relatively normal-appearing foal born to a
mare recovering from endotoxemia had a serum K + of 8.0 mEq per
L (normal is 4.6 ± .5 mEq per L), a creatinine of 16.7 mg per dl
(normal is 2.5 ± .6 mg per dl, day 1 of age) and severe metabolic
acidosis 1 hour after birth, indicating that there had been some com-
promise to the foal in utero. Another extremely depressed and weak
foal had a calcium of5.9 mg per dl (normal is 11.7 ± 1.0 mg per dl)
and a phosphorus of 8.2 mg per dl (normal is 5.6 ± .9 mg per dl) on
admission. After the electrolyte imbalances were corrected, the foal
began to act completely normal; the primary abnormality was never
diagnosed. Because of the unpredictability of the electrolyte status,
we recommend that N a +, K +, CI +, Ca +, P +, creatinine, and
glucose be run as part of work-up of the foal (see Table 2). While
awaiting the results, a balanced electrolyte solution with glucose
added may be provided for emergency volume replacement.
The volume of fluid required depends on maintenance require-
ments, fluid deficits, current losses, and renal function. In most neo-
natal foals that do not have conditions that increase sensible or in-
sensible water losses, such as diarrhea, increased breathing effort, or
seizures, 70 to 90 ml per kg per day or 3 to 4 L of fluids per day to
a 45-kg foal (125 to 170 ml per hour) is usually adequate, once initial
deficits are replaced. If serum creatinine is elevated or renal function
is questionable, it is important to monitor urine output closely to
avoid fluid overloading an oliguric animal.
Urinary catheters may facilitate volume quantitation but they
also serve as a nidus for infection and have been difficult to maintain
in place in the male foal. As the healthy neonatal foal receives most
of his entire caloric requirements from a liquid diet, the usual specific
gravity of the urine is very low (1.001 to 1.012). Although specific
studies have not been performed, the concentrating ability of the
neonatal foal's kidney, like the kidneys of other neonates, is probably
not as efficient as the adult's. 3 A urine specific gravity of greater than
1.025 has rarely been observed in the neonatal foal, in spite of the
coexistence of severe hemoconcentration. Rate of fluid administra-
* ChelTIstrips. BiodynalTIics, Inc., Indianapolis, Indiana. Dextrostix. AlTIeS Division,

Miles Laboratories, Elkhart, Indiana.
26 ANNE M. KOTERBA, WILLA H. DRUMMOND AND PHILLIP KOSCI
tion is increased from maintenance level according to urine specific

gravity and output, packed cell volume, total protein, and physical
parameters, especially weight and observed losses.
Replacement of Specific Fluid Deficits
In calculation of specific electrolyte replacement, it should be
remembered that in the newborn, the extracellular fluid volume is
relatively larger than in the adult. In the term 7-day-old pony foal,
extracellular fluid volume was measured at 43 per cent of body
weight24 compared to previous measurements in adult horses of 25
per cent of body weight. 10 Thus, in calculation of NaHC0 3 replace-
ment requirements, the following formula would be appropriate:
Body weight (kg) x base deficit x 0.4 = replacement (mEq)
Metabolic acidosis is a common acid-base derangement in the
foal that has a compromised cardiovascular system. About 40 per cent
of 33 septicemic foals had metabolic acidosis diagnosed by blood gas
analysis. 27 Venous blood from a large vessel such as the jugular is
adequate for acid-base determination. As discussed earlier, much of
the acidosis secondary to poor tissue perfusion can be corrected with
volume expansion without the use of hypertonic NaHC0 3 solutions.
However, when metabolic acidosis is severe or when losses of bicar-
bonate are pronounced, such as in many diarrheic states, bicarbonate
therapy may be indicated. The total deficit is calculated, one half of
which is replaced over 1 hour and values are rechecked.
Hypokalemia is also a common finding in the sick neonatal foal,
particularly when anorexia and/or diarrhea is present. Because the
majority of K + resides in the intracellular compartment (150 mEq
per L) as opposed to the extracellular space (4 to 5 mEq per L),
estimates of K + deficits based on serum levels may grossly under-
estimate the real replacement requirements, especially if sizable
water and solute losses have taken place from the intracellular
space. 43 Potassium deficits may be replaced either by the intravenous
or oral route. If the intravenous route is selected, 20 mEq KCI is
usually added to each liter of replacement fluids and is given slowly
to minimize any cardiac side effects. Oral administration of KCI in
milk or in syrup has certain advantages. Deficits may be replaced
more quickly because larger amounts can be given safely in a shorter
period of time. Before potassium is administered, renal function
should be assessed to avoid production of a hyperkalemic state.
Frequently, in spite of adequate replacement fluid therapy, the
foal still has poor pulse quality and perfusion; many of these animals
are in septic shock or have myocardial dysfunction, and so on. Volume
expansion and inotropes may be needed.
Blood Volume Depletion
Newborn mammals have several potent neurohormonal com-
pensatory systems that act in concert to allow them to adjust to the
cardiocirculatory demands of birth. The process of labor elevates cir-
I TENSI\'E CARE OF THE NEO ATAL FOAL 27
culating cathecholamines, triggers release of renin, which the fetus
converts to angiotensin II, and stimulates a many-fold increase in
circulating levels of arginine vasopressin (antidiuretic hormone).
Each of these normally hyperactive vasopressor systems further in-
crease in hormone production if asphyxia and/or peripartum fetal
hemorrhage supervene during the birth process.
Owing to interplay of these VaSOlTIotor support systems, terlTI
neonates may lose up to 30 to 50 per cent of their circulating blood
volume before acute cardiovascular collapse is noted clinically. In the
immediate postpartum period, a significantly hemorrhaged neonate
may exhibit minimal or confusing sylTIptomatology, for cyanosis or
respiratory symptoms, without obvious pallor, may predominate. The
blood pressure, if taken, might be normal, because numerous cap-
illary capacitance beds have been constricted by catecholamines, high
a-adrenergic sympathetic tone, angiotensin II and antidiuretic hor-
mone. The correct diagnosis of hypovolemia might be overlooked in
the absence of a high index of suspicion. With time, however, the
acute stresses lessen. Levels of circulating catecholamines and va-
soactive peptides fall. Exogenous warmth vasodilates the skin.
During these hours, as poorly perfused regional vascular beds con-
vert to anaerobic metabolism, a previously hemorrhaged neonate
whose initial blood pressure was normal may develop progressive
hypotension and lactic acidosis. In some term foals, the acidosis may
trigger reactive pulmonary vasoconstriction, pulmonary pressure will
exceed the falling systemic pressure, and right to left shunting can
begin.
Unrecognized peripartum hemorrhage can be a common ante-
cedent event leading to volume depletion. Other contributing con-
ditions are massive third-space volume losses, as could occur with
ruptured bladders, or endotoxemia, which can cause massive capil-
lary leak with secondary intravascular volume depletion. Documen-
tation of hypovolemic shock requires measurement of subnormal cen-
tral venous pressure (normal is 0 to 4 mmHg). This can be accom-
plished in the neonate by passing a catheter from the jugular vein
into the right atrium. Hypovolemic shock is easily rectified if blood
and plasma losses are replaced early in the course. If hypovolemia is
unrecognized, secondary subcellular organelle dysfunction in the
heart, lungs, brain, liver, kidney, and so on can result in "irreversible
shock" in the neonate, just as in adults.
Autonomic Dysfunction
In health, a complex array of negative and positive feedback
systems operate to maintain cardiocirculatory homeostasis. Periph-
eral carotid and aortic arch baroreceptors, and right and left atrial
mechanoreceptors send afferents to the brain stem where impulses
are integrated and translated into appropriate efferent information.
Efferent neural impulses travel via vagal and sympathetic nerves to
effect heart rate and contractility changes and, acting in concert with
local autoregulation, to adjust systemic and pulmonary arteriolar and
venous tone so that blood flow and tissue oxygen and nutrient de-
mands are matched. Atrial mechanoreceptors sense changes in atrial
wall stretch (which is directly related to vascular volume change, in
the absence of positive pressure ventilation) transmitting that infor-
mation via the vagus to the hypothalamus. When the atria expand,
artrial stretch receptors are activated and arginine vasopressin secre-
tion is halted. When the atria contract (or are squeezed- by inappro-
priately high ventilator pressure), the loss of stretch receptor afferent
input results in increased central production of arginine vasopressin.
The kidney senses pulse pressure directly and activates the
renin-angiotensin system when pulse pressure decreases. Angio-
tensin II directly increases systemic and pulmonary vascular tone,
stimulates the central production of arginine vasopressin, and, acting
via aldosterone, which it also triggers, stimulates salt and water re-
tention by the kidney. These major neurohormonal mechanisms func-
tion to facilitate adaption of the organism to influences of dehydration
or overhydration, and other environmental stresses relating to body
position, temperature, and venous return.
Appropriate stress response in an adult depends upon complete
vagal and sympathetic innervation of the heart and the various pe-
ripheral vascular beds, and upon maturation of the target organ's
ability to respond. These pathways can be dysfunctional in infants
because of developmental immaturity. Complete adrenergic inner-
vation of the heart is absent until after birth in several animal spe-
cies,15 and cardiac ~-receptor maturation is known to lag behind (X-
receptor maturation in fetal lambs. 45 Moreover, newborn lambs differ
in ~-receptor development compared to lambs that are days to weeks
0Ider. 4o ,47 Responses to adrenergic agonists and antagonists evolve
from fetus through neonate to adult. For most parameters (for ex-
ample, change in heart rate, systemic or pulmonary blood pressure),
neither the term fetus's response nor the adult's response to various
drugs is predictably similar to that of the neonate.
Influences that cause brain malfunction may alter the ability of
a given neonate to respond appropriately to circulatory stress. Cen-
tral nervous system hemorrhage or edema may permanently or telu-
porarily limit the neonates' ability to respond by systemic vasocon-
striction to vascular volume loss or hypoxic stress. This is important
in neonates because the "resting" circulatory milieu of normal neo-
nates is also different from adults. Imluediately (up to 12 hours) after
birth, circulating catecholamines are high. 21 The combined effect of
the hypersensitivity to ~-adrenergic stimulation, high metabolic de-
mands of the neonatal adaptation, and the various transient intracar-
diac and intravascular shunts combine to make "resting" cardiac
output near to maximal cardiac output in the ilumediate neonatal
period. 7 Thus, "baseline" performance of the neonatal heart repre-
sents a stress response. If additional stresses are superimposed, the
heart may fail simply because its myocardium can pUIUp no harder
and because endogenous stores of catecholaluines, which are devel-
opmentally subnormal (versus adults),21 have been further depleted
by severe birth stresses and may be completely exhausted. Thus, in

these situations, inotropic agents such as dopamine, which depend
upon ~-receptor stimulated release of endogenous norepinephrine
for their cardiotonic effects,12,15 may be ineffective.
Available pressor agents include isoproterenol, dopamine, and
dobutamiQe.
Isoproterenol is a pure ~-receptor agonist that affects both ~1
and ~2 receptors, thus effecting bronchodilation and cardiac stimu-
lation. It is also a potent vasclliar vasodilator that lowers peripheral
resistance by dilating vascular beds in skeletal muscle, kidneys, and
gut. The combined effects of myocardial stimulation and augmented
venous return usually increase cardiac output and maintain systemic
arterial pressure. In some disease states (hypovolemia, for example),
however, isoproterenol-induced hypotension can occur. Neonates of
some species (dogs, humans) frequently develop severe tachycardia
from isoproterenol, whereas other species (lambs) do not have as
marked a chronotropic effect. Usual doses are 0.05 to 1.0 f-Lg per kg
per minute given as a continuous intravenous infusion.
In adults of various species, dopamine vasodilates renal, cere-
bral, mesenteric and coronary vascular beds via a specific dopamine
receptor mechanism. At higher doses (4 f-Lg per kg per minute) pe-
ripheral a-receptor activation results in systemic vasoconstriction,
with lesser effects in the coronary, cerebral, and pulmonary circula-
tion. 33 In neonates of various species, some of these regional vaso-
dilator effects are modified by both age and dopamine dose.
The primary determinants of dopamine;>s - inotropic action are
endogenous myocardial norepinephrine stores and left ventricular
afterload. Both can be affected by developmental immaturity (for
example, decreased norepinephrine stores and subadult levels of
maximal ventricular myocardial performance under pressure stress)
and varied pathologic states (for example, chronic congestive failure,
pathologically high systemic vascular resistance). Thus, in some clin-
ical situations, the neonatal heart may be unable to respond as ex-
pected to dopamine infusion, especially at higher doses, unless the
a-mediated systemic afterload increase in simultaneously blockaded.
Renal perfusion may improve in neonates if low (less than 4 f-Lg
per kg per minute) doses are given. In human neonates (age 4 hours
to 29 days) with circulatory disturbances severe enough to cause renal
dysfunction, low-dose dopamine (2 to 4 f-Lg per kg per minute) im-
proved renal function as determined by urine output, creatinine
clearance, and fractional excretion of sodium. 49 Higher dopamine
doses (more than 5 f-Lg per kg per minute) may cause a.-adrenergic
vasoconstriction. In lambs, dopamine does not increase cardiac
output at any dose unless the alpha effects are blocked.
Dobutamine is a synthetic catecholamine that acts by direct
stimulation of cardiac ~ receptors. In adults, its inotropic effects are
independent of stored catecholamines and it increases cardiac output
in both norlnal and failing hearts, with minimal tachycardia. 6 It has
very weak cross-reactivity with peripheral a and ~ receptors. 35 Heart
rate increase after dobutamine is often greater than with dopamine

in adults, although in the only existing comparatives neonatal study,
in puppies, 16 dobutamine was less chronotropic than either dopamine
or isoproterenol. Dobutamine has no selective vasodilator effects on
regional vascular beds. Thus, some researchers have suggested com-
bining low-dose dopamine (less than 3 IJ-g per kg per minute) with
dobutamine, for treatment of cardiogenic shock. 34
Supportive Intensive Care Techniques
The value of good nursing care in treatment of the abnormal neo-
natal foal cannot be overemphasized. Although it is often a tedious,
unglamorous, time-consuming, and frustrating undertaking, the sur-
vival of many foals is utterly dependent on this type of 24-hours-a-
day attention.
One of the first important questions is usually where to put the
foal while care is provided. Although the foal is often left in the stall
with its mother both to preserve maternal bonding and for lack of a
better place, a number of disadvantages are associated with this prac-
tice, including poor lighting, unsanitary (and sometimes downright
dirty) surroundings, the presence of rough, easily inhaled or swal-
lowed bedding, and poor maternal cooperation. Therefore, when a
foal is too weak to stand and nurse effectively from the mare, or when
sterile procedures must be done, the foal is usually removed from
the stall and placed in a cleaner, more controlled environment. Ide-
n
ally, this "clean area is placed within viewing range of the mother,
but this is not always possible; often, the foal and mare must be
reintroduced at a later date. The area in which the foal is treated
should be warm, easily cleaned and disinfected, and provide soft
bedding for the recumbent foal. A thermal neutral environment is
vital for sick or premature foals. Thermoneutrality minimizes energy
requirements, prevents hypothermia, and improves survival. Ancil-
lary heat sources routinely used include infrared heating lamps and
water-circulating heating pads. Servo-controlled radiant warmers,
which are used in human neonatology to maintain a constant skin
temperature, may be modified for more precise temperature regu-
lation in the newborn foal as well.
The environment of the neonatal foal should be designed to
minimize the potential for self-inflicted injury. Decubital and corneal
ulcers are common complications in the recumbent, struggling foal,
and bedding and restraint must be chosen carefully to minimize this
sequela. Utilization of a twin-sized waterbed mattress with heater
was found to help decrease the incidence of pressure sores, and pro-
vided a heat source as well (Fig. 5). In addition, frequent change of
the foal's position and effective control of seizures and thrashing are
important additional considerations. Development of corneal ulcer-
ations have prolonged hospitalization more frequently than any com-
plication in intensive care. They usually occur secondary to trauma
associated with thrashing, entropion, or a combination of the two.
Because severe corneal ulcers can develop in an extremely short
Figure 5. Premature foal reclining on twin-sized, heated waterbed placed on

custom-designed elevated foal bed. (Photo courtesy Woodford Veterinary Clinic, Ver-
sailles, Kentucky)
period of time, the eyes should be thoroughly examined at frequent

intervals for abnormalities; and treatment instituted promptly when
a problem is detected. Treatment goals include elimination of the
inciting cause and institution of appropriate therapy. Details will be
provided in the article, "Neonatal Ophthalmology. ~~
The normal, hydrated foal produces a large quantity of dilute urine.
If urine scalding is to be prevented in the down foal, much time can
be devoted to simply mopping up urine. The best time-saving solu-
tion to this problem has not been identified. Unless it is important
to quantitate urine output for some medical reason, indwelling uri-
nary catheters are felt to present too great a risk of introducing in-
fection to the compromised foal than is justified for the sake of con-
venience. It may be possible, however, to adapt human adult colos-
tomy bags for use for effective urine collection in the foal.
Another common complication observed in the down, or debili-
tated, foal is development of a p~tent urachus. A patent urachus is
also commonly observed in foals whose umbilical cords were cut and!
or tied at parturition. Our standard treatment has involved cauteri-
zation at least three times a day with silver nitrate sticks or iodine
solutions. In all surviving foals treated conservatively in this manner,
the urachus closed within a few days and no further complications
were noted. However, if there is reason to suspect that the urachus
or remnants of the umbilical vessels are infected because of pain on
palpation or an inflammatory hemogram, ultrasound examination
may help to identify areas of abscessation that need surgical resection.
Besides providing for all the basic needs of the foal, another ex-
tremely important goal of intensive care is to help the animal to
develop into a functional animal. Many recovering foals must be
taught from scratch even such basic activities as how to suckle effec-
tively and to stand and walk unassisted. However, in spite of the

large investment of time often necessary, this process can prove to
be extremely rewarding when a normal, useful horse results.
Unfortunately, knowledge concerning optimal physical therapy of
the premature, growth-retarded, or recumbent term foal is rudimen-
tary. How best to manage the foal with immature bones and/or con-
nective tissue, and the resulting angular limb deformities, is unclear.
The optimal types of manipulation, external support devices, and
nutritional supplementation required are simply not known at the
present time. However, as increasing numbers of immature foals
survive the early neonatal period, these questions will need to be
answered.
Conclusion
As the area of veterinary neonatology is quite new, the ideas pre-
sented in this article are not all established facts but are the result
of 4 years~ experience in providing intensive care to a large group of
sick neonatal foals at the University of Florida. Some techniques have
been successfully adapted from human neonatology; in other in-
stances, however, what is feasible in human infants is simply not
possible in domestic animals. Most importantly, there are still many
problems to solve and much basic information still to be gained con-
cerning the neonatal foal. At this time, it is clear that intensive care
is not indicated for every abnormal foal. The decision to go to heroic
efforts to support a critically ill foal is not an easy one and, in certain
situations, this type of care is neither possible, desirable, or justifi-
able. However, in many other foals, careful, intelligent observation,
judicious intervention, and utilization of a few basic principles of
intensive care can go a long way to improving the compromised foal's
chances for survival.
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Department of Medical Sciences

College of Veterinary Medicine
University of Florida

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Symposium on Neonatal Equine Disease

Intensive Care of the Neonatal Foal

Anne M. Koterba, D.V.M.,*

Throughout the years, a prevailing attitude of horse owners,

Froln University of Florida, Gainesville, Florida

Veterinary Clinics of North America: Equine Practice-Vol. 1, No.1, April 1985 3

General Concepts of Neonatal Intensive Care

Identification of the High-Risk Foal

Table 1. Conditions Associated with High-Risk Neonatal Foal

1. Purulent vaginal discharge

CONDITIONS OF LABOR OR DELIVERY

1. Meconium-stained fluid or foal

cental insufficiency, congenital defects, in utero infections, or twin

Initial Work-Up of the Neonatal Foal

Table 2. Protocol for Receiving Neonatal Foals at University of Florida

3. Perfonn whole blood glucose determination. If result is less than 40 mg per

4. Assess fluid balance. Aseptically insert intravenous catheter if fluid therapy

6. Draw blood for aerobic and anaerobic blood cultures.

8. Cauterize umbilicus with 3 per cent iodine if newborn or stump is moist.

9. When condition is stabilized, radiograph thorax and, if indicated, abdomen.

11. Evaluate laboratory data, physical examination results and decide on

Initial Assessment: Rule Out Need for Immediate Intervention

Begin external cardiac Entubate trachea

Table 3. Emergency Drugs and Their Doses for Neonatal Resuscitation

Epinephrine .1 mI/kg, 1: 10, 000 solution IV

in intervening when the animal is making adequate progress on his

* Bivona. Surgical, Inc., Gary, Indiana.

* Valiuln. Hoflinan-LaRoche Inc., Nutley, New Jersey.

* ROlnpun. Haver-Lockhart, Shawnee, Kansas.

is often overlooked clinically. In one report of 37 foals less than 1

Figure 2. Lateral thoracic radiograph of a 7-day-old Arabian foal with Escherichia

Figure 3. A, Lateral thoracic radiograph of 305-day gestational age, 3-hour-old foal

sequent hyperventilation. A small gauge needle (25 gauge, 5/8 inch)

Figure 4. A, Chest radiograph of a 6-day-old Thoroughbred foal in respiratory

catheter in the great metatarsal artery is not difficult if pulse quality

the advantages of continuous access to an artery must be carefully

are repeated in this position. If sternal position is not possible, foals

* Dopram-V A. H. Robins Co., RichlTIond, Virginia.

* Bivona. Surgical, Inc., Gary, Indiana.

of ventilator also has the capacity to deliver humidified and heated

* Hudson Oxygen TherCl:PY Sales Co., Orange Park, Florida.

catheters can also serve as an important source of infection for the

* Quick-cath. Travenol Labs, Deerfield, Illinois. .

* ChelTIstrips. BiodynalTIics, Inc., Indianapolis, Indiana. Dextrostix. AlTIeS Division,

tion is increased from maintenance level according to urine specific

by severe birth stresses and may be completely exhausted. Thus, in

rate increase after dobutamine is often greater than with dopamine

Figure 5. Premature foal reclining on twin-sized, heated waterbed placed on

period of time, the eyes should be thoroughly examined at frequent

tively and to stand and walk unassisted. However, in spite of the

Department of Medical Sciences

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