Vol. 22, No.
4 April 2000 V
CE Refereed Peer Review
FOCAL POINT
★Clinicians must thoroughly
understand the differences
between neonatal and adult
dogs and cats to be able
to efficiently address life-
threatening disorders.
KEY FACTS
■ Neonates are prone to
hypoglycemia for several
reasons, including immature
glucose feedback mechanisms,
inefficient hepatic gluconeogenesis,
and decreased glycogen stores.
■ Obtaining baseline data and
meticulous monitoring are
essential to detect and treat
dehydration and shock.
■ Common bacterial infections
in puppies include species of
Staphylococcus, Streptococcus,
and Pseudomonas as well as
Escherichia coli.
■ Dramatic differences in
pulmonary vascular resistance
and adequate surfactant are
essential for survival at birth.
■ Epinephrine is the drug of choice
in most cases of cardiopulmonary
arrest.
Pediatric Critical Care
Medicine: Specific
Syndromes*
Tufts University
Maureen McMichael, DVM
Angell Memorial Animal Hospital
Boston, Massachusetts
Nishi Dhupa, BVM
ABSTRACT: Similar to their human counterparts, neonatal puppies and kittens have physio-
logic parameters that differ from those of adults. Thus puppies and kittens require monitoring
and treatment specific to their unique biochemistry and physiology. Knowledge of these differ-
ences becomes even more important when treatment decisions for life-threatening conditions,
such as hypovolemia or respiratory distress, must be made quickly.
D
ata on critical care of pediatric and neonatal veterinary patients are sparse.
Hemodynamic parameters in neonates can differ markedly from those in
adults. Clinicians must be aware of these differences to make a rapid diag-
nosis and facilitate treatment. Awareness of the unique homeostasis of neonates aids
in diagnosis and successful treatment. In veterinary medicine, the term pediatric
refers to an animal younger than 6 months of age. The information in this article is
limited to dogs and cats 0 to 12 weeks of age and focuses on the neonatal age range
(0 to 2 weeks). Clinical manifestations and treatment of specific life-threatening
syndromes in very young puppies and kittens are summarized.
HYPOGLYCEMIA
Neonatal Response
Neonates are prone to hypoglycemia because of immature glucose feedback
mechanisms, inefficient hepatic gluconeogenesis, and decreased glycogen stores.
Renal losses also contribute to this problem because glucose reabsorption does
not normalize until day 21.1,2 The neonatal brain depends heavily on glucose for
energy, and permanent brain damage can result from hypoglycemia.2 In addi-
tion, the fetal myocardium primarily uses carbohydrate as a substrate rather than
the long-chain fatty acids used by the adult heart.3
In neonates, clinical signs of hypoglycemia may be difficult to recognize until the
*A companion article entitled “Pediatric Critical Care Medicine: Physiologic Considera-
tions” appeared in the March 2000 (Vol. 22, No. 3) issue of Compendium.
Small Animal/Exotics
process is advanced. Serial measurements of blood glucose
are essential in this age group. Early signs of hypoglycemia
may include lethargy, anorexia, and a limp body. Epi-
nephrine, one of the most essential counterregulatory hor-
mones, is not released in response to hypoglycemia in neo-
natal puppies.2 In adult dogs, counterregulatory hormones
(epinephrine, glucagon, growth hormone, cortisol) provide
essential maintenance of euglycemia by antagonizing in-
sulin levels and increasing the rate of glycolysis, gluconeo-
genesis, and lipolysis. This system seems to be inefficient
in neonates.2
Monitoring and Treatment
Neonatal hypoglycemia is most commonly caused by
vomiting, diarrhea, inadequate fluid intake, and infec-
tion. Treatment of hypoglycemia involves an intra-
venous (IV) bolus of 1 ml/kg of 25% dextrose followed
by continuous-rate infusion (CRI) of isotonic fluids
supplemented with 2.5% to 5% dextrose. Oversupple-
mentation of dextrose can cause prolonged hypergly-
cemia (puppies are relatively insensitive to insulin) and
osmotic diuresis, leading to dehydration.4
HYPOVOLEMIC SHOCK
Neonatal Response
Hypovolemia results in inadequate tissue perfusion
causing decreased oxygen delivery and subsequent cel-
lular hypoxia. In adult animals, hypovolemia causes
varying degrees of tachycardia, prerenal azotemia, con-
centrated urine, and decreased urine output. Many of
the compensatory mechanisms that are maximally stim-
ulated in adults during shock are not fully functional in
neonates. Because these mechanisms are measured to
diagnose dehydration and shock, the disorders can be
difficult to detect in neonates.
Contractile elements make up approximately 60% of
adult cardiac muscle but only 30% of fetal cardiac mus-
cle. Cardiac output (i.e., the heart rate multiplied by the
stroke volume) in the fetus and neonate cannot be in-
creased by increasing contractility; neonates depend on
a rapid heart rate to maintain cardiac output.5 However,
neural control of heart rates seems to be incomplete in
newborn puppies, which have a lower density of sympa-
thetic nerve fibers in the myocardium than do adults.6
Complete maturation of both divisions of the autonom-
ic nervous system occurs after 8 weeks of age.6 Tachycar-
dia in response to hypovolemia may not occur in nor-
mal neonates because of this variation in maturity.
Decreased mean arterial pressure is found in normal
neonates, with an average arterial pressure of 49 mm Hg
at 2 months of age compared with an average pressure
of 94 mm Hg at 9 months of age.7 This decrease is be-
lieved to be caused by immaturity of the muscular com-
HYPOGLYCEMIA TREATMENT ■ ARTERIAL PRESSURE ■ NEPHROGENESIS
Compendium April 2000
ponent of the arterial wall at birth. Therefore, blood
pressure changes are also unreliable for diagnosing shock
in neonates.
Nephrogenesis is incomplete at birth, with glomeru-
lar maturation preceding tubular maturation.4,8 In pup-
pies 2 days of age, glomerular filtration rate (GFR)
measurements were only 14% those of puppies at 77
days of age. 4,8 Adult values may be achieved by 10
weeks of age. In kittens, the GFR reaches adult values
by 9 weeks of age.9 In adult dogs, the kidneys have the
ability to regulate their blood supply independently of
systemic arterial pressures (as long as the pressure re-
mains above 70 to 80 mm Hg).10 Young puppies have
decreased autoregulation of renal blood flow in re-
sponse to changes in arterial blood pressure, such as
those occurring in shock states.10
In one study of puppies,10 acute decreases in arterial
blood pressure resulted in similar decreases in the GFR,
reflecting the inability of immature kidneys to maintain
glomerular filtration in the presence of hypovolemia.
Concentration and dilution of urine in response to
changes in extracellular fluid volume is limited in new-
born puppies and increases with age.10 The capacity to
concentrate urine increases almost linearly during the
first year of life in humans.11 Decreased urea concentra-
tion, inefficient countercurrent mechanisms caused by
relatively short loops of Henle, and inefficient sodium
reabsorption in the thick ascending limb of the loop of
Henle may all contribute to inefficiency of the concen-
trating mechanism.11 Levels of blood urea nitrogen and
creatinine are lowest during the neonatal phase. Prere-
nal azotemia and a concentrated urine specific gravity
may not be found at this age even if dehydration is se-
vere. These aspects of the neonatal kidney make treat-
ment (particularly fluid loading and drug dosing and
interval adjusting) and interpretation of laboratory data
particularly challenging.
Deaths that occur immediately after birth are often
caused by problems during the birthing process (e.g.,
trauma, inadequate oxygenation), problems occurring
to the dam or queen, congenital anomalies, neonatal
isoerythrolysis, or inadequate intake. Deaths and ill-
nesses occurring during this period are often referred to
as the fading puppy (or kitten) syndrome. Illnesses that
occur after 2 weeks of age are usually caused by viral or
bacterial infection.
The most common viral infections in kittens are fe-
line herpesvirus type 1 and calicivirus. Both viruses
cause mild upper respiratory infection in healthy kit-
tens, but disease in immune-compromised kittens can
be severe. Sources of bacteria include the umbilicus,
placenta, or trauma during the birthing process.12 Or-
ganisms most commonly isolated from septicemic kit-
Compendium April 2000 Small Animal/Exotics

tens are Escherichia coli and β- maintenance fluids (80 ml/kg/

hemolytic Streptococcus. Fluid Therapy for Shock day) plus fluids to compensate
The most common viral in- for dehydration and losses (e.g.,
fections in puppies are canine ■ Initial dose of lactated Ringer’s solution—30 to 2 tbsp of diarrhea requires 30
herpesvirus and canine par- 45 ml/kg for dogs, 20 to 30 ml/kg for cats; more ml of fluids) replaced
vovirus type 1. Both viruses monitor for response over a 12-hour period is rec-
can be fatal in an entire litter ■ Maintenance dose of lactated Ringer’s solution— ommended. One dose of 0.01
of puppies, often within 24 80 ml/kg for dogs, 80 ml/kg for cats to 0.1 mg/kg of vitamin K ad-
hours of the appearance of ■ Preferred fluids—Warmed isotonic crystalloids ministered subcutaneously is
clinical signs.12 Common bac- often recommended for kit-
terial infections in puppies in- ■ Blood glucose—Monitor two to four times per tens13 and 0.5 to 2.5 mg/kg sub-
clude species of Staphylococcus, day cutaneously for puppies.12
Streptococcus, and Pseudomonas ■ Nutritional support—Encourage natural nursing,
as well as E. coli. β-Lactam an- provide a foster dam, or feed warmed milk SEPSIS AND
timicrobials (e.g., cephalo- replacer using a bottle or tube SEPTIC SHOCK
sporins, amoxicillin–clavulanic Neonatal Response
acid) are the first drug choice Sepsis in neonates is most of-
for treating bacteremic puppies and kittens pending ten associated with umbilical, respiratory, and GI infec-
culture and sensitivity results. tions and with tail docking. Neonatal sepsis can be
frustrating to diagnose because of the lack of specific
Monitoring and Treatment indicators, such as tachycardia, hyperthermia, and de-
One of the most common causes of hypovolemic creased blood pressure as a result of immaturity of the
shock in neonates is dehydration, which can occur autonomic nervous system. Clinical signs include pale
rapidly because of the higher fluid requirements in mucous membranes, decreased urine output, cold ex-
neonates (see Fluid Therapy for Shock). Gastrointesti- tremities, constant crying, and reluctance to suckle.
nal (GI) disturbances (e.g., vomiting, diarrhea), inabili-
ty to nurse, or competition for milk are common causes Monitoring and Treatment
of dehydration in neonates. Rapid and aggressive fluid resuscitation is strongly as-
Severe limitations in the ability to monitor physio- sociated with survival in children; this outcome has also
logic parameters in this age group necessitate estima- been shown in an animal model of septic shock in rats,
tions and assumptions. Because skin turgor (decreased mice, and rabbits.14 Septic neonates may need large vol-
fat content and increased water content make this unre- umes of replacement fluids because of continued capil-
liable), moistness of mucous membranes (they often re- lary permeability and peripheral vasodilation. Septic
main moist despite significant dehydration), heart rate, neonates that have had adequate volume repletion but
or urine specific gravity cannot be used as monitoring still have hypoperfusion may need inotropic support;
measures, practitioners must make some assumptions such support must be individually tailored because of
about the patient’s status, such as diagnosing dehydra- variations in maturation of the autonomic nervous
tion in neonates with moderate to severe diarrhea. Pa- system. Perfusion can be assessed by serial checks of
tients should be weighed every 6 to 12 hours; mucous mucous membrane color, pulse quality, extremity temp-
membrane color (pale mucous membranes suggest ane- erature, lactate levels, and mentation. In addition, fre-
mia or hypovolemia), blood glucose, hematocrit, oxy- quent blood glucose checks are essential, and supple-
genation (pulse oximetry), urine output and specific mentation with IV dextrose is warranted if there is any
gravity, and central venous pressure should be moni- indication of hypoglycemia.
tored and checked using baseline values as indicators of The choice of antibiotic should ideally be based on
improvement or decline. Serial measurement of hemato- culture results of the affected area. Administration of
crit and total protein and body weight provides objec- broad-spectrum antibiotics may be required if a source of
tive information about the patient’s hydration status infection is not found. First-generation cephalosporins,
and response to fluid therapy. Urine specific gravity which have minimal toxicity and provide coverage for
greater than 1.015 to 1.020 suggests dehydration and gram-positive and some gram-negative organisms, are a
can be monitored as an indicator of sufficient rehydra- good choice pending culture results.
tion.12 Oxygen therapy may help counteract tissue hypoxia,
In severely dehydrated animals, an IV bolus of 45 ml but excessive amounts can be toxic and cause retrolen-
of warm isotonic fluids/kg followed by the CRI of tal fibroplasia—a retinopathy that can lead to perma-

VIRAL INFECTION ■ SEVERE DEHYDRATION ■ FLUID RESUSCITATION

Small Animal/Exotics
nent vision loss.15 Supplementation to achieve inspired
oxygen concentrations of no more than 40% seems to
be safe in newborn infants and may be achieved with
an oxygen cage or incubator.15
Use of plasma or serum from well-vaccinated adult
dogs for septic puppies has been advocated but has not
been proven to be beneficial.17 However, it may benefit
neonates that have not received colostrum.
In summary, sepsis can be very difficult to detect in
neonates and must be treated early and aggressively.
Clinical and diagnostic signs include pale mucous mem-
branes, cold extremities (indicative of decreased perfu-
sion), decreased urine output, hypoglycemia, and dull
mentation. Treatment consists of aggressive fluid thera-
py, warmth, antibiotics, oxygen supplementation, and
possibly plasma or serum transfusion from an immuno-
competent vaccinated adult.
RESPIRATORY DISTRESS
Neonatal Response
Although placental blood is oxygenated, the fetus is
considered to be in a relatively hypoxic state through-
out gestation. Pulmonary pressure in the fetus is much
higher than that in the adult. Higher pressure causes
the right side of the heart to be under greater pressure
than the left side; both ventricles are equal in thickness.
After birth, with decreased pulmonary vascular resis-
tance, the right ventricular workload decreases and the
right ventricle becomes thinner than the left.16
In several species, pulmonary arteries in the fetus and
newborn have a greater proportion of smooth muscle
than do those in adults.17 This adds to elevated pul-
monary vascular resistance and preferential shunting of
blood from the pulmonary trunk through the patent
ductus arteriosus to the aorta and into the systemic cir-
culation. At birth, physical expansion of the lungs caus-
es release of prostacyclin, which increases pulmonary
blood flow through pulmonary vasodilation. Nitric ox-
ide synthesis is probably induced by fetal oxygenation
and contributes to pulmonary vasodilation. These
changes lead to less pulmonary vascular resistance after
birth and closure of the patent ductus arteriosus.18
In the lungs, type I epithelial cells line the alveoli,
where gas exchange occurs; type II cells produce surfac-
tant in response to glucocorticoid stimulation.19 Surfac-
tant consists mainly of lipids and reduces the tension of
the air–fluid interface of alveoli and prevents them
from collapsing. By reducing compliance (stiffness),
surfactant also reduces the work of breathing. At birth,
a large amount of surfactant is secreted in response to
lung inflation.19 Dramatic decreases in pulmonary vas-
cular resistance and adequate surfactant are essential for
survival at birth. If pulmonary vascular resistance re-
PULMONARY VASCULAR RESISTANCE ■ DRUG REVERSAL ■ SPONTANEOUS RESPIRATION
Compendium April 2000
mains high, blood continues to be shunted from right
to left (via the foramen ovale and patent ductus arterio-
sus), thereby bypassing the lungs.
Monitoring and Treatment
In veterinary medicine, respiratory distress is most
commonly encountered at birth. This distress may be as-
sociated with fluid in the airways, meconium aspiration,
decreased surfactant levels, or several congenital defects
that cause persistent pulmonary hypertension. The anes-
thesia involved in cesarean section commonly causes re-
spiratory and heart rate depression. Reversal of the drugs
used during induction or surgery is essential in neonates
delivered in this manner. In older neonates, respiratory
distress occurs secondary to infectious or inflammatory
disease (e.g., parvovirus infection, canine distemper,
pneumonia), pulmonary edema associated with congeni-
tal cardiac defects, electrocution, or head trauma.
A crucial first line of treatment consists of oxygen
supplementation and lung expansion. Oxygen may be
supplied via an endotracheal tube, face mask, incuba-
tor, or oxygen cage. Lung expansion, for reasons not
understood, is essential to surfactant release in new-
borns and causes release of prostacyclin, which increas-
es pulmonary blood flow and pulmonary vasodilation.
We recommend attaching a pediatric ambubag to the
endotracheal tube and using gentle compressions while
watching the chest expand. Overexpansion can damage
the lungs; thus it is essential to use minimal pressure at
first. In older puppies and kittens, treating the primary
disease while supporting the lungs is essential.
Resuscitation
The need for resuscitation at birth most often results
from the presence of fluid in the airways and the high
pressure needed to expand collapsed alveoli. Drugs that
may have been used during cesarean section must be re-
versed immediately while supportive care is being giv-
en. Gentle stimulation (rubbing) and gentle clearing of
the oropharynx (bulb syringe or finger sweeps) should
be attempted before aggressive suctioning.
The aim is to stimulate spontaneous respiration by
using the least-aggressive most-effective method. Shak-
ing or hitting the newborn is contraindicated and can
cause complications. Aggressive suctioning can cause
vagal-induced bradycardia and laryngospasm. Doxa-
pram hydrochloride is a general central nervous system
stimulant that also causes direct stimulation of the
medullary respiratory centers and has a rapid onset of
action. Neonates can be given one to two drops under
the tongue.20 If there is no response, mouth-to-nose re-
suscitation should be attempted along with suctioning
of the oropharynx. Another method of clearing the lungs
Small Animal/Exotics Compendium April 2000

is to hold the neonate and re- myocardial contractility and

peatedly move the head to-
ward the tail (accordion-like
motion) (Figure 1).
The next step is intubation
and ventilation if respiration
has not spontaneously started.
Ventilation can be achieved
with a pediatric ambubag at-
tached to an oxygen line and
use of minimal pressure.
Many ambubags have inlet
valves that do not allow pa- Figure 1—If mouth-to-nose resuscitation fails, practitio- dioxide cannot be eliminated.
tients to breathe on their ners should attempt to clear fluid from the respiratory Buffers may also increase so-
own. Detaching the endotra- tract by repeatedly moving the newborn’s head toward its dium levels and cause hyper-
cheal tube from the bag when tail as shown.
respiration begins sponta-
neously is recommended. Ventilation should be main-
tained for 10 to 15 seconds at a rate of 25 to 30 breaths
per minute before starting cardiac compression. Initiat-
ing respiration is often all that is needed to improve the well as of neonatal myocardium. Frequent monitoring of
heart rate. However, if no response occurs, cardiac
compression should be started.
Because of the patient’s small size, cardiac compres-
sions are most safely done by placing the thumb and
forefinger on either side of the thorax and compressing
at a rate of 100 to 120 times per minute. IV or in-
traosseous access is the preferred route for drug and flu- toring parameters used for adults may not be suitable.
id delivery. Although many drugs (e.g., epinephrine,
naloxone, atropine) can be administered by endotra-
cheal tube, an amount twice the normal dose is needed
by this route; greater and more prolonged toxicity seems
to occur when endotracheal tubes are used. Certain
drugs are contraindicated because they can cause per-
manent pulmonary damage (e.g., sodium bicarbonate
destroys surfactant and causes atelectasis).
Epinephrine remains the drug of choice in almost all
cases of cardiopulmonary arrest. This drug has α- and
β-adrenergic activity and causes increased coronary per-
fusion pressure; increased myocardial and cerebral blood
flow; and increased vascular resistance in skin, muscle,
and splanchnic vascular beds. The current recommenda-
tion in newborn infants is to use low-dose epinephrine
(0.01 mg/kg) early during cardiopulmonary resuscita-
tion because high doses are more likely to cause toxicity
if the patient is not severely acidotic and ischemic. If
there is no effect after 3 to 5 minutes, a higher dose (0.1
mg/kg) should be administered and repeated every 3 to
5 minutes until the heart beat resumes.21
Acidosis can become severe during cardiopulmonary
resuscitation because of a combination of metabolic
acidosis (decreased perfusion) and respiratory acidosis
(decreased ventilation). Severe acidosis can decrease
blunt responses to exogenous
catecholamines. Restoring
perfusion and providing ade-
quate ventilation are the keys
to treating acidosis. The use
of buffers (e.g., sodium bicar-
bonate) is controversial be-
cause they increase the levels
of carbon dioxide in the
blood; if perfusion and venti-
lation are compromised, carbon
osmolar states. If the patient
is successfully resuscitated and
perfusion has been restored, administration of a buffer
may be beneficial.
Glucose is the main energy substrate of the brain as
glucose levels in critically ill neonates is therefore essential.
CONCLUSION
Neonates pose significant challenges because of their
unique anatomic and physiologic characteristics, physi-
cal examination parameters, and drug doses. Thus moni-
Unfortunately, veterinary medicine lacks published
physiologic values for neonates and pediatric patients.
Thus awareness of the unique homeostasis of puppies
and kittens and their response to disease can aid practi-
tioners in diagnosing and successfully treating diseases
and syndromes.
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About the Authors
When this article was submitted for publication, Drs.
McMichael and Dhupa were affiliated with the Depart-
ment of Clinical Sciences, School of Veterinary Medicine,
Tufts University, North Grayton, Massachusetts. Dr. Dhu-
pa is now affiliated with Angell Memorial Animal Hospital,
Boston, Massachusetts.