Essentials of Anesthesia for Infants and Neonates

Visit the link below to download the full version of this book:

https://medidownload.com/product/essentials-of-anesthesia-for-infants-and-neonat
es/

Click Download Now

 Cambridge University Press
978-1-107-06977-0 — Essentials of Anesthesia for Infants and Neonates
Edited by Mary Ellen McCann , Edited in association with Christine Greco , Kai Matthes
Frontmatter
More Information
vi

Contents

22 Anesthesia for Plastic Surgery 211 33 Anesthesia for Conjoined Twins 347
Petra M. Meier Philip D. Bailey and Lynne G. Maxwell
23 Anesthesia for Abdominal Wall 34 Anesthesia for Fetal Surgery 354
Reconstruction Procedures 233 Linda A. Bulich, Arielle Y. Mizrahi-Arnaud,
Ellen Choi and Samuel H. Wald and Kha M. Tran
24 Anesthesia for Intra-Abdominal
Procedures 242
Raymond Park and Edward Cooper
Section 4 – Pain Management and
Other Newborn and Infant Anesthesia
25 Anesthesia for Urologic Surgery 252
Deepa Kattail, Jessica A. George, and Concerns
Myron Yaster 35 Pain Management in Neonates and
26 Anesthesia for Thoracic Surgery 264 Infants 369
Cornelius A. Sullivan Christine Greco and Charles Berde

27 Congenital Diaphragmatic Hernia 276 36 Regional Anesthesia in Neonates and

Elizabeth C. Eastburn and Bridget L. Muldowney Infants 382
Karen Boretsky
28 Congenital Heart Disease in the Neonate
and Infant: Cardiac Catheterization and 37 Procedural Sedation 398
Cardiac Surgery 280 Mary Ellen McCann and Christine Greco
Morgan L. Brown, James A. DiNardo, and 38 Ambulatory Anesthesia in Infants 405
Kirsten C. Odegard Sharon Redd and Ethan Sanford
29 Noncardiac Surgery in Neonates and 39 Apnea and Bradycardia 410
Infants With Cardiac Disease 302 Puneet Sayal and Samuel Rodriguez
Annette Y. Schure
40 Neonatal Outcomes 415
30 Neonatal and Infant Tumors 321 Joseph P. Cravero
Laura H. Leduc
41 Research on Newborns and Infants 426
31 Anesthesia for Transplant Surgery 332 Patcharee Sriswasdi
Evan Burke and Franklyn Cladis
32 Anesthesia for Interventional Radiology
Procedures 340
Mary Landrigan-Ossar Index 439

vi

© in this web service Cambridge University Press www.cambridge.org

 Cambridge University Press
978-1-107-06977-0 — Essentials of Anesthesia for Infants and Neonates
Edited by Mary Ellen McCann , Edited in association with Christine Greco , Kai Matthes
Frontmatter
More Information
vii

Contributors

Richard Anderson, MD Kathleen Chen, MD

Massachusetts General Hospital; Harvard Medical Boston Children’s Hospital, Boston, MA, USA
School, Boston, MA, USA
Ellen Choi, MD
T. Anthony Anderson, MD, PhD David Geffen School of Medicine, University of
Massachusetts General Hospital; California, Los Angeles, CA, USA
Harvard Medical School, Boston, MA, USA
Franklyn Cladis, MD, FAAP
Philip D. Bailey, DO University of Pittsburgh Medical Center,
The Children’s Hospital of Philadelphia, Pittsburgh, PA, USA
Philadelphia, PA, USA
Edward Cooper, MD
Dusica Bajic, MD, PhD Boston Children’s Hospital, Boston, MA, USA
Boston Children’s Hospital; Harvard
Medical School, Boston, MA, USA Joseph P. Cravero, MD
Boston Children’s Hospital; Harvard
Hubert Benzon, MD Medical School, Boston, MA, USA
Ann & Robert H. Lurie Children’s Hospital of
Chicago; Northwestern University Feinberg James A. DiNardo, MD
School of Medicine, Chicago, IL, USA Boston Children’s Hospital; Harvard
Medical School, Boston, MA, USA
Charles Berde, MD, PhD
Boston Children’s Hospital; Harvard Laura Downey, MD
Medical School, Boston, MA, USA Boston Children’s Hospital, Boston, MA, USA

Karen Boretsky, MD Elizabeth C. Eastburn, DO

Boston Children’s Hospital, Boston Children’s Hospital; Harvard
Boston, MA, USA Medical School, Boston, MA, USA

Morgan L. Brown, PhD, MD Lynne R. Ferrari, MD

Boston Children’s Hospital; Harvard Boston Children’s Hospital; Harvard
Medical School, Boston, MA, USA Medical School, Boston, MA, USA

Linda A. Bulich, MD Tiffany Frazee, MD

Boston Children’s Hospital; Harvard Children’s Hospital Los Angeles; Keck School
Medical School, Boston, MA, USA of Medicine, University of Southern California,
Los Angeles, CA, USA
Evan Burke, MD
Hasbro Children’s Hospital and Rhode Katherine R. Gentry, MD
Island Hospital; The Warren Alpert Medical Seattle Children’s Hospital; University of Washington
School of Brown University, Providence, RI, USA School of Medicine, Seattle, WA, USA
vii

© in this web service Cambridge University Press www.cambridge.org

 Cambridge University Press
978-1-107-06977-0 — Essentials of Anesthesia for Infants and Neonates
Edited by Mary Ellen McCann , Edited in association with Christine Greco , Kai Matthes
Frontmatter
More Information
viii

Contributors

Jessica A. George, MD Justin Long, MD, FAAP

Johns Hopkins University, Baltimore, MD, USA Children’s Healthcare of Atlanta at Egleston
Children’s Hospital; Emory University School of
Christine Greco, MD Medicine, Atlanta, GA, USA
Boston Children’s Hospital; Harvard
Medical School, Boston, MA, USA Anne M. Lynn, MD
Seattle Children’s Hospital; University of Washington
Monica Hoagland, MD School of Medicine, Seattle, WA, USA
Boston Children’s Hospital; Harvard
Medical School, Boston, MA, USA Thomas J. Mancuso, MD, FAAP
Boston Children’s Hospital; Harvard
Robert S. Holzman, MD, MA (Hon.), FAAP Medical School, Boston, MA, USA
Boston Children’s Hospital; Harvard
Medical School, Boston, MA, USA Kai Matthes, MD, PhD
Boston Children’s Hospital; Harvard
Vincent Hsieh, MD Medical School, Boston, MA, USA
Seattle Children’s Hospital; The University of
Washington, Seattle, WA, USA Lynne G. Maxwell, MD
The Children’s Hospital of Philadelphia;
Narasimhan Jagannathan, MD Perelman School of Medicine at the
Ann & Robert H. Lurie Children’s Hospital of University of Pennsylvania,
Chicago; Northwestern University Feinberg Philadelphia, PA, USA
School of Medicine, Chicago, IL, USA
Mary Ellen McCann, MD, MPH
Deepa Kattail, MD Boston Children’s Hospital; Harvard
Johns Hopkins University School of Medicine, Medical School, Boston, MA, USA
Baltimore, MD, USA
Craig D. McClain, MD
Lauren R. Kelly Ugarte, MA, MD, FAAP Boston Children’s Hospital; Harvard Medical School,
Boston Children’s Hospital; Harvard Boston, MA, USA
Medical School, Boston, MA, USA
Petra M. Meier, MD, DEAA
Michael R. King, MD Boston Children’s Hospital; Harvard Medical School,
Ann & Robert H. Lurie Children’s Hospital of Boston, MA, USA
Chicago; Northwestern University Feinberg
School of Medicine, Chicago, IL, USA Arielle Y. Mizrahi-Arnaud, MD
Boston Children’s Hospital; Harvard
Monica E. Kleinman, MD Medical School, Boston, MA, USA
Boston Children’s Hospital; Harvard
Medical School, Boston, MA, USA Phil G. Morgan, MD
Seattle Children’s Hospital; The University of
Benjamin Kloesel, MD Washington, Seattle, WA, USA
University of Minnesota, Minneapolis, MN, USA
Bridget L. Muldowney, MD
Mary Landrigan-Ossar, MD, PhD University of Wisconsin School of Medicine and
Boston Children’s Hospital; Harvard Public Health, Madison, WI, USA
Medical School, Boston, MA, USA
Charles Nargozian, MD
Laura H. Leduc, MD Boston Children’s Hospital; Harvard
The Greenville Health System, Greenville, SC, USA Medical School, Boston, MA, USA

viii

© in this web service Cambridge University Press www.cambridge.org

 Cambridge University Press
978-1-107-06977-0 — Essentials of Anesthesia for Infants and Neonates
Edited by Mary Ellen McCann , Edited in association with Christine Greco , Kai Matthes
Frontmatter
More Information
ix

Contributors

Viviane G. Nasr, MD Augusto Sola, MD

Boston Children’s Hospital; Harvard Medical School, New York Medical College, Valhalla, NY, USA;
Boston, MA, USA Maimonides University, Buenos Aires, Argentina;
Universidad del Norte, Barranquilla, Colombia
Kirsten C. Odegard, MD
Boston Children’s Hospital, Boston, MA, USA Sulpicio G. Soriano, MD
Boston Children’s Hospital, Boston, MA, USA
Raymond Park, MD
Boston Children’s Hospital, Boston, MA, USA Patcharee Sriswasdi, MD
Boston Children’s Hospital; Harvard
Shivani S. Patel Medical School, Boston, MA, USA
Northwestern University Feinberg School of
Medicine, Chicago, IL, USA Cornelius A. Sullivan, MD, FACS
Boston Children’s Hospital, Boston, MA, USA
Sharon Redd, MD
Boston Children’s Hospital; Harvard Kha M. Tran, MD
Medical School, Boston, MA, USA The Children’s Hospital of Philadelphia,
Philadelphia, PA, USA
Lawrence Rhein, MD
Boston Children’s Hospital, Cynthia Tung, MD, MPH
Boston, MA, USA Boston Children’s Hospital; Harvard
Medical School, Boston, MA, USA
Samuel Rodriguez, MD
Boston Children’s Hospital, Amy Vinson, MD
Boston, MA, USA Boston Children’s Hospital; Harvard
Medical School, Boston, MA, USA
Ethan Sanford, MD
Boston Children’s Hospital, Samuel H. Wald, MD, MBA
Boston, MA, USA Stanford University, Stanford, CA, USA

Puneet Sayal, MD Thomas Weismueller, MD

Massachusetts General Hospital, Brigham and Women’s Hospital, Boston, MA, USA
Boston, MA, USA
Gerhard K. Wolf, MD, PhD
Annette Y. Schure, MD, DEAA Ludwig-Maximillians-University, Munich, Germany;
Boston Children’s Hospital, Boston, MA, USA Children’s Hospital Traunstein, Traunstein, Germany

Roby Sebastian Myron Yaster, MD

Nationwide Children’s Hospital, University of Colorado Denver; Children’s Hospital
Columbus, OH, USA Colorado, Aurora, CO, USA

ix

© in this web service Cambridge University Press www.cambridge.org

 Cambridge University Press
978-1-107-06977-0 — Essentials of Anesthesia for Infants and Neonates
Edited by Mary Ellen McCann , Edited in association with Christine Greco , Kai Matthes
Frontmatter
More Information
xi

Preface

The mortality of infants in the United States during There is ongoing research in humans to try to
the last 100 years has decreased from approximately determine whether general anesthesia is neurotoxic.
100 infants for every 1000 births to about 7 infants for The epidemiologic studies have been confounded by
every 1000 births. Most of the decline in infant mor- the effects of surgery and presurgical pathology on
tality has been due to improvements in medical care, the neurodevelopment of babies. Prospective stud-
sanitation, improved standards of living, and better ies examining the effects of general anesthesia on
nutrition. But relatively speaking, infancy is still the human development have shown that there are great
time of highest mortality during childhood. In some hemodynamic differences between general anesthesia
studies, almost 10 percent of children will undergo an compared with awake regional anesthesia in young
anesthetic in the first year of life. The leading cause of infants. Physiologically there are great differences in
neonatal death is prematurity, accounting for 30 per- infants compared to older children and adults, which
cent of all deaths in the first month of life. The lead- may not always be intuitive to anesthesiologists who
ing cause of infant death is congenital cardiac disease, do not routinely care for very young infants. It is
with about 25 percent of neonatal deaths attributed to very possible that aspects of general anesthesia other
heart defects. than neurotoxicity may predispose young infants
There are great concerns within the pediatric anes- to later learning disabilities. Other factors might
thesia community about effects of anesthetic exposure include overwarming the infants, hypocapnia and
during infancy on long-term neurologic development hypotension under anesthesia, and hypo- or hyper-
in humans. Many juvenile animal studies have shown glycemia. Over the last ten years there has been lots
that exposure to a wide variety of general anesthetics of research that has demonstrated the importance of
and sedatives at a young age lead to widespread neuro- hemodynamic and other physiologic variables in the
apoptosis and brain cell death. In addition, when care of newborns in critical care nurseries and the
these exposed animals are allowed to reach maturity, operating room.
they demonstrate learning difficulties. Several human This textbook focuses on the practical aspects of
studies have shown an association between anesthetic anesthesia care for our youngest patients. Interwoven
exposure before the age of four years and later neuro- through the chapters is information about the devel-
cognitive deficits. It is not clear that general anes- opment and changing physiology of infants and how
thetic exposure causes learning disabilities or is just a this should impact anesthetic practice. The chapters
marker for other possible causes, such as the effects of are written by nationally recognized experts in their
the surgery itself or the underlying reasons that these topics who focus on state-of-the-art, evidence-based
young children require surgery. practice.

xi

© in this web service Cambridge University Press www.cambridge.org

1

Section 1 Newborn and Infant Physiology for Anesthetic Management

Chapter
The Term Infant

1 Mary Ellen McCann

Introduction Immediately after delivery, with the first breath of

life, the expansion of the lungs causes the pulmonary
The first moment of healthy extrauterine life is usually
vascular resistance to drop. Concurrently, the umbil-
heralded by a deep breath followed by a cry. Within
ical vessels begin to narrow due to traction and the
a few breaths, the color of the infant changes from a
increased oxygen levels in the umbilical artery from
mottled dusky blue to a rosy hue and the infant is gen-
the infant breathing the room air. Once these vessels
erally alert, looking around at his new environs. Once
are fully constricted or clamped during delivery, the
he is swaddled and brought to his mother, he may
vascular resistance of the systemic circulation is mark-
instinctively root and suck even though the mother is
edly increased. The result of this is less blood flow
not yet able to nourish him. The physiologic changes
through the ductus venosus to the inferior vena cava.
that occur in the first few minutes of life are astound-
The decrease in pulmonary vascular resistance leads
ing. During development, the fetus develops an organ
to more blood flow to the lungs and higher flows into
physiology that was adapted to the low-oxygen envir-
the left atrium. Thus, the right- and left-sided cardiac
onment of the maternal circulation and then the first
pressures begin to reverse, with the left atrium develop-
breath of extrauterine life initiates a process of phys-
ing higher pressures, which causes the foramen ovale
iologically altering his circulation and respiration. In
to functionally close. The flow across the ductus arte-
order to care for neonates during the perioperative
riosus becomes left-to-right as the pulmonary artery
period, it is important to understand the physiologic
pressure decreases and the system vascular pressure
changes that occur during the first few hours, days,
increases. Normally the combination of decreased cir-
and months of life.
culating prostaglandin PGE2 and the increased oxy-
gen levels within the duct lead to functional closure
Cardiac within 2–3 days in greater than 99 percent of term
In utero, oxygenated placental blood is divided to infants [3]. Complete closure does not occur nor-
pass through either the liver or to the inferior vena mally until 4–8 weeks, which means that under cer-
cava via the ductus venosus. This oxygenated blood tain circumstances the ductus arteriosus can reopen.
from the inferior vena cave preferentially streams If the vascular resistances of the pulmonary circuit
across the right atrium through the foramen ovale become elevated during this period, it is possible for
into the left atrium. This blood passes through the the foramen ovale to act as a right-to-left shunt, as it
left ventricle and aorta to supply the myocardium, did during fetal life. This condition is known as per-
head, and upper torso. Deoxygenated blood returns sistent pulmonary hypertension of the newborn and
to the right atrium via the superior and inferior vena can be exacerbated by hypoxia, acidemia, or primary
cava and is pumped out into the pulmonary arteries structural cardiac diseases. Figures 1.1 and 1.2 offer an
via the right ventricle [1]. About 11 percent of this overview of the circulatory system.
blood is distributed to the highly resistant pulmon-
ary vascular bed and 89 percent is distributed to
the aorta via the ductus arteriosus [2]. Aortic blood Neonatal Heart
then divides to supply the lower extremities and to In a full-term infant, the neonatal cardiac output
return to the placenta via the umbilical arteries to be at 200 ml–1 kg–1 min–1 or greater is roughly double
reoxygenated. that of adults to meet the metabolic demands of
1

10:56:18
02
2

Section 1: Newborn and Infant Physiology for Anesthetic Management

4 Mixed blood travels

to the head and body,
and back to the
placenta via the aorta.

3 The ductus
arteriosus connects
the aorta with the
pulmonary artery,
further shunting blood
Placenta away from the lungs
Umbilical and into the aorta.
vein The foramen ovale
2
allows oxygenated
blood in the right
atrium to reach the
left atrium.
1 Oxygenated blood from placenta enters
right atrium via inferior vena cava.

Inferior vena cava

2 The ductus
venosus shunts
oxygenated
blood from
Umbilical the placenta
Umbilical cord artery away from the
(contains umbilical semifunctional
artery and umbilical vein) liver and toward
the heart.
1 Blood arrives
via umbilical
vein.

Figure 1.1 The fetal circulatory system (from Rice University’s OpenStax course in Anatomy & Physiology under CCC license 4.0
http://cnx.org/content/col11496/1.6/).

eating, breathing, thermogenesis, and growing [4,5]. young infants is often heralded by sweatiness, tachy-
Because the myocardium is immature at birth, with cardia, tachypnea, difficulties in feeding, and may
a reduced, chaotic arrangement of myofibrils, there be missed during a preoperative examination. In
is limited compliance at birth [5]. Although fill- cases of moderate to severe congestive failure there
ing pressures can increase stroke volume to a small will be signs of acidosis, hypothermia, and oliguria.
degree, functionally the neonatal heart is primarily Management consists of diagnosing the underlying
dependent on an increase in heart rate to increase physiology, fluid restriction, diuretics, and inotropic
cardiac output. At birth the ECG reflects the right- agents.
sided dominance of the fetal heart with right axis Normal heart rates at birth at rest vary between
deviation and R-wave dominance in lead V1 and S- 104 and 156 (mean 130 + 13 mmHg). The first day
wave dominance in lead V6. After the left ventricle of life, the mean systolic blood pressure is 70 mmHg,
grows and hypertrophies, the ECG assumes the adult which rapidly increases over the next three days to
configuration of left-sided dominance by about six 77 mmHg [6]. Mean blood pressure rises by 15 per-
2 months of age [5]. Mild congestive heart failure in cent over the first month of life [7].

10:56:18
02
3

Chapter 1: The Term Infant

patients dying before surgical repair was done [12].

Presentation usually occurs when the ductus arterio-
sus begins to close and the infants manifest either
shock or cyanosis. Careful physical examination of
term newborns scheduled for surgery is important,
but may not detect all infants with critical CDH. A car-
diac murmur is present in many patients with CDH,
but in approximately 44 percent of murmur detections
in a healthy newborn there is no structural heart dis-
ease [13]. A careful physical examination along with
a screening pulse oximetry test should be carried
out for every preoperative patient. Attention should
be paid to abnormal heart rates, precordial activity,
S2 splitting, other heart sounds, murmurs, periph-
eral pulses, and cyanosis. In patients with cyanosis,
a hyperoxia test can be done to help discern cardiac
from noncardiac causes of decreased oxygen desatu-
ration. In addition to the hyperoxia test, pulse oxime-
ters can be placed both preductally (right hand) and
postductally (left limb) to determine whether there is
differential saturations. In medical centers with access
to echography, a cardiac echo can rapidly determine
the structural integrity of the heart.

Respiratory
The process of extrauterine breathing occurs with
Figure 1.2 Fetal blood circulation © BSIP/UIG.
fluid being squeezed from the lung during vaginal
delivery. The first breath is characterized by high
inspiratory negative pressures to overcome the airway
Congenital Cardiac Defects resistance of residual fluid in the airways, and pul-
The most common birth defect in neonates is congen- monary collapse. With alveolar expansion, the alveo-
ital heart disease (CDH) with a prevalence of between lar size increases and the wall tension of the alveolus
6 and 13 per 1000 live births [8]. It is 2–3 times more decreases. Alveolar collapse between breaths is lim-
common in premature births compared with full- ited by a coating of surfactant that maintains surface
term births [9]. Critical CDH is defined as lesions tension within the alveolus. Type II pneumocytes are
requiring surgery or catheterizations within the first responsible for surfactant production and begin to
year of life, and constitute 15 percent of CDH at birth differentiate at 24 weeks of gestation; however, surfac-
[10,11]. Approximately 30 percent of critical CDH tant synthesis for appropriate pulmonary function is
is diagnosed after initial hospital discharge because not adequate until 34–36 weeks of gestation [5]. Once
the ductus arteriosus is still functioning, masking oxygenated blood reaches the pulmonary and cen-
symptomatology [10,11]. The most common lesions tral circulation, the pulmonary vascular resistance
involved include coarctation of the aorta, interrupted drops and facilitates the transition from fetal to adult
aortic arch, aortic stenosis, transposition of the great circulation.
vessels, and hypoplastic left heart syndrome. Some Neonatal lung mechanics put young infants at a
nondependent duct lesions associated with mild cya- disadvantage compared with older children and adults.
nosis such as truncus arteriosus, Tetralogy of Fallot, The chest wall is exceedingly compliant and the lungs
and total anomalous venous return can be missed themselves relatively noncompliant; both of which
during the perinatal period. Missed critical CDH can facilitate lung collapse. In fact, the closing capac-
has a high mortality rate, with more than half of ity for neonates exceeds functional residual capacity. 3

10:56:18
02
4

Section 1: Newborn and Infant Physiology for Anesthetic Management

Neonates compensate for this by producing auto pos- desaturations. Some studies – but not all – have shown
itive end-expiratory pressure (auto-PEEP) by partial an association between anemia and an increased risk
closure of the vocal cords and breathing through the of postoperative apnea [18].
high-resistance nasal passages. The horizontal nature
of the ribs and the relatively flat diaphragm make the
work of breathing inefficient and increases in minute Hematologic
ventilation are achieved by increasing respiratory rate. At birth, 50–95 percent of the hemoglobin in an infant
Also, infants have a relatively low functional residual is fetal hemoglobin, which has an increased attrac-
capacity compared with adults. Any surgical pathol- tion for oxygen compared to adult hemoglobin. Fetal
ogy that decreases the compliance of the abdomen hemoglobin is made up of two alpha chains and two
will necessarily affect the ability of the neonate to gamma chains, and is gradually replaced by hemoglo-
adequately ventilate. During the first day of life, venti- bin A, which is made up of two alpha chains and two
lation flow mismatch accounts for up to 24 percent of beta chains, by the time the infant is six months old.
cardiac output. This fraction decreases to 10 percent The fetus lives in a relatively hypoxic zone compared
by one week of life [14]. In addition to the disadvan- with the maternal environment and compensates
tageous lung mechanics, neonates consume twice as for this with a much higher hemoglobin concentra-
much oxygen per kilogram as adults, thus their alve- tion of 19.3 g dl–1. Within one week of birth in term
olar ventilation needs to be roughly double that of infants, hemoglobin levels begin to drop and reach a
adults. Because of all these factors, modest decreases nadir of about 9–11 g dl–1 at about 8–12 weeks of life
in either ventilation or fraction of inspired oxygen [19]. Anemia can occur at birth as a result of blood
(FiO2) will incline neonates to develop hypoxia. loss before, after, or during delivery. Feto-maternal
The ventilatory centers of respiration in the brain or twin–twin transfusion, placental abruption, or
at birth are not fully developed, and responses to hyp- delayed cord clamping can cause increased blood
oxia are immature in the term neonate. The peripheral loss. Decreased erythrocyte production can occur
chemoreceptors do not respond to hypoxia during the as a result of iron deficiency, or chronic infection.
first 48 hours of life because they are effectively sup- Decreased red blood cell destruction can be caused
pressed by the rise in PaO2 following delivery and by Rh and autoimmune hemolytic disease, enzyme
need to be reset [15]. This effect is exacerbated in abnormalities such as G6 PD, membranopathies such
infants resuscitated with 100 percent O2 in the deliv- as spherocytosis and elliptocytosis, and hemoglobin-
ery room [16]. The feedback mechanisms by which opathies such as sickle cell disease, thalassemia, and
the peripheral chemoreceptors send messages to the hemoglobin C disease.
central centers of ventilation are also not mature, lead- Term infants can also be born with polycythemia,
ing to unstable respiratory control mechanisms, espe- which can lead to a hyperviscous state and complica-
cially in sick, unstable neonates. tions when the hematocrit is greater than 65 percent
Apnea and bradycardia is one of the nonspecific [20]. Maternal uterine insufficiency can lead to pla-
signs that a neonate is suffering from stress such cental hypoxic state in which the fetus responds with
as hypoxemia, sepsis, or hypothermia. This apnea increased red cell production. Postnatally polycythe-
can lead to an unstable metabolic state that further mia can cause decreased blood flow to vital organs
increases the risk of apnea and hypoxia. Apnea, which including the brain, heart, and lungs, increased biliru-
is generally defined as a cessation of breathing for bin production, and is associated with hypoglycemia.
longer than 15 seconds, can also result from airway Treatment is a partial exchange transfusion.
obstruction, especially in those neonates with con- The coagulation profile of neonates also differs
genital abnormalities of the head and neck region or from adults. Many of the proteins needed for coagu-
neonates that have been sedated with anesthetic drugs lation are diminished in newborns, including factors
[17]. It is very common for term infants after a gen- II, VII, IX, X, XI, XII; others that promote fibrinoly-
eral anesthetic to exhibit periodic breathing, which sis are increased, such as thrombomodulin, tPA, and
is a breathing pattern in which the tidal volumes plasminogen activator inhibitor-1 [21,22]. These pro-
become shallower and shallower to the point of brief bleeding tendencies are balanced by an alteration in
cessation, and then become deeper again. This pat- some procoagulant proteins such as an increase in
4 tern is repeated and generally does not lead to oxygen Von Willibrand factor and a decrease in antithrombin,

10:56:18
02
5

Chapter 1: The Term Infant

heparin cofactor II, alpha-2-macroglobulin, protein supply of energy for neonates that may not be getting
C, protein S, and plasminogen [22]. The end result is adequate enteral nutrition in the first days of life. It is
that neonates normally have a prolongation of their also responsible for the production of clotting factors
prothrombin time (PT), and activated partial throm- and serum proteins, bile synthesis, and the biotrans-
boplastin time (aPTT), but a shortened bleeding formation of medications and other xenobiotics, as
time [21]. well as the endogenous metabolic byproducts.
Newborns can be adversely affected by low vita- Maturation of the many liver functions occurs at
min K levels. Bleeding can occur because of a decrease differential rates. Albumin synthesis is at adult levels
of the vitamin K-dependent coagulation factors (II, at birth in term infants. The coagulation factors (all
VII, IX, X). Treatment includes prophylactic vitamin are synthesized in the liver except for factor VIII)
K intramuscular injections and fresh frozen plasma are initially low at birth but reach adult levels by 2–
transfusions in infants with symptomatic bleeding. 3 days of life. The expression of the hepatic enzyme
Early thrombocytopenia in the newborn is usually uridine diphosphate glucuronyl transferase is poor in
related to maternal–placental factors, and late throm- the fetus, but by age 2–3 weeks postnatally it reaches
bocytopenia is usually caused by excessive platelet adult levels. This enzyme is needed to conjugate bil-
consumption, such as seen in necrotizing enterocoli- irubin in order to facilitate biliary excretion into the
tis and sepsis [23]. Thrombocytopenia is a risk factor enteric system. Some of this conjugated bilirubin is
for intraventricular hemorrhage even in term infants, then unconjugated by intestinal B glucuronidase and
so many centers administer platelet transfusions to then reabsorbed into the body by way of the entero-
infants whose levels are below 50 000. hepatic circulation. It is very common for term infants
to have neonatal jaundice in the first few days to weeks
Thermoregulation of life because of increased erythrocyte breakdown,
deficiencies of their ability to conjugate free bilirubin,
Regulation of body temperature depends on a bal-
and decreased amounts of enteric organisms available
ance between heat loss and heat generated. Although
to break down unconjugated bilirubin for fecal excre-
thermogenesis is suppressed in utero, heat produc-
tion [26]. Clearance of medications depends on either
tion is actually greater in the fetus than the mother so
a drug metabolism pathway or a hepatic transport
the heat gradient flows from the fetus to the mother.
mechanism. Metabolic pathways are usually divided
Humans are a precocial species in regards to thermo-
into phase 1 reactions that involve oxidation, reduc-
genesis, with responses capable of generating heat
tion, hydrolysis, cyclization, and decyclization reac-
within minutes of birth. Stimulation of the preoptic
tions, and phase 2 reactions that involve the addition
chiasma/anterior hypothalamic nuclei from periph-
(conjugation) of polar groups to phase 1 metabolites
eral cutaneous receptors activate non-shivering ther-
[25]. Neonates are unable to metabolize medications
mogenesis by sympathetic norepinephrine-secreting
as rapidly as adults because the cytochrome p450
nerve fibers that innervate brown adipose tissue and
system (which oxidizes medications) does not reach
shivering thermogenesis through the posterior hypo-
adult levels until one year of age [27]. For phase 2
thalamic nucleus [24].
metabolism, infants preferentially must use sulfation
rather than glucuronidation for conjugation reactions
Hepatic [28]. Table 1.1 summarizes the maturation of liver
During fetal development, the umbilical vein brings functions.
blood to the liver. Between 20 to 30 percent of this
blood bypasses the liver and is carried directly to the
inferior vena cava by way of the ductus venosus [25]. Renal
The remaining umbilical vein enters the liver, where The kidney matures over the first two years of life.
some of it joins the portal vein. The ductus venosus Nephrogenesis is completed by 36 weeks postconcep-
typically closes by the first week of life and is then tion but the nephrons are immature at birth. During
known as the ligamentum venosum. fetal development the primary role of the kidney is to
Liver function is not fully mature until about two maintain amniotic fluid levels and renal blood flow is
years postnatally. Initially, its primary role is to regu- a very small percentage of the fetal cardiac output. For
late glucose and fatty acid metabolism to maintain a the first week of life, renal blood flow is only 10 percent 5

10:56:18
02
6

Section 1: Newborn and Infant Physiology for Anesthetic Management

Table 1.1 Maturation of liver functions

Oxidative enzyme activity Glucuronide conjugation Sulfate conjugation Effect on drug

metabolism
Premature Decreased oxidative enzyme Decreased glucuronide Slightly decreased sulfate Decreased
neonates activity (20–70 percent of adult conjugation conjugation
values for cytochrome p450
activity)
Neonates Same as premature infants Same as premature infants Slightly decreased from Decreased
adults
Infants Cytochrome p450 reaches Reaches adult levels by Reaches adult levels in early Decreased
adult activity by 6–12 months 24 months of age infancy
of age

of cardiac output and does not reach the adult level of responsible for the increase in blood pressure seen
25 percent until 24 months of life [29]. The glomeru- over the first weeks of life.
lar filtration rate (GFR) is also diminished for the first
two years of life. At birth it is about 40 ml kg–1 1.73 m–2 Neurologic
and reaches 66 ml kg–1 1.73 m–2 at two weeks of age, The neonatal and infancy period represents a time of
which is about one-half of the normal adult GFR [30]. dramatic brain growth, with the brain size as a neo-
The nephrons for the first few days of life are very nate being 36 percent of the size of an adult brain and
immature and allow for some resorption of creatinine, growing to 70 percent of its adult size by one year of
which makes creatinine clearance a poor estimate of age and 80 percent by two years of age [31]. During late
GFR during this period. These leaking nephrons gestation, brain development includes gray and white
rapidly mature and then creatinine levels drop. matter myelination, synaptogenesis, pruning, and
One of the main functions of the kidney is to synaptic modification. These processes continue into
maintain fluid and electrolyte balance. At birth the early infancy. Although all the cortical layers of cells
extracellular volume is approximately 40 percent by are present at term and the primary cortical areas such
body weight; this decreases to about 30 percent at as motor, somatosensory, visual, and auditory corti-
six months of age and 20 percent by one year of age. ces are morphologically identifiable, the association
Term infants generally do not have difficulty main- cortices are less delineated. There is pronounced gray
taining sodium balance, but excessive administration matter growth in the parietal and occipital areas in the
of sodium can overwhelm their kidneys, leading to first month of life. The newborn brain still exhibits a
peripheral edema. Likewise, the term kidney is able small degree of cortical neurogenesis and neuronal
to maintain potassium, calcium, and phosphorus migration, but the dramatic brain growth is mainly
balance. Acid–base status is accomplished through due to the growth of glia and subsequent myelination
ventilation, buffering capacity of serum proteins, during infancy. Abnormal brain growth in infancy is
bicarbonate-carbonic acids, hemoglobin–oxyhemo- often a harbinger of poor neurocognitive outcomes.
globin and phosphorus, and the renal system. These Microcephaly can be a result of malnutrition, and
mechanisms are all mature enough within three days macrocephaly has been associated with autism.
of birth to handle nonrespiratory-induced acid loads. MRI and autopsy studies of infants in the first
The kidney also produces renin, which triggers the year of life reveal a robust expansion of gray matter by
formation of angiotensin, which is converted to angio- way of elaboration of dendrites, spines, and synapses.
tensin II by angiotensin-converting enzyme. This Conversely, this is also a time of increased apoptosis
enzyme increases the peripheral vascular resistance or pruning. The pruning process time course begins
and cardiac contractility, leading to an increase in sys- with the primary cortices followed by the association
temic blood pressure. The excretion of renin increases cortices, and lastly in late childhood by pruning in the
after birth and is higher in infants than older children. frontal lobes.
The renin angiotensin system, other humoral agents, Along with synaptic pruning, there is remodeling
6 and an increase in sympathetic activity at birth are of existing synapses and fine-tuning of neural circuits.

10:56:18
02
7

Chapter 1: The Term Infant

Synaptic remodeling is dependent on the strengthen- shown that chlorhexidine in term infants can be safely
ing of certain synaptic pathways and weakening of used perioperatively and decreases surgical site infec-
others. Some of these are time-dependent during tions [34–36]. There is evidence that chlorhexidine
infantile maturation, such as the development of bin- absorption does occur and increases after repeated
ocular vision. Lack of input from an eye with a con- exposures. Povidine iodine is an excellent bacterio-
genital cataract will lead to potentiation of synapses cidal agent but causes thyroid suppression second-
from the functioning retina and inhibition of synap- ary to iodine absorption [37]. This effect is greater in
ses from the poorly stimulated retina. This in com- premature infants but even in infants less than three
bination with pruning can lead to permanent visual months of age, increased levels of serum iodine have
impairment in infants who get delayed treatment for been found after skin exposure. Skin rashes and burns
congenital cataracts. have been seen after surgical preparations in term
There is a dramatic increase in the volume of glial infants exposed to isopropyl alcohol, chlorhexidine,
cells postnatally, which leads to an increase in myelin- and povidine iodine.
ation during the first year of life. Myelination proceeds There are several very common rashes seen in
in a differential pattern starting with the sensory path- term babies. Erythema toxicum neonatorum affects
ways, then motor and finally association pathways. It almost 50 percent of term newborns and is heralded
also proceeds subcortically before cortically in any by an erythematous macular papular rash with pus-
given neural pathway. At birth in full-term infants, tules. It usually occurs in the first week of life and lasts
there are functional networks that include the visual, a few days. Milia are pinpoint pearly white bumps
sensorimotor, and auditory processing networks. seen most often on the nose, mouth, or palate which
The effects of harmful toxins, illness, and envir- are also seen in 50 percent of neonates and generally
onmental deprivation may be greater in very young resolve by the first month of life. Neonates often get
infants whose brains are growing rapidly in a time- miliaria or heat rash from overbundling. It is caused
dependent fashion. The long-term effects of general by occlusion of the sweat ducts and features 1–3 mm
anesthetics on the neonatal brain have not been ade- vesicles or papules. Treatment is to limit humid or hot
quately characterized yet. environments. Neonates are also susceptible to neo-
natal acne [38]. This is also self-limited and resolves as
circulating maternal hormones diminish.
Dermatologic
The term newborn has a dermis that is 40–60 percent
the depth of adult dermis, and a larger surface area to Endocrine
body weight ratio than adults [32]. This means that There are many endocrine changes that occur perina-
the infant is more likely to lose heat and body fluids as tally. Normally neonatal blood glucose levels drop in
well as absorb any materials placed on the skin com- the first few hours of birth, sometimes to levels below
pared to an adult. The pH of adult skin is acidotic at 30 mg dl–1. A compensatory stress response involving
4.7, which is protective by decreasing the colonization the secretion of epinephrine and cortisol increases
of pathogenic bacteria. At term birth, the pH is 6.0 the plasma glucose to levels above 40 mg dl–1. There
but decreases to less than 5.0 by four days of age. The are no universally agreed guidelines as to the defini-
skin colonization of neonates resembles adult flora tion of hypoglycemia in term infants, but many neo-
after the first few weeks of life. There are differences natologists consider a plasma glucose of <40 mg dl–1
between the skin biome of infants delivered vaginally in the first three hours of life, <45 mg dl–1 in the first
compared with caesarian section, with 60–82 per- day of life, and <60 mg dl–1 after three days of life to
cent of neonatal methicillin-resistant staphylococcus be abnormal [39]. Infants who are born of diabetic
infections occurring in surgically delivered babies mothers, large for gestational age, or have suffered
[33]. The vernix caseosa is a sebaceous material made severe perinatal stress or asphyxia may have transient
from sebum, desquamated skin, water, and lanugo hyperinsulinemia. Glucose requirements in excess of
that is present in term infants, which enhances the 8 mg kg–1 min–1 in order to maintain normoglycemia
skin barrier to infection, heat, and fluid loss. suggests a hyperinsulinemic state. Because insulin
The best type of disinfective skin preparation for inhibits ketone body formation, decreases glycogen-
surgery has not been determined. Many studies have olysis and gluconeogenesis, and increases peripheral 7

10:56:18
02
8

Section 1: Newborn and Infant Physiology for Anesthetic Management

glucose uptake by cells, the brain is very vulnerable to seen in infants who are hypomagnesemic and infants
damage such as permanent injury and seizures during born of mothers with diabetes mellitus and hyper-
hyperinsulinemia. parathyroidism [39]. Abnormal thyroid gland devel-
Thyroid homeostasis is necessary for brain devel- opment is seen in DiGeorge’s syndrome, which can
opment and growth, cardiac function, and energy lead to hypocalcemia. Hypercalcemia of the neonate
balance. Prior to birth, the neonate is primarily is most commonly iatrogenically caused, but is also
dependent on maternal T3 and T4, but postnatally seen in patients with Williams syndrome. In this con-
there is a dramatic increase (up to a 50-fold increase) dition, the hypercalcemia usually resolves by one year
in thyroid stimulating hormone (TSH) over the first of age. Infants with Williams syndrome can present
24 hours. It is important to recognize that a TSH in with pulmonary artery stenosis and supravalvular
the first day of life in the 60–80 mU/L range is not stenosis with associated coronary artery abnormal-
indicative of thyroid disease [40]. One of the most ities. Sudden death from this syndrome is rare during
common causes of abnormally low thyroid hormone infancy but has occurred.
levels in term infants is nonthyroidal critical illnesses,
but there is no evidence that treating low levels bene-
fits these patients [41,42]. Other causes include exces-
References
1. Odegard KC, DiNardo JA, Laussen PC. Anesthesia
sive iodine intake such as may be seen in iodinated for Congenital Heart Disease, in Gregory’s Pediatric
contrast dyes or surgical preparations, and inadequate Anesthesia, 5th edn. Oxford: Wiley-Blackwell; 2012.
iodine intake. Congenital hypothyroidism is rare
2. Mielke G, Benda N. Cardiac output and central
and is usually tested for at birth in the United States. distribution of blood flow in the human fetus.
Transient hyperthyroidism occasionally occurs in Circulation. 2001;103:1662–8.
infants exposed to maternal hyperthyroidism. 3. Schneider DJ, Moore JW. Patent ductus arteriosus.
At birth the adrenal system is mature, with adre- Circulation. 2006;114:1873–82.
nocorticotropic hormone (ACTH) stimulating the 4. Walther FJ, Siassi B, Ramadan NA, Ananda AK,
adrenal gland to secrete cortisol. Primary adrenal Wu PY. Pulsed Doppler determinations of cardiac
insufficiency is most often seen in infants that lack the output in neonates: normal standards for clinical use.
enzyme 21 hydroxylase, which is necessary to synthe- Pediatrics. 1985;76:829–33.
size corticosteroids and aldosterone. The symptoms 5. Brusseau R, McCann ME. Anaesthesia for urgent and
include life-threatening salt wasting, hypotension, emergency surgery. Early Hum Dev. 2010;86:703–14.
and poor growth. Affected infants also have very high 6. Tan KL. Blood pressure in full-term healthy neonates.
levels of 17 hydroxyprogesterone and other adre- Clin Pediatr (Phila). 1987;26:21–4.
nal androgens, leading to viralized infants. Female 7. Second Task Force on Blood Pressure Control in
infants will have abnormal external genitalia but male Children. Task Force on Blood Pressure Control in
infants may appear normal leading to a delayed diag- Children: National Heart, Lung, and Blood Institute,
nosis. Secondary adrenal insufficiency is common Bethesda, Maryland. Pediatrics. 1987;79:1–25.
in extremely stressed term infants or in infants that 8. van der Linde D, Konings EE, Slager MA, et al. Birth
have been treated with exogenous steroids. The mor- prevalence of congenital heart disease worldwide: a
systematic review and meta-analysis. J Am Coll
tality for infants with known adrenal insufficiency
Cardiol. 2011;58:2241–7.
in the setting of sepsis is as high as 86 percent [43].
9. Kenna AP, Smithells RW, Fielding DW. Congenital
Treatment with glucocorticoids in infants with known
heart disease in Liverpool: 1960–69. Q J Med.
adrenal insufficiency will improve blood pressure. 1975;44:17–44.
Aldosterone is stimulated by the renin angiotensin
10. Wren C, Reinhardt Z, Khawaja K. Twenty-year trends
system and thus is unaffected by low ACTH levels. in diagnosis of life-threatening neonatal cardiovascular
Serum calcium levels are regulated by parathyroid malformations. Arch Dis Child Fetal Neonatal Ed.
hormone release and special calcium-sensing receptors 2008;93:F33–5.
within the parathyroid glands. Parathyroid hormone 11. Hoffman JI. It is time for routine neonatal screening by
(PTH) stimulates bone resorption to mobilize skele- pulse oximetry. Neonatology. 2011;99:1–9.
tal calcium and conversion of inactive vitamin D to 12. Chang RK, Gurvitz M, Rodriguez S. Missed diagnosis
active vitamin D to increase dietary absorption of cal- of critical congenital heart disease. Arch Pediatr
8 cium and phosphate. Transient hypoparathyroidism is Adolesc Med. 2008;162:969–74.

10:56:18
02
9

Chapter 1: The Term Infant

13. Ainsworth S, Wyllie JP, Wren C. Prevalence and 30. Schwartz GJ, Brion LP, Spitzer A. The use of plasma
clinical significance of cardiac murmurs in neonates. creatinine concentration for estimating glomerular
Arch Dis Child Fetal Neonatal Ed. 1999;80:F43–5. filtration rate in infants, children, and adolescents.
14. Rennie J, ed. Robertson’s textbook of Neonatology. 4th Pediatr Clin North Am. 1987;34:571–90.
ed. Oxford: Elsivier; 2005. 31. Tau GZ, Peterson BS. Normal development of brain
15. Hertzberg T, Lagercrantz H. Postnatal sensitivity of the circuits. Neuropsychopharmacol. 2010;35:147–68.
peripheral chemoreceptors in newborn infants. Arch 32. SYSTOLIC blood pressure determination in the
Dis Child. 1987;62:1238–41. newborn and infant. Anesthesiol. 1952;13:648–9.
16. Martin RJ, Bookatz GB, Gelfand SL, et al. 33. Watson J, Cortes C. Community associated methicillin
Consequences of neonatal resuscitation with resistant Staphylococcus aureus infection among
supplemental oxygen. Sem Perinatol. 2008;32:355–66. healthy newborns: Chicago and Los Angeles County,
17. Craven PD, Badawi N, Henderson-Smart DJ, O’Brien 2004. JAMA. 2006;296:36–8.
M. Regional (spinal, epidural, caudal) versus general 34. Da Cunha ML, Procianoy RS, Franceschini DT, De
anaesthesia in preterm infants undergoing inguinal Oliveira LL, Cunha ML. Effect of the first bath with
herniorrhaphy in early infancy. Cochrane Database of chlorhexidine on skin colonization with Staphylococcus
Syst Rev. 2003:CD003669. aureus in normal healthy term newborns. Scand J Infect
18. Cote CJ, Zaslavsky A, Downes JJ, et al. Postoperative Dis. 2008;40:615–20.
apnea in former preterm infants after inguinal 35. Mullany LC, Darmstadt GL, Khatry SK, et al. Topical
herniorrhaphy: a combined analysis. Anesthesiology. applications of chlorhexidine to the umbilical cord
1995;82:809–22. for prevention of omphalitis and neonatal mortality
19. Kett JC. Anemia in infancy. Pediatr Rev. in southern Nepal: a community-based, cluster-
2012;33:186–7. randomised trial. Lancet. 2006;367:910–18.
36. Tielsch JM, Darmstadt GL, Mullany LC, et al. Impact
20. Rosenkrantz TS. Polycythemia and hyperviscosity in
of newborn skin-cleansing with chlorhexidine on
the newborn. Semin Thromb Hemost. 2003;29:515–27.
neonatal mortality in southern Nepal: a community-
21. Diaz-Miron J, Miller J, Vogel AM. Neonatal based, cluster-randomized trial. Pediatrics.
hematology. Semin Pediatr Surg. 2013;22:199–204. 2007;119:e330–40.
22. Ignjatovic V, Lai C, Summerhayes R, et al. Age- 37. L’Allemand D, Gruters A, Heidemann P, Schurnbrand
related differences in plasma proteins: how plasma P. Iodine-induced alterations of thyroid function in
proteins change from neonates to adults. PLoS One. newborn infants after prenatal and perinatal exposure
2011;6:e17213. to povidone iodine. J Pediatr. 1983;102:935–8.
23. Kamphuis MM, Paridaans NP, Porcelijn L, Lopriore 38. Cantatore-Francis JL, Glick SA. Childhood
E, Oepkes D. Incidence and consequences of neonatal acne: evaluation and management. Dermatol Ther.
alloimmune thrombocytopenia: a systematic review. 2006;19:202–9.
Pediatrics. 2014;133:715–21.
39. Wassner AJ, Modi BP. Endocrine physiology in the
24. Morrison SF, Nakamura K, Madden CJ. Central newborn. Semin Pediatr Surg. 2013;22:205–10.
control of thermogenesis in mammals. Exp Physiol.
40. Fisher DA, Klein AH. Thyroid development and
2008;93:773–97.
disorders of thyroid function in the newborn. N Engl J
25. Grijalva J, Vakili K. Neonatal liver physiology. Semin Med. 1981;304:702–12.
Pediatr Surg. 2013;22:185–9. 41. Dimmick S, Badawi N, Randell T. Thyroid hormone
26. Dennery PA, Seidman DS, Stevenson DK. Neonatal supplementation for the prevention of morbidity
hyperbilirubinemia. N Engl J Med. 2001;344:581–90. and mortality in infants undergoing cardiac surgery.
27. Treluyer JM, Cheron G, Sonnier M, Cresteil T. Cochrane Database Syst Rev. 2004:CD004220.
Cytochrome P-450 expression in sudden infant 42. Shih JL, Agus MS. Thyroid function in the critically ill
death syndrome. Biochem Pharmacol. newborn and child. Curr Opin Pediatr. 2009;21:536–40.
1996;52:497–504. 43. Soliman AT, Taman KH, Rizk MM, et al. Circulating
28. Alcorn J, McNamara PJ. Ontogeny of hepatic and renal adrenocorticotropic hormone (ACTH) and cortisol
systemic clearance pathways in infants: part I. Clin concentrations in normal, appropriate-for-gestational-
Pharmacokinet. 2002;41:959–98. age newborns versus those with sepsis and respiratory
29. Sulemanji M, Vakili K. Neonatal renal physiology. distress: cortisol response to low-dose and standard-
Semin Pediatr Surg. 2013;22:195–8. dose ACTH tests. Metabolism. 2004;53:209–14.
9

10:56:18
02
10

Section 1 Newborn and Infant Physiology for Anesthetic Management

Chapter
The Preterm Infant

2 Lauren R. Kelly Ugarte and Thomas J. Mancuso

Background on the Preterm Newborn PCA group and one report showed that 93 percent of
these patients will have respiratory distress, 46 percent
The preterm newborn is defined as a baby born from
will have patent ductus arteriosis (PDA), 16 percent
22 to 36 weeks postconceptual age (PCA) [1]. More
will have severe intraventricular hemorrhage (IVH),
specifically, preterm is defined by the Center for
11 percent will have necrotizing enterocolitis (NEC),
Disease Control as less than 37 completed weeks of
and 36 percent will have late sepsis [4]. The most com-
gestation, with early preterm being less than 34 weeks
mon issues for the smallest of patients are broncho-
of gestation and late preterm being 34–36 weeks [2].
pulmonary dysplasia (BPD) and infections [4]. All of
There were 3.95 million live births in the United
these issues in and of themselves may require surgical
States in 2011, with the preterm birthrate declining
attention or add to the anesthetic risk if the patient
for the fifth year in a row, with a rate of 11.72 per-
is taken to surgery. Other common problems that are
cent of all births being younger than 36 weeks, down
seen in or result from preterm birth include: retinop-
from 11.99 percent in 2010 [2]. Overall, 0.7 percent
athy of prematurity (ROP), hypoglycemia, and neuro-
of births in 2011 were babies younger than 28 weeks
developmental delay [1,4].
PCA (Figure 2.1) [3].
Pediatric anesthesiologists must be vigilant and
Categorization of birth age allows for stratification
thoughtful in the provision and planning of care for
of risk. Data show that survival is least favorable in the
all of their patients. Preterm newborns who present
smallest and youngest patients. Recently, with greatly
for surgery are uniquely challenging due to the imma-
improved accuracy in gestational age (GA) measure-
turity of all the organ systems, the complexity of their
ments, it has become clear that perinatal complica-
ongoing medical care, and the often emergent reasons
tions most closely follow GA, not birth weight. In
for any surgical procedures. It is unlikely that the sur-
extremely low gestational age newborns (ELGAN)
gical issues these patients deal with today will change
born at 22–28 weeks PCA, there is improved survival
drastically over the coming years as there seems to be
with longer gestation as there is about a 6 percent
a current plateau in survival [4]. That being said, these
survival to discharge in a 22-week GA newborn and
patients are usually not cared for on a daily basis by
92 percent for a 28-week GA newborn [1,4]. The sur-
pediatric anesthesiologists and this fact contributes to
vival in very low birth weight patients has increased
their challenging care.
since the 1980s due to advances in prenatal, obstet-
ric, and neonatal care, and we now see a majority of
infants born at 24 weeks GA survive to leave the hos- Neurologic Issues
pital (Figure 2.2) [4]. Over the past few decades, anesthetic care for preterm
Medically intervening in newborns born at 22–24 newborns has improved as research has allowed us to
weeks’ gestation is a controversial area of obstetrics understand their complex physiology. We have come to
and neonatology and it is not possible to standardize learn that fetuses at 20 weeks’ gestation have the neural
the data available [4]. We see that every week in utero substrate to transmit impulses due to noxious stimuli.
confers better survival as the risk of death is 2.5 times All newborns the pediatric anesthesiologist deals with
higher in infants born from 24 to 27 weeks compared will require either pain medications or anesthetics to
to those who are born at 28 weeks and more than three minimize the detrimental stress responses related to
times higher for the 22-week newborns [4]. However, surgical procedures [5]. Currently, there are concerns
10 morbidity in the survivors is high in the 22–28 week about the long-term neurologic sequelae of exposing

11:05:44
03