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Chapter 22

The Neonate

Cardiopulmonary Transition 469 Clinical Applications 480 Perinatal Infection 487

Pulmonary Development 469 Delivery Room 480 Early-Onset Bacterial Infection 487
First Breaths 472 Nursery 480 Respiratory Distress 487
Fetal Breathing 472 Neonatal Nutrition and Cardiovascular Causes 487
Mechanics of the First Breath 472 Gastroenterology 481 Pulmonary Causes 488
Circulatory Transition 473 Infant Feeding 481 Neonatal Neurology 490
Abnormalities of Cardiopulmonary Neonatal Hypoglycemia 482 Intraventricular Hemorrhage and
Transition 474 Congenital Gastrointestinal Surgical Periventricular Leukomalacia 490
Birth Asphyxia 474 Conditions 483 Classification of Newborns by
Delivery Room Management of the Necrotizing Enterocolitis 483 Growth and Gestational Age 490
Newborn 475 Neonatal Jaundice 483 Nursery Care 491
Cord Clamping 478 Neonatal Hematology 486 Care of the Parents 493
Sequelae of Birth Asphyxia 478 Anemia 486 Kangaroo Care 494
Birth Injuries 478 Polycythemia 486 Outcome of Neonatal Intensive Care
Neonatal Thermal Thrombocytopenia 486 and Threshold of Viability 495
Regulation 480 Vitamin KDeficiency Bleeding of the Late Preterm Infant 496
Physiology 480 Newborn 486

American College of Obstetricians and ACOG Large for gestational age LGA
Gynecologists Magnetic resonance imaging MRI
Appropriate for gestational age AGA Meconium aspiration syndrome MAS
Central nervous system CNS Necrotizing enterocolitis NEC
Chronic lung disease CLD Neonatal resuscitation program NRP
Continuous positive airway pressure CPAP Periventricular hemorrhage PVH
Computed tomography CT Periventricular leukomalacia PVL
Cyclic adenosine monophosphate cAMP Persistent pulmonary hypertension of PPHN
Dipalmitoylphosphatidylcholine DPPC the newborn
Docosahexaenoic acid DHA Pulmonary vascular resistance PVR
Functional residual capacity FRC Rapid eye movement REM
Glucose-6-phosphate dehydrogenase G6PD Respiratory distress syndrome RDS
Group B Streptococcus GBS Small for gestational age SGA
Hyaline membrane disease HMD Surfactant protein SP
Human immunodeficiency virus HIV Thyrotropin-releasing hormone TRH
Idiopathic thrombocytopenic purpura ITP Thyroid-stimulating hormone TSH
Inferior vena cava IVC Uridine diphosphoglucuronosyl UDPGT
Insulin-like growth factor 1 IGF-1 transferase
Intrauterine growth restriction IUGR Vascular endothelial growth factor VEGF
Intraventricular hemorrhage IVH Very low birthweight VLBW
Kangaroo maternal care KMC

The first 4 weeks of an infants life, the neonatal period, are hours after birth, the newborn must assume responsibility
marked by the highest mortality rate in all of childhood. The for thermoregulation, metabolic homeostasis, and respira-
greatest risk occurs during the first several days after birth. tory gas exchange and must also undergo the conversion
Critical to survival during this period is the infants ability from fetal to postnatal circulatory pathways. This chapter
to adapt successfully to extrauterine life. During the early reviews the physiology of a successful transition as well as the

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Chapter 22 The Neonate 469

implications of circumstances that disrupt this process. Implicit surface is thin and continuous with two alveolar cell types: type
in these considerations is the understanding that the newborn I cells are thin and contain few subcellular organelles, whereas
reflects the sum total of its genetic and environmental past, type II cells contain subcellular organelles that aid in the produc-
which includes any minor or major insults to which it was sub- tion of surfactant (Fig. 22-1). Surfactant lipids and surfactant
jected during gestation and parturition. The period of neonatal proteins B and C are secreted by exocytosis as lamellar bodies
adaptation is then most meaningfully viewed as continuous with and unravel into tubular myelin. The other surfactant proteins
fetal life. (SPs), SP-A and SP-D, are secreted independently of the lamellar
bodies. Tubular myelin is a loose lattice of phospholipids and
surfactant-specific proteins. The surface active component of
CARDIOPULMONARY TRANSITION surfactant then adsorbs at the alveolar interface between air and
Pulmonary Development water in a monolayer. With repetitive expansion and compres-
Lung development and maturation require a carefully regulated sion of the surface monolayer, material is extruded that is either
interaction of anatomic, physiologic, and biochemical pro- cleared by alveolar macrophages through endocytic pathways or
cesses. The outcome of these events provides an organ with ade- is taken up by the type II cell for recycling back into lamellar
quate surface area, sufficient vascularization, and the metabolic bodies.3
capability to sustain oxygenation and ventilation during the Because of the development of high surface forces along
neonatal period. Five stages of morphologic lung devel- the respiratory epithelium when breathing begins, the avail-
opment have been identified in the human fetus1: (1) the ability of surfactants in terminal airspaces is critical to post-
embryonic period, from 0 to 6 weeks postconception; (2) the natal lung function. Just as surface tension acts to reduce the
pseudoglandular period, from 6 to 16 weeks; (3) the canalicular size of a bubble in water, it also acts to reduce lung inflation,
period, from 16 to 24 weeks; (4) the saccular period, from 24 to which promotes atelectasis. This is described by the LaPlace
38 weeks; and (5) the alveolar period, from 36 weeks gestation law, which states that within a sphere the pressure (P) is directly
to 2 years of age. proportional to surface tension (T) and is inversely propor-
The lung arises as a ventral diverticulum from the foregut tional to the radius (r) of curvature (Fig. 22-2). Surfactant
during the fourth week of gestation, in the embryonic period. has the physical property of variable surface tension depen-
During the ensuing weeks, in the pseudoglandular period, branch- dent on the degree of surface area compression. In other
ing of the diverticulum occurs and forms a tree of narrow tubes words, as the radius of the alveolus decreases, surfactant
with thick epithelial walls composed of columnar cells. Molecu- serves to reduce surface tension, which prevents collapse
lar mechanisms involved in lung development include expres- of the alveolus. If this property is extrapolated to the lung,
sion of transcription factors important for specification of the smaller alveoli will remain more stable than larger alveoli because
foregut endoderm, endogenous secretion of polypeptides impor- of their lower surface tension. This feature is emphasized in
tant for pattern formation, and the production of growth and Figure 22-3, which compares pressure-volume curves from
differentiation factors critical to cell development. By 16 weeks, surfactant-deficient and surfactant-treated preterm rabbits. Sur-
the conducting portion of the tracheobronchial tree up to factant deficiency is characterized by high opening pressure,
and including the terminal bronchioles has been established. low maximal lung volume, and lack of deflation stability at
The vasculature derived from the pulmonary circulation devel- low pressures.
ops concurrently with the conducting airways, and by 16 weeks, Natural surfactant contains mostly lipids, phospholipids
preacinar blood vessels are formed. The canalicular period is specifically, and some protein (Fig. 22-4).3 Approximately
characterized by differentiation of the airways, with widening of half of the protein is specific for surfactant. The principal
the airways and thinning of epithelium. In addition, primitive classes of phospholipids are:
respiratory bronchioles begin to form, marking the start of the Saturated phosphatidylcholine compounds, the surface
gas-exchanging portion of the lung. Vascular proliferation con- tension-reducing component of surfactant, 45%more
tinues, along with a relative decrease in mesenchyme, which than 80% of which is dipalmitoylphosphatidylcholine
brings the vessels closer to the airway epithelium. The saccular (DPPC)
period is marked by the development of the gas-exchanging Unsaturated phosphatidylcholine compounds, 25%
portion of the tracheobronchial tree (acinus) composed of respi- Phosphatidylglycerol, phosphatidylinositol, and phospha-
ratory bronchioles, alveolar ducts, terminal saccules, and finally, tidylethanolamine, 10%
alveoli. During this stage, the pulmonary vessels continue to Saturated phosphatidylcholine is found in lung tissue of the
proliferate with the airways and surround the developing air human fetus earlier in gestation than in other species. Surfactant
sacs. The final phase of prenatal lung development, the alveolar is released from storage pools into fetal lung fluid at a basal rate
period, is marked by the formation of thin secondary alveolar during late gestation and is stimulated by labor and the initiation
septa and the remodeling of the capillary bed. of air breathing. Four unique surfactant-associated proteins have
Throughout these periods, mesenchymal and epithelial cell been identified, and all are synthesized and secreted by type II
cross-talk directs the normal processes of lung alveolarization alveolar cells. Surfactant protein A (SP-A) functions coopera-
and vascularization.2 Several million alveoli will form before tively with the other surfactant proteins and lipids to enhance
birth, which emphasizes the importance of the last few weeks the biophysical activity of the surfactant, but its most important
of pregnancy to pulmonary adaptation. Postnatal lung growth role is in the innate host defense of the lung. SP-B and SP-C
is characterized by generation of alveoli, and over 85% of alveo- are lipophilic proteins that facilitate the adsorption and spread-
larization takes place after birth.1 ing of lipid to form the surfactant monolayer. SP-B deficiencies
The critical determinants of extrauterine survival are the are associated with neonatal pulmonary complications and
formation of the thin air-blood barrier and production of death, whereas SP-C deficiencies are associated with interstitial
surfactant. By birth, the epithelial lining of the gas-exchanging lung disease that presents at a more variable age. SP-D plays a

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470 Section IV Postpartum Care


Tubular myelin
Surfactant protein A Subphase
Surfactant protein B
Surfactant protein C
Phospholipids Endocytosis

Lamellar bodies

Golgi Rough endoplasmic

Type I cell reticulum Type I cell
Type II cell

Basement Capillary
membrane endothelial cell

Red blood

Type I cell

FIG 22-1 Metabolism of surfactant. Surfactant phospholipids are synthesized in the endoplasmic reticulum, transported through the Golgi appa-
ratus to multivesicular bodies, and finally packaged in lamellar bodies. After lamellar body exocytosis, phospholipids are organized into tubular
myelin before aligning in a monolayer at the air-fluid interface in the alveolus. Surfactant phospholipids and proteins are taken up by type II cells
and are either catabolized or reused. Surfactant proteins are synthesized in polyribosomes and are modified in endoplasmic reticulum, Golgi
apparatus, and multivesicular bodies. (Modified from Whitsett JA, Pryhuber GS, Rice WR, etal. Acute respiratory disorders. In Avery GB, Fletcher
MA, MacDonald MG [eds]: Neonatology: Pathophysiology and Management of the Newborn, 5th ed. Philadelphia: Lippincott, Williams & Wilkins;

P r

r r
r T r

Alveolar wall T

FIG 22-2 LaPlaces law. The pressure (P) within a sphere is directly proportional to surface tension (T) and is inversely proportional to the radius
of curvature (r). In the normal lung, as alveolar size decreases, surface tension (thin arrows) is reduced because of the presence of surfactant.
This serves to decrease the collapsing pressure that must be opposed and maintains equal pressures in the small and large interconnected
alveoli. (Modified from Netter FH. The Ciba Collection of Medical Illustrations. The Respiratory System, Vol 7. Summit, NJ: Ciba-Geigy; 1979.)

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Chapter 22 The Neonate 471


80 Natural

Volume (mL/kg)

Maximal lung volume


Volume stability Control

20 Opening

0 5 10 15 20 25 30 35 40
Pressure (cm H2O)
FIG 22-3 Pressure-volume relationships for the inflation and deflation of surfactant-deficient and surfactant-treated (red line) preterm rabbit lungs.
Surfactant deficiency (black line) is indicated by high opening pressure, low maximal volume at a distending pressure of 30cm of water, and
lack of deflation stability at low pressures on deflation. (Modified from Jobe AH. Lung development and maturation. In Fanaroff AA, Martin RJ
[eds]: Neonatal-Perinatal Medicine: Diseases of the Fetus and Infant, 7th ed. St. Louis: Mosby; 2002:973.)

Other phospholipids




8% SP-C
phosphatidylcholine SP-D
FIG 22-4 Composition of pulmonary surfactant. SP, surfactant protein. (Modified from Jobe AH. Lung development and maturation. In Fanaroff
AA, Martin RJ [eds]: Neonatal-Perinatal Medicine: Diseases of the Fetus and Infant, 7th ed. St Louis: Mosby; 2002:973.)

role in the regulation of surfactant lipid homeostasis, inflamma- 50% in the incidence of respiratory distress syndrome (RDS)
tory responses, and host defense mechanisms.3 is seen in infants born to mothers who received antenatal
Several hormones and growth factors contribute to the regula- corticosteroids. In a secondary analysis, a 70% reduction in
tion of pulmonary phospholipid metabolism and lung matu RDS was seen among babies born between 24 hours and 7 days
ration: glucocorticoids, thyroid hormone, thyrotropin-releasing after corticosteroid administration. In addition, evidence sug-
hormone, retinoic acid, epidermal growth factor, and others. gests reductions in mortality and RDS even with treatment
Glucocorticoids are the most important and are used clini- started less than 24 hours before delivery. Although most babies
cally to augment the synthesis of surfactant and accelerate in the trials were between 30 and 34 weeks gestation, clear
morphologic development.4 Pregnant women with anticipated reduction in RDS was evident when the population of babies
preterm delivery have received corticosteroid treatment since less than 31 weeks was examined, and given the impact on
1972. Numerous controlled trials have since been performed. neonatal morbidity and mortality, prenatal steroid use can be
Based on a meta-analysis,5 a significant reduction of about recommended in pregnancies as early as 23 weeks gestation.6

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472 Section IV Postpartum Care

Gender and race do not influence the protective effect of corti- Mechanics of the First Breath
costeroids. In the population of patients with preterm premature With its first breaths, the neonate must overcome several
rupture of the membranes (PPROM), antenatal corticosteroids forces that resist lung expansion: (1) viscosity of fetal lung
also reduce the frequency of RDS. fluid, (2) resistance provided by lung tissue itself, and (3) the
Corticosteroids also accelerate maturation of other organs forces of surface tension at the air-liquid interface.12-14 Viscos-
in the developing fetus, including the cardiovascular, gas ity of fetal lung fluid is a major factor as the neonate attempts
trointestinal (GI), and central nervous systems. Corticoste- to displace fluid present in the large airways. As the passage of
roid therapy reduces the chances of periventricular hemorrhage air moves toward small airways and alveoli, surface tension
(PVH) and intraventricular hemorrhage (IVH) in addition to becomes more important. Resistance to expansion by the lung
necrotizing enterocolitis (NEC).5 The significant reductions in tissue itself is less significant. The process begins as the infant
serious neonatal morbidity are also reflected in a reduction in passes through the birth canal; the intrathoracic pressure caused
the risk of early neonatal mortality. The short-term beneficial by vaginal squeeze is up to 200cmH2O. With delivery of the
effects of antenatal corticosteroids are enhanced by reassuring head, approximately 5 to 28mL of tracheal fluid is expressed.
reports about long-term outcome. The children of mothers Subsequent delivery of the thorax causes an elastic recoil of the
treated with antenatal corticosteroids show no lag in intellectual chest. With this recoil, a small passive inspiration (no more than
or motor development, no increase in learning disabilities or 2mL) occurs. This is accompanied by glossopharyngeal forcing
behavioral disturbances, and no effect on growth compared with of some air into the proximal airways (frog breathing) and the
untreated infants.7,8 introduction of some blood into pulmonary capillaries. This
Since the advent of antenatal steroids for the prevention of pulmonary vascular pressure may have a role in producing con-
RDS, other therapies have been introduced that decrease mortal- tinuous surfaces throughout the small airways of the lung, into
ity and morbidity. Surfactant replacement therapy to treat which surfactant can deploy.
specifically the surfactant deficiency that is the cause of RDS The initial breath is characteristically a short inspiration,
has been shown to decrease mortality and the severity of followed by a more prolonged expiration.13 The initial breath
RDS.9 The effects of antenatal corticosteroids and postnatal begins with no air volume and no transpulmonary pressure
surfactant appear to be additive in terms of decreasing the gradient. Considerable negative intrathoracic pressure during
severity of RDS and the mortality caused by it.10 inspiration is provided by diaphragmatic contraction and chest
wall expansion. An opening pressure of about 25cmH2O
First Breaths usually is necessary to overcome surface tension in the smaller
A critical step in the transition from intrauterine to extra- airways and alveoli before air begins to enter. The volume of
uterine life is the conversion of the lung from a fluid-filled this first breath varies between 30 and 67mL and correlates
organ to one capable of gas exchange. This requires aeration with intrathoracic pressure. The expiratory phase is prolonged,
of the lungs, establishment of an adequate pulmonary circula- because the infants expiration is opposed by intermittent closure
tion, ventilation of the aerated parenchyma, and diffusion of at the pharyngolaryngeal level with the generation of significant
oxygen and carbon dioxide through the alveolar-capillary mem- positive intrathoracic pressure. This pressure serves to aid both
branes. This process has its origins in utero as fetal breathing. in maintenance of a functional residual capacity (FRC) and with
fluid removal from the air sacs. The residual volume after this
Fetal Breathing first breath ranges between 4 and 30mL, averaging 16 to 20mL.
Fetal respiratory activity is initially detectable at 11 weeks. The No major systematic differences are apparent among the first
most prevalent pattern is rapid, small-amplitude movements three breaths, which demonstrate similar pressure patterns of
(60 to 90 per minute), which are present 60% to 80% of the decreasing magnitude. The FRC rapidly increases with the first
time. Less commonly, irregular low-amplitude movements inter- several breaths and then increases more gradually. By 30 minutes
spersed with slower, larger amplitude movements are seen.11 of age, most infants attain a normal FRC with uniform lung
Initially, fetal breathing was thought to depend on behavioral expansion. The presence of functional surfactant is instru-
influences. However, subsequent work has shown responses mental in the accumulation of an FRC.
to chemical stimuli and other agents. Acute hypercapnea stimu- In utero, alveoli are open and stable at a nearly neonatal lung
lates breathing. Hypoxia abolishes fetal breathing, whereas an volume because they are filled with fetal lung liquid, probably
increase in oxygen tension to levels above 200mmHg induces produced by ultrafiltration of pulmonary capillary blood as
continuous fetal breathing. Although peripheral and central well as by secretion by alveolar cells. Transepithelial chloride
chemoreflexesas well as vagal afferent reflexescan be dem- secretion appears to be a major factor responsible for the produc-
onstrated in the fetus, their role in spontaneous fetal breathing tion of luminal liquid in the fetal lung. Normal expansion and
appears to be minimal. The role of fetal breathing in the con- aeration of the neonatal lung is dependent on removal of
tinuum from fetal to neonatal life is still not completely under- fetal lung liquid. Liquid is removed by a combination of
stood. Fetal respiratory activity is probably essential to the mechanical drainage and absorption across the lung epi
development of chest wall muscles, including the diaphragm, thelium.15 This process begins before a normal term birth
and serves as a regulator of lung fluid volume and thus lung because of decreased fluid secretion and increased absorp-
growth. tion. Once labor is initiated, a reversal of liquid flow occurs
The mechanism responsible for the transition from intermit- across the lung epithelium. Active transcellular sodium absorp-
tent fetal to continuous neonatal breathing is unknown. Pros tion drives liquid from the lumen to the interstitial space, where it
taglandins may be involved in addition to other factors that is drained through the pulmonary circulation and lymphatics.16
surround birth, including blood gas changes and various sensory In normal circumstances, the process is complete within 2 hours
stimuli. Another possibility is the release from a placental of birth. Cesarean-delivered infants without benefit of labor and
inhibitory factor that is removed after cord occlusion. premature infants have delayed lung fluid clearance. In both

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Chapter 22 The Neonate 473

Superior vena cava

Ascending aorta
Ductus arteriosus

Pulmonary artery

Ductus venous

Inferior vena cava

Umbilical vein
Descending aorta

Umbilical arteries

Low High
Oxygen concentration of blood

FIG 22-5 The fetal circulation.

groups, the prenatal decrease in lung water does not occur. In blood from the lower body and the renal, mesenteric, and right
addition, in the premature neonate, fluid clearance is diminished hepatic veins streams across the tricuspid valve to the right ven-
by increased alveolar surface tension, increased left atrial pres- tricle. Almost all the return from the superior vena cava (SVC)
sure, and hypoproteinemia. and the coronary sinus passes through the tricuspid valve to the
right ventricle, with only 2% to 3% crossing the foramen ovale.
Circulatory Transition In the near-term fetus, the combined ventricular output is about
The circulation in the fetus (Fig. 22-5) has been studied in a 450mL/kg/min; two thirds from the right ventricle and one
variety of species using several techniques (see Chapter 2).17,18 third from the left ventricle. The blood in the left ventricle has
Umbilical venous blood returning from the placenta has a a PO2 of 25 to 28mmHg (saturation of 60%) and is distributed
PO2 of about 30 to 35mmHg. Because of the left-shifted to the coronary circulation, brain, head, and upper extremities
fetal hemoglobin-oxyhemoglobin disassociation curve, this cor- with the remainder (10% of combined output) passing into
responds to a saturation of 80% to 90%. About 60% of this the descending aorta. The major portion of the right ventricu-
blood perfuses the liver, mainly to the middle and left lobes, lar output (60% of combined output) is carried by the ductus
and it ultimately enters the inferior vena cava (IVC) through arteriosus to the descending aorta, with only 7% of combined
the hepatic veins. The remainder (40% in mid-gestation, 20% output going to the lungs. Thus 70% of combined output passes
at term) bypasses the hepatic circulation through the ductus through the descending aorta, with a PO2 of 20 to 23mmHg
venosus and empties directly into the IVC. Because of streaming (saturation of 55%) to supply the abdominal viscera and lower
in the IVC, the more oxygenated blood from the ductus venosus extremities. Forty-five percent of combined output goes through
and left hepatic vein, as it enters the heart, is deflected by the the umbilical arteries to the placenta. Thus blood of a higher
crista dividens through the foramen ovale to the left atrium. The PO2 supplies the critical coronary and cerebral circulations,
remainder of left atrial blood is the small amount of venous and umbilical venous blood is diverted to where oxygenation
return from the pulmonary circulation. The less oxygenated IVC is critical.

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474 Section IV Postpartum Care

The diversion of right ventricular output away from the With occlusion of the umbilical cord, the low-resistance
lungs through the ductus arteriosus is caused by the very placental circulation is interrupted, which causes an increase
high pulmonary vascular resistance (PVR) in the fetus. This in systemic pressure. This coupled with the decrease in PVR
high PVR is maintained by multiple mechanisms. With advanc- serves to reverse the shunt through the ductus arteriosus
ing gestational age, an increase in the number of small pulmo- to a predominantly left-to-right shunt. By 15 hours of age,
nary vessels occurs that increases the cross-sectional area of the shunting in either direction is physiologically insignificant.
pulmonary vasculature. This contributes to the gradual decline Although functionally closed by 4 days, the ductus arteriosus is
in PVR that begins during later gestation (Fig. 22-6). With not anatomically occluded for 1 month. The role of an increased
delivery, a variety of factors interact to decrease PVR acutely; oxygen environment and prostaglandin metabolism in ductal
these include mechanical ventilation, increased oxygen closure is well established. Ductal closure occurs in two phases:
tension, and the production of endothelium-derived relaxing constriction and anatomic occlusion. Initially, the muscular
factor or nitric oxide (NO).19 wall constricts, followed by permanent closure achieved by
With the increase in pulmonary flow, left atrial return increases endothelial destruction, subintimal proliferation, and con-
with a rise in left atrial pressure (Table 22-1). In addition, with nective tissue formation.20 The ductus venosus is functionally
the removal of the placenta, IVC return to the right atrium is occluded shortly after the umbilical circulation is interrupted.
diminished. The foramen ovale is a flap valve, and when left
atrial pressure increases over that on the right side, the opening
is functionally closed. It is still possible to demonstrate patency ABNORMALITIES OF
with insignificant right-to-left shunts in the first 12 hours of life CARDIOPULMONARY TRANSITION
in a human neonate, but in a 7- to 12-day newborn, such a Birth Asphyxia
shunt is rarely seen. Anatomic closure is not complete for a Even normal infants may experience some limitation of oxy-
longer time. genation (asphyxia) during the birth process. A variety of
circumstances can exaggerate this problem and can result in
respiratory depression in the infant, including (1) acute
TABLE 22-1 PRESSURES IN THE interruption of umbilical blood flow, as occurs during cord
PERINATAL CIRCULATION compression; (2) premature placental separation; (3) mater-
FETAL (mmHg) NEONATAL (mmHg) nal hypotension or hypoxia; (4) any of the above-mentioned
Right atrium 4 5 problems superimposed on chronic uteroplacental insuffi-
Right ventricle 65/10 40/5 ciency; and (5) failure to execute a proper resuscitation.
Pulmonary artery 65/40 40/25 Other contributing factors include anesthetics and analgesics
Left atrium 3 7
Left ventricle 60/7 70/10 used in the mother, mode and difficulty of delivery, maternal
Aorta 60/40 70/45 health, and prematurity.
The neonatal response to asphyxia follows a predictable
Modified from Nelson NM. Respiration and circulation after birth. In Smith CA, Nelson
NM (eds): The Physiology of the Newborn Infant, 4th ed. Springfield, IL: Charles C. pattern. Dawes21 investigated the responses of the newborn
Thomas; 1976:117. rhesus monkey (Fig. 22-7). After delivery, the umbilical cord was

60 Primary Onset of
50 apnea Last gasp gasping
40 6

30 4
mean pressure
20 Secondary or
(mm Hg) 2
10 terminal apnea
160 Heart rate
120 200
blood flow 80

40 150
1.8 100
1.4 50 Resuscitation
Pulmonary 1.2
1.0 Blood pressure
resistance .8 60
(mm Hg/mL/min/kg) .6
.4 40
mm Hg

Birth 20
7 5 3 1 1 3 5 7 Brain damage
0 5 10 15 20
FIG 22-6 Representative changes in pulmonary hemodynamics during
Time from onset of asphyxia (min)
transition from the late-term fetal circulation to the neonatal circula-
tion. (Modified from Rudolph AM. Fetal circulation and cardiovascular FIG 22-7 Schematic depiction of changes in rhesus monkeys during
adjustments after birth. In Rudolph CD, Rudolph AM, Hostetter MK, asphyxia and on resuscitation by positive-pressure ventilation. (Modi-
etal [eds]: Rudolphs Pediatrics, 21st ed. New York: McGraw-Hill; fied from Dawes GS. Foetal and Neonatal Physiology. Chicago: Year
2003:1749.) Book; 1968.)

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Chapter 22 The Neonate 475

tied, and the monkeys head was placed in a saline-filled plastic TABLE 22-2 EQUIPMENT FOR
bag. Within about 30 seconds, a short series of respiratory efforts NEONATAL RESUSCITATION
began. These were interrupted by a convulsion or a series of
clonic movements accompanied by an abrupt fall in heart rate.
The animal then lay inert with no muscle tone. Skin color Thermoregulation Radiant heat source with platform, mattress
covered with warm sterile blankets, servo
became progressively cyanotic and then blotchy because of vaso- control heating, temperature probe
constriction in an effort to maintain systemic blood pressure. Airway management Suction: Bulb suction, meconium aspirator,
This initial period of apnea lasted about 30 to 60 seconds. The wall vacuum suction with sterile catheters
monkey then began to gasp at a rate of three to six breaths per Ventilation: Manual infant resuscitation bag
minute. The gasping lasted for about 8 minutes, becoming connected to a pressure manometer capable
of delivering 100% oxygen, appropriate
weaker terminally. The time from onset of asphyxia to last gasp masks for term and preterm infants, oral
could be related to postnatal age and maturity at birth; the more airways, stethoscope, gloves, compressed air
immature the animal, the longer the time. Secondary or terminal source with oxygen blender, pulse oximeters,
apnea followed, and if resuscitation was not quickly initiated, and probe (optional)
Intubation: Neonatal laryngoscope with #0
death ensued. As the animal progressed through the phase of and #1 blades; extra bulbs and batteries;
gasping and then on to terminal apnea, heart rate and blood endotracheal tubes 2.5, 3.0, 3.5, and
pressure continued to fall, which indicated hypoxic depression 4.0mm OD with stylet; scissors and tape;
of myocardial function. As the heart failed, blood flow to critical and end-tidal CO2 detection device
organs decreased and resulted in organ injury. Gastric decompression Nasogastric tube, 8Fr with 20-mL syringe
Administration of Sterile gloves and sterile umbilical
The response to resuscitation is qualitatively similar in many drugs/volume catheterization tray with scalpel or scissors,
species, including humans. During the first period of apnea, antiseptic prep solution, umbilical tape,
almost any physical or chemical stimulus causes the animal to three-way stopcock, umbilical catheters (3.5
breathe. If gasping has already ceased, the first sign of recovery and 5Fr), volume expanders (normal saline),
drug box with appropriate neonatal vials and
with initiation of positive-pressure ventilation is an increase in dilutions (see Table 22-5), sterile syringes
heart rate. The blood pressure then rises, rapidly if the last gasp and needles
has only just passed, but more slowly if the duration of asphyxia Transport Warmed transport isolette with an oxygen source
has been longer. The skin then becomes pink, and gasping
ensues. Rhythmic spontaneous respiratory efforts become estab-
lished after a further interval. For each minute past the last gasp,
2 minutes of positive-pressure breathing is required before
gasping begins, and it takes 4 minutes to reach rhythmic breath- SIGN 0 1 2
ing. Later, the spinal and corneal reflexes return. Muscle tone Heart rate Absent <100 beats/min >100 beats/min
gradually improves over the course of several hours. Respiratory Apneic Weak, irregular Regular
effort gasping
Reflex No response Some response Facial grimace,
Delivery Room Management of the Newborn irritability* sneeze, cough
A number of situations during pregnancy, labor, and delivery Muscle tone Flaccid Some flexion of Good flexion
place the infant at increased risk for asphyxia: (1) maternal arms and legs
diseases, such as diabetes mellitus and hypertension, in Color Blue, pale hands Body pink Pink
and blue feet
addition to third-trimester bleeding and prolonged rupture
of membranes; (2) fetal conditions, such as prematurity, Modified from Apgar V. A proposal for a new method of evaluation of the newborn
infant. Anesth Analg. 1953;32:260.
multiple gestation, growth restriction, fetal anomalies, and *Elicited by suctioning the oropharynx and nose.
rhesus isoimmunization; and (3) conditions related to labor
and delivery, including fetal distress, meconium staining,
breech presentation, and administration of anesthetics and For the initial inflations, pressures of 30 to 40cmH2O may
analgesics. be necessary to overcome surface active forces in the lungs.
When an asphyxiated infant is expected, a resuscitation team Adequacy of ventilation is assessed by observing expansion
should be in the delivery room. The team should comprise at of the infants chest with bagging and watching for a gradual
least two people, one to manage the airway and one to monitor improvement in color, perfusion, and heart rate. Rate of
heart rate and provide whatever assistance is needed. The neces- bagging should be 40 to 60 beats/min. If the infant does not
sary equipment for an adequate resuscitation is listed in Table initially respond to bag and mask ventilation, try to reposi-
22-2. The equipment should be checked regularly and should tion the head in slight extension, reapply the mask to achieve
be in a continuous state of readiness. The steps in the resuscita- a good seal, consider suctioning the mouth and oropharynx,
tion process22 are outlined in the algorithm in Figure 22-8. and try ventilating with the mouth open. It may be necessary
Some key points of the algorithm follow. to increase the pressure used. However, if no favorable
1. Do not allow the infant to become hyperthermic under the response is seen in 30 to 40 seconds, proceed to intubation
warmer. (Fig. 22-10).
2. The best criteria to use for assessing the infants condition are 4. Failure to respond to intubation and ventilation can result
respiratory effortwhether it is apneic, gasping, or regular from mechanical causes or severe asphyxia. The mechanical
and heart rate (>100 or <100; Table 22-3). causes listed in Table 22-4 should quickly be ruled out.
3. Most neonates can be effectively resuscitated with a bag 5. It is very unusual for a neonatal resuscitation to require either
and face mask. The proper bagging devices are pictured in cardiac massage or drugs, and almost all newborns respond
Figure 22-9. In addition, a T-piece resuscitator can be used. to ventilation with supplemental oxygen. If compressions are

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476 Section IV Postpartum Care

Term gestation? Yes Routine care
Breathing or crying? Provide warmth
Good tone? Stay with mother Clear airway if necessary
No Ongoing evaluation
clear airway if necessary
Dry, stimulate No

HR <100 beats/min, No Labored breathing or

30 sec
gasping, or apnea? persistant cyanosis?

PPV Clear airway

60 sec SPO2 monitoring SPO2 monitoring
Consider CPAP
HR <100 beats/min?

Take ventilation Postresuscitation care

corrective steps

HR <60 beats/min? Target preductal SPO2

after birth
Yes 1 min 60%-65%
Consider intubation 2 min 66%-70%
Chest compressions
Coordinate with PPV 3 min 71%-75%
4 min 76%-80%
5 min 81%-85%
HR <60 beats/min?
10 min 86%-95%

Take ventilation IV epinephrine

corrective steps
If no chest
movement, intubate!


FIG 22-8 Delivery room management of the newborn. CPAP, continuous positive airway pressure; HR, heart rate; IV, intravenous; PPV, positive
pressure ventilation; SPO2, peripheral capillary oxygen saturation. (From the American Heart Association and American Academy of Pediatrics.
Neonatal Resuscitation Textbook, Elk Grove, IL; 2011.)

TABLE 22-4 MECHANICAL CAUSES OF required, they need to be coordinated with bagging at a 3:1
FAILED RESUSCITATION ratio (90 compressions to 30 breaths/min). It is even less
CATEGORY EXAMPLES common to need medications (Table 22-5). The optimal
Equipment failure Malfunctioning bag, oxygen not delivery route is through an umbilical venous line.
connected or running 6. The appropriateness of continued resuscitative efforts should
Endotracheal tube malposition Esophagus, right mainstem bronchus always be reevaluated in an infant who fails to respond to all
Occluded endotracheal tube of the previously mentioned efforts. Today, resuscitative
Insufficient inflation pressure to
expand lungs efforts are made even in apparent stillbirths, that is, infants
Space-occupying lesions in the Pneumothorax, pleural effusions, whose 1-min Apgar scores are 0 to 1. However, efforts should
thorax diaphragmatic hernia not be sustained in the face of little or no improvement
Pulmonary hypoplasia Extreme prematurity, despite an appropriate resuscitation over a reasonable period
oligohydramnios of time (i.e., 10 to 15 minutes).22

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Chapter 22 The Neonate 477

Pressure guage
100% O2

Flow-control valve

90%-100% O2 reservoir
FIG 22-9 Bags used for neonatal resuscitation. A, A flow-inflating bag with a pressure manometer and flow-control valve. B, A self-inflating bag
with an oxygen reservoir to maintain 90% to 100% oxygen. (From the American Heart Association and American Academy of Pediatrics. Neo-
natal Resuscitation Textbook, Elk Grove, IL; 2000.)

Tongue A few special circumstances merit discussion at this point.

Vallecula Infants in whom respiratory depression secondary to narcotic
Glottis administration is suspected may be given naloxone, although
evidence to support efficacy is limited. However, this should not
be done until the airway has been managed and the infant is
resuscitated in the usual fashion. In addition, naloxone should
not be given to the infant of an addicted mother because it will
Epiglottis Main bronchi precipitate withdrawal.
Lung A second special group are the preterm infants. Minimizing
heat loss improves survival, so prewarmed towels should be
available, and the environmental temperature of the delivery
suite should be raised. The infant should be placed in a plastic
covering after birth to minimize evaporative heat loss.26 In the
FIG 22-10 Anatomy of laryngoscopy for endotracheal intubation. (From
the American Heart Association and American Academy of Pediatrics. infant with an extremely low birthweight (<1000g), proceed
Neonatal Resuscitation Textbook, Elk Grove, IL 2000.) quickly to administration of continuous positive airway pressure
(CPAP) and consider early intubation for surfactant adminis
tration. Volume expanders should be infused slowly to avoid
rapid swings in blood pressure. Resuscitation in preterm infants
DRUG DOSE ROUTE HOW SUPPLIED should begin with 21% to 30% oxygen.24,27
Epinephrine 0.1 to 0.3mL/kg IV or ET 1:10,000 dilution A third special circumstance is the presence of meconium-
Sodium 1 to 2mEq/kg IV 0.5mEq/mL (4.2% stained amniotic fluid. Meconium aspiration syndrome (MAS)
bicarbonate* solution)
Normal saline, 10mL/kg IV is a form of aspiration pneumonia that occurs most often in term
whole or postterm infants who have passed meconium in utero (7%
blood to 20% of all deliveries).28 Overall, 2% to 9% of children born
Naloxone 0.1mg/kg IV, ET 1mg/mL IM, SC through meconium-stained fluid are diagnosed with MAS.28
Modified from the American Heart Association and American Academy of Pediatrics. Delivery room management of meconium in the amniotic fluid
Neonatal Resuscitation Textbook. American Heart Association and American Academy of has been historically based on the notion that aspiration takes
Pediatrics; 2006.
*For correction of metabolic acidosis only after adequate ventilation has been achieved;
place with the initiation of extrauterine respiration and that the
give slowly over several minutes. There is no evidence to support routine use. pathologic condition is related to the aspirated contents, which

Infuse slowly over 5 to 10 minutes. resulted in the practice of oropharyngeal suction on the perineum
Insufficient evidence to support safety and efficacy of subcutaneous dose.

Use after proceeding with proper airway management and other resuscitative techniques. after delivery of the head, followed by airway visualization and
ET, endotracheal; IM, intramuscular; IV, intravenous; SC, subcutaneous. suction by the resuscitator after delivery. However, both of the
foregoing assumptions are not entirely true. In utero aspiration
Resuscitation of term newborns should begin with room air has been induced in animal models and confirmed in autopsies
because of the potential harmful effects of 100% oxygen, in of human stillbirths. In addition, the combined suction approach
particular the generation of oxygen free radicals.23,24 Oxygen has not been uniformly successful in decreasing the incidence of
should be used and titrated to achieve normal saturations for MAS. These data have been confirmed by a large multicenter,
age in minutes (see Fig. 22-8).22 If resuscitation is started with prospective, randomized controlled trial (RCT) that assessed
room air and no improvement is seen, supplemental oxygen can selective intubation of apparently vigorous meconium-stained
be given. Normal healthy term infants require approximately infants.29 Compared with expectant management, intubation
10 to 15 minutes to achieve oxygen saturations above 90%.25 and tracheal suction did not result in a decreased incidence of

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478 Section IV Postpartum Care

MAS or other respiratory disorders. Finally, oropharyngeal in minimizing cerebral injury after asphyxia are still being
suction on the perineum before delivery of the shoulders does investigated.
not prevent MAS.30 The current recommended approach to If the infant survives, the major long-term concern is perma-
meconium in the amniotic fluid is as follows: nent central nervous system (CNS) damage. The challenge lies
1. The obstetrician carefully performs bulb suctioning of the in the identification of criteria that can provide information
oropharynx and nasopharynx after delivery of the baby. about the risk of future problems for a given infant. A variety
2. If the baby is active and breathing and requires no resuscita- of markers have been examined to identify birth asphyxia and
tion, the airway need not be inspected, thus avoiding the risk risk for adverse neurologic outcome. Marked fetal bradycardia
of inducing vagal bradycardia. is associated with increased risk, but use of electronic fetal moni-
3. Any infant in need of resuscitation does not need the airway toring and cesarean delivery have not altered the incidence of
inspected and suctioned before instituting positive-pressure cerebral palsy over the last several decades. Low Apgar scores
ventilation. at 1 and 5 minutes are not predictive, but infants with low
4. Suction the stomach when airway management is complete scores that persist at 15 and 20 minutes after birth have a
and vital signs are stable. 50% chance of manifesting cerebral palsy if they survive.
Cord pH is predictive of adverse outcome only if the pH
Cord Clamping is less than 7. The best predictor of outcome is the severity
Although delayed cord clamping is not currently part of the of the neonatal neurologic syndrome.38 Infants with mild
Neonatal Resuscitation Program (NRP), the practice is now encephalopathy survive and are normal on follow-up exami
recommended for both term and preterm births. Historically, nation. Moderate encephalopathy carries a 25% to 50% risk
clamping and cutting of the umbilical cord took place within of severe handicap or death, whereas the severe syndrome
seconds; however, it has been found that delaying this separation carries a greater than 75% risk of death or disability. Although
of the newborn from the placental circulation for 30 to 60 outcomes are improved with hypothermia initiated in the
seconds results in (1) a more gradual perinatal transition after first 6 hours of life, these patients remain at high risk for poor
birth, (2) transfusion of placental blood to the newborn, and neurodevelopment.35-37 Diagnostic aids that include electroen-
(3) a variety of improved outcomes, in particular, for preterm cephalograms and magnetic resonance imaging (MRI) scans
newborns.31-33 This practice is now endorsed for preterm births can also aid in predicting outcome. The circulatory response
by the American College of Obstetricians and Gynecologists to hypoxia is to redistribute blood flow to provide adequate
(ACOG), although specific patient populations and situations oxygen delivery to critical organs (e.g., brain, heart) at the
require further study.33 expense of other organs. Thus an insult severe enough to damage
the brain should be accompanied by evidence of other organ
Sequelae of Birth Asphyxia dysfunction.
The incidence of birth asphyxia is about 0.1% in term infants, The long-term neurologic sequelae of intrapartum asphyxia
with an increased incidence in infants at lower gestational are cerebral palsy with or without associated cognitive defi-
ages.34 The acute sequelae that need to be managed in the cits and epilepsy. Although cerebral palsy can be related to
neonatal period are listed in Table 22-6. With asphyxia, wide- intrapartum events, the large majority of cases are of unknown
spread organ injury is evident. Management focuses on sup- causes. Furthermore, cognitive deficits and epilepsy, unless asso-
portive care and treatment of specific abnormalities; this includes ciated with cerebral palsy, cannot be related to asphyxia or to
careful fluid management, blood pressure support, intravenous other intrapartum events. To attribute cerebral palsy to peri-
(IV) glucose, and treatment of seizures. Phenobarbital (40mg/ partum asphyxia, there must be an absence of other demon-
kg) given 1 to 6 hours after the event as neuroprotective therapy strable causes, substantial or prolonged intrapartum asphyxia
is associated with an improved neurologic outcome. Especially (fetal heart rate abnormalities, fetal acidosis), and clinical
if started within the first 6 hours of life, hypothermia (whole evidence during the first days of life of neurologic dysfunc-
body or selective head cooling) improves outcomes at 6 to 7 tion in the infant (Box 22-1).39
years of age.35-37 The roles of oxygen free-radical scavengers,
excitatory amino acid antagonists, and calcium channel blockers
Birth injuries are those sustained during labor and delivery.
Factors that predispose to birth injury include macrosomia,
TABLE 22-6 ACUTE SEQUELAE OF ASPHYXIA cephalopelvic disproportion, shoulder dystocia, prolonged
or difficult labor, precipitous delivery, abnormal presenta-
tions (including breech), and use of operative vaginal deliv-
Central nervous Cerebral edema, seizures, hemorrhage, hypoxic- ery.40 Injuries range from minor, requiring no therapy, to life
ischemic encephalopathy threatening (Table 22-7).
Cardiac Papillary muscle necrosis, transient tricuspid
insufficiency, cardiogenic shock Soft tissue injuries are most common. Most are related to
Pulmonary Aspiration syndromes (meconium, clear fluid), dystocia and to the use of operative vaginal delivery. Accidental
acquired surfactant deficiency, persistent pulmonary lacerations of the scalp, buttocks, and thighs may be inflicted
hypertension, pulmonary hemorrhage with the scalpel during cesarean delivery. Cumulatively, these
Renal Acute tubular necrosis with anuria or oliguria
Adrenal Hemorrhage with adrenal insufficiency injuries are of a minor nature and respond well to therapy. Hy-
Hepatic Enzyme elevations, liver failure perbilirubinemia, particularly in the premature infant, is the
Gastrointestinal Necrotizing enterocolitis, feeding intolerance major neonatal complication related to soft tissue bruising.
Metabolic Hypoglycemia, hypocalcemia A cephalohematoma occurs in 0.2% to 2.5% of live births.
Hematologic Coagulation disorders, thrombocytopenia Caused by rupture of blood vessels that traverse from the skull

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Chapter 22 The Neonate 479

BOX 22-1 RELATIONSHIP OF INTRAPARTUM EVENTS in 5.4% of cases but are of no major consequence except in the
AND CEREBRAL PALSY unlikely event that a leptomeningeal cyst develops. Most cepha-
lohematomas are reabsorbed in 2 weeks to 3 months. Subgaleal
Neonatal Signs Consistent With an Acute Peripartum bleeds, which are not limited by suture lines, can occur in asso-
or Intrapartum Event ciation with vacuum extraction aloneespecially with multiple
Evidence of a metabolic acidemia in fetal umbilical cord pop-offs and prolonged tractionin combination with the use
arterial blood obtained at delivery (pH <7.00 and base of forceps or with difficult forceps deliveries, and they can result
deficit 12mmol/L)
in life-threatening anemia, hypotension, or consumptive coagu-
Apgar score of less than 5 at 5 and 10min
Neuroimaging evidence of acute brain injury seen on
lopathy. Depressed skull fractures are also seen in neonates, but
brain magnetic resonance imaging or magnetic most do not require surgical elevations.
resonance spectroscopy consistent with Intracranial hemorrhages related to trauma include epidu-
hypoxia-ischemia ral, subdural, subarachnoid, and intraparenchymal bleeds.41
Presence of multisystem organ failure consistent with With improvements in obstetric care, subdural hemorrhages
hypoxic-ischemic encephalopathy fortunately are now rare. Three major varieties of subdural
bleeds have been described: (1) posterior fossa hematomas due
Type and Timing of Contributing Factors Consistent
With an Acute Peripartum or Intrapartum Event
to tentorial laceration with rupture of the straight sinus, vein of
Galen, or transverse sinus or due to occipital osteodiastasis (a
Sentinel hypoxic or ischemic event occurring
separation between the squamous and lateral portions of the
immediately before or during labor and delivery such as
a severe placental abruption
occipital bone); (2) falx laceration, with rupture of the inferior
Fetal heart rate monitor patterns consistent with an sagittal sinus; and (3) rupture of the superficial cerebral veins.
acute peripartum or intrapartum event The clinical symptoms are related to the location of bleeding.
Timing and type of brain injury patterns based on With tentorial laceration, bleeding is infratentorial, leading to
imaging studies consistent with an etiology of an acute brainstem signs and a rapid progression to death. Falx tears cause
peripartum or intrapartum event bilateral cerebral signs (e.g., seizures and focal weakness) until
No evidence of other proximal or distal factors that blood extends infratentorially to the brainstem. Subdural hem-
could be contributing factors orrhage over the cerebral convexities can cause several clinical
Developmental Outcome Is Spastic Quadriplegia or states that range from an asymptomatic newborn to one with
Dyskinetic Cerebral Palsy seizures and focal neurologic findings. Infants with lacerations
of the tentorium and falx have a poor outlook. In contrast, the
Modified from American College of Obstetricians and Gynecologists prognosis for rupture of the superficial cerebral veins is much
(ACOG), American Academy of Pediatrics (AAP). Neonatal Encephalopa- better, and the majority of survivors are normal. Primary
thy and Neurologic Outcome. Washington DC: ACOG; 2014.
subarachnoid hemorrhage is the most common variety of
neonatal intracranial hemorrhage.41 Clinically, these infants
are often asymptomatic, although they may present with a char-
TABLE 22-7 BIRTH INJURIES acteristic seizure pattern that begins on day 2 of life, and the
infants are well between convulsions. In general, the prognosis
for subarachnoid bleeds is good.
Soft tissue injuries* Lacerations, abrasions, fat necrosis Trauma to peripheral nerves produces another major group
Extracranial bleeding Cephalohematoma,* subgaleal bleed
Intracranial hemorrhage Subarachnoid, subdural, epidural, cerebral, of birth injuries. Brachial plexus injuries are caused by stretch-
cerebellar ing of the cervical roots during delivery, usually when shoul-
Nerve injuries Facial nerve,* cervical nerve roots (brachial der dystocia is present. Upper arm palsy (Erb-Duchenne
plexus palsies,* phrenic nerve, Horner paralysis), the most common brachial plexus injury, is caused
syndrome), recurrent laryngeal nerve (vocal
cord paralysis)
by injury to the fifth and sixth cervical nerves; lower arm
Fractures Clavicle,* facial bones, humerus, femur, skull, paralysis (Klumpke paralysis) results from damage to the
nasal bones eighth cervical and first thoracic nerves. Damage to all four
Dislocations Extremities, nasal septum nerve roots produces paralysis of the entire arm. Outcome for
Eye injuries Subconjunctival* and retinal hemorrhages, these injuries is variable, and some infants are left with signifi-
orbital fracture, corneal laceration, breaks
in Descemet membrane with corneal cant residual damage. Horner syndrome as a result of damage
opacification to sympathetic outflow through nerve root T1 may accompany
Torticollis Klumpke paralysis, and approximately 5% of patients with Erb
Spinal cord injuries paralysis have an associated phrenic nerve paresis. Facial palsy is
Visceral rupture Liver, spleen
Scalp laceration* Fetal scalp electrode, scalpel
another fairly common injury caused either by pressure from the
Scalp abscess Fetal scalp electrode sacral promontory or fetal shoulder as the infant passes through
the birth canal or by operative vaginal delivery. Most of these
*More common occurrences.

Secondary to hemorrhage into the sternocleidomastoid muscle. palsies resolve, although in some infants, paralysis is persistent.
The majority of bone fractures that result from birth trauma
involve the clavicle and result from shoulder dystocia or breech
to the periosteum, the bleeding is subperiosteal and is therefore extractions that require vigorous manipulations. Clinically,
limited by suture lines; the most common site of bleeding is over many of these fractures are asymptomatic, and when present,
the parietal bones. Associations include prolonged or difficult symptoms are mild. Prognosis for both clavicular and limb
labor and mechanical trauma from operative vaginal delivery. fractures is uniformly good. The most commonly fractured long
Linear skull fractures beneath the hematoma have been reported bone is the humerus.

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480 Section IV Postpartum Care

Spinal cord injuries are a relatively infrequent but often TABLE 22-8 NEONATAL RESPONSE TO
severe form of birth injury. Accurate incidence is difficult to THERMAL STRESS
assess, because symptoms mimic other neonatal diseases and
autopsies often do not include a careful examination of the
spine. Depressed tone, hyporeflexia, and respiratory failure are Cold Vasoconstriction ++ ++
Exposed surface area
clues to this diagnosis. Excessive longitudinal traction and head (posture change)
rotation during forceps delivery predispose to spinal injury, and Oxygen consumption ++ +
hyperextension of the head in a footling breech is particularly Motor activity, shivering +
dangerous. Outcomes include death or stillbirth caused by high Heat Vasodilation ++ ++
cervical or brainstem lesions, long-term survival of infants with Sweating +
paralysis from birth, and minimal neurologic symptoms or ++, Maximum response; +, intermediate; , may have a role; , no response.


Physiology Delivery Room
The range of environmental temperatures over which the In utero, fetal thermoregulation is the responsibility of the pla-
neonate can survive is narrower than that of an adult as a centa and is dependent on maternal core temperature; fetal
result of the infants inability to dissipate heat effectively in temperature is 0.5 C higher than maternal temperature. At
warm environments and, more critically, to maintain tem- birth, the infants core temperature drops rapidly from 37.8 C
perature in response to cold. This range narrows with decreas- because of evaporation from its wet body and radiant and con-
ing gestational age. vective losses to the cold air and walls of the room. Even with
Although some increases in activity and shivering have been an increase in oxygen consumption to the maximum capability
observed, nonshivering thermogenesis is the most important of the newborn (15mL/kg/min), the infant can produce only
means of increased heat production in the cold-stressed 0.075cal/kg/min and will rapidly lose heat. Measures taken to
newborn.42 It can be defined as an increase in total heat pro- reduce heat loss after birth depend on the clinical situation.
duction without detectable (visible or electrical) muscle For the well term infant, drying the skin and wrapping the
activity. The site of this increased heat production is brown baby with warm blankets is sufficient. When it is necessary
fat located between the scapulae; around the muscles and to leave an infant exposed for close observation or resuscita-
blood vessels of the neck, axillae, and mediastinum; between tion, the infant should be dried and placed under a radiant
the esophagus and trachea; and around the kidneys and heat source. Room temperature can be elevated as an added
adrenal glands. Brown fat cells contain more mitochondria precaution for the low-birthweight infant.
and fat vacuoles and have a richer blood and sympathetic
nerve supply compared with white fat cells. Nursery
Heat loss to the environment is dependent on both an Babies are cared for in the newborn nursery wrapped in blankets
internal temperature gradient, from within the body to the in bassinets (cot-nursed), in isolettes, or under a radiant heat
surface, and an external temperature gradient, from the source. Healthy full-term infants (>2.5kg) need only be clothed
surface to the environment. The infant can change the internal and placed in a bassinet under a blanket. Infants weighing 2 to
gradient by altering vasomotor tone and, to a lesser extent, by 2.5kg who are either slightly premature or growth restricted
postural changes that decrease the amount of exposed surface should be allowed 12 to 24 hours to stabilize in an isolette and
area. The external gradient is dependent on purely physical vari- should then be advanced to a bassinet. Lower-birthweight babies
ables. Heat transfer from the surface to the environment (<2kg) will require care in either isolettes or under radiant heat
involves four routes: radiation, convection, conduction, and sources. Adequate thermal protection of the low-birthweight
evaporation. Radiant heat loss, heat transfer from a warmer to (LBW) infant is essential. This is especially important for the
a cooler object that is not in contact, depends on the tempera- very-low-birthweight (VLBW) infant (<1.5kg), who often
ture gradient between the objects. Heat loss by convection to the does not behave like a mature homeotherm. These neonates
surrounding gaseous environment depends on air speed and can react to a small change in environmental temperature with
temperature. Conduction, heat loss to a contacting cooler object, a change in body temperature rather than a change in oxygen
is minimal in most circumstances. Heat loss by evaporation is consumption. In addition, warmer environments hasten growth
cooling secondary to water loss at the rate of 0.6cal/g water of the premature infant.
evaporated and is affected by relative humidity, air speed, The isolette, which heats by convection, is the most com-
exposed surface area, and skin permeability. In infants in exces- monly used heating device for the LBW nude infant. The major
sively warm environments, such as those under overhead radiant source of heat loss while in a neutral thermal environment is
heat sources, or in very immature infants with thin, permeable radiant to the walls of the isolette. The magnitude of this loss is
skin, evaporative losses increase considerably. Table 22-8 sum- predictable if room temperature is known, and losses can be
marizes the neonates efforts to maintain a stable core tempera- minimized using double-walled isolettes in which the inner wall
ture in the face of cold or heat stress. It is advantageous to temperature is very close to the air temperature within the iso-
maintain an infant in a neutral thermal environment (Fig. lette. Once clinical status has been stabilized, the infant can be
22-11). The neutral thermal environment for a given infant dressed, which will afford increased thermal stability.
depends on size, gestational age, and postnatal age.43 In general, Radiant warmers can also be used to ensure thermal stability
maintaining the abdominal skin temperature at 36.5 C of both LBW and full-sized infants. Radiant warmers are
minimizes energy expenditure. used most effectively for short-term warming during initial

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Chapter 22 The Neonate 481


Inevitable Thermoregulatory Inevitable

body cooling range body heating

Death from heat

Death from cold
oxygen consumption

Summit metabolism
Heart production or

Range of
thermal neutrality

Decreasing Chemical Increasing

body temperature regulation body

Environmental temperature
FIG 22-11 Effect of environmental temperature on oxygen consumption and body temperature. (Modified from Klaus MH, Fanaroff AA. The
physical environment. In Klaus MH, Fanaroff AA [eds]: Care of the High-Risk Neonate, 5th ed. Philadelphia: WB Saunders; 2001:130.)

resuscitation and stabilization and for performing procedures. efficiently, such infants face a number of problems: (1) relatively
They provide easy access to the infant while ensuring thermal high caloric demand; (2) small stomach capacity; (3) incompe-
stability. The main heat losses are convection, which can be tent esophageal-cardiac sphincter that leads to gastroesophageal
significant because of variable air speed in a room, and evapora- reflux; (4) poor gag reflex, which creates a tendency for aspira-
tion. Evaporative heat loss that results in significant fluid tion; (5) decreased digestive capability, especially for fat; and (6)
losses is a major concern for the VLBW premature infant slow gastric emptying and intestinal motility. These infants can
cared for under a radiant warmer. Placing a plastic shield over initially be supported adequately with parenteral nutrition, fol-
the infant or covering the skin with a semipermeable membrane lowed by institution of nasogastric tube feedings when their
can minimize these fluid losses. cardiopulmonary status is stable.
The most economical means of thermal support for the Although a wide range of infant formulas satisfy the nutri-
LBW infant is skin-to-skin contact with a parent.44 tional needs of most neonates, breast milk remains the
standard on which formulas are based (see Chapter 24). The
distribution of calories in human milk is 7% protein, 55% fat,
NEONATAL NUTRITION and 38% carbohydrate. The whey/casein ratio is 70:30, which
AND GASTROENTEROLOGY enhances ease of protein digestion and gastric emptying, whereas
At birth, the newborn infant must assume various functions fat digestion is augmented by the presence of a breast milk lipase.
performed by the placenta during fetal life. Cardiopulmonary Despite the low levels of several vitamins and minerals, bioavail-
transition and thermoregulation have already been discussed. ability is high. In addition to the nutritional features, breast
The final critical task for the newborn is the assimilation of calo- milks immunochemical and cellular components provide
ries, water, and electrolytes. protection against infection.45
The growth demands of the LBW infant exceed what can
Infant Feeding be provided by human milk in terms of protein, calcium, phos-
For the well term or slightly preterm infant, institution of oral phorus, sodium, zinc, copper, and possibly other nutrients.
feedings within the first 2 to 4 hours of life is reasonable practice. These shortcomings can be addressed through the addition of
For infants who are small for gestational age (SGA) or large for human milk fortifiers to mothers preterm breast milk.46 Advan-
gestational age (LGA), earlier feedings may be indicated to avoid tages of breast milk for the premature infant include its antiin-
hypoglycemia. Premature infants (<34 weeks gestation) who are fective properties, possible protection against NEC, and its role
unable to nipple feed present a more complex set of circum- in enhancing neurodevelopmental outcome.47 The importance
stances. In addition to an inability to suck and swallow of breast milk for the preterm infant has been emphasized with

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482 Section IV Postpartum Care


Milk supply You may be able to express a few Milk should come in between days 2 and 4. Milk should be Breasts should
drops of milk. in. Breasts feel softer
may be firm after
and may leak nursing.
Babys Baby is usually Wake up your Baby should be Look for early feeding cues such as rooting, lip smacking, Baby should
activity wide awake in baby. Babies more and hands to the face. appear
the first hour may not cooperative satisfied
of life and wake up on and less after
should be put their own to sleepy. feedings.
to the breast feed.
within 30
Feeding Baby may go into Use a chart to write down each feeding time. Baby may go one
routine a deep sleep 2 Feed your baby every 1 to 4hr or as often as the baby wants to nurse but at longer interval
to 4 hours least 8 to 12 times a day. (up to 5hr
after birth. between feeds)
in a 24-hour
Breastfeeding Baby will wake As long as the Try to nurse on Consider hand Nurse a minimum of 10 to Mothers
up and be mother is both sides at expressing or 30min per side every feeding nipple
alert and comfortable, each feeding, pumping a few for the first few weeks of life. tenderness
responsive for nurse at aiming at 10 drops of milk to Once milk supply is well is
several more both breasts min per side. soften the nipple established, allow baby to improving
hours after as long as Expect some if the breast is too finish the first breast before or is gone.
initial sleep. the baby is nipple firm for the baby offering the other one.
actively tenderness. to latch on.
Babys urine Baby must have Baby must have You should see an Babys urine Baby should have
output a minimum at least one increase in wet should six to eight
of one wet wet diaper diapers (four to be light wet diapers
diaper in the every 8 to six) in 24hr. yellow. per day of
first 24hr. 11hr. colorless or
light yellow
Babys stools Baby may have Baby may have a Babys stools should be in transition Baby should have The number of
a very dark second very from black green to yellow. three to four stools may
(meconium) dark yellow, seedy decrease
stool. (meconium) stools a day. gradually
stool. after 4 to 6
Courtesy Beth Gabrielski, RN, The Childrens Hospital, Denver, Colorado.

the use of donor banked human milk as a bridge until the Neonatal Hypoglycemia
mother is producing an adequate amount of milk for her Glucose is a major fetal fuel transported by facilitated diffusion
infant.48,49 across the placenta. After birth, before an appropriate supply of
Few contraindications to breastfeeding exist. Infants with exogenous calories is provided, the newborn must maintain
galactosemia should not ingest lactose-containing milk. Infants blood glucose through endogenous sources. Hepatic glycogen
with other inborn errors of metabolism such as phenylketonuria stores are almost entirely depleted within the first 12 hours after
may ingest some human milk with close monitoring of the birth in the healthy term neonate and even more rapidly in the
amount. The presence of environmental pollutants has been preterm or stressed infant if no other glucose source is available.
documented in breast milk, but to date no serious side effects Fat and protein stores are then used for energy, and glucose levels
have been reported. Most drugs do not contraindicate breast- are maintained by hepatic gluconeogenesis.
feeding, but a few exceptions do exist (see Chapter 8). Trans In the healthy unstressed neonate, glucose falls over the
mission of some viral infections via breast milk is a concern as first 1 to 2 hours after birth, stabilizes at a minimum of about
well. Mothers who are human immunodeficiency virus (HIV) 40mg/dL, and then rises to 50 to 80mg/dL by 3 hours
positive should not breastfeed if safe and effective alternatives of life.50 Low glucose concentrations can be defined as less
to breast milk are available. The nursery staff must be aware than 45mg/dL. Infants at risk for low blood glucose concen-
of problems associated with breastfeeding, and lactation con trations and in whom glucose should be monitored include
sultants should be available to deal with poor infant latch-on, preterm infants, SGA infants, hyperinsulinemic infants
sore nipples, poor milk supply, and excessive hyperbiliru (infant of a diabetic mother [IDM]), LGA infants, and in-
binemia. The obstetrician and pediatrician should serve as a fants with perinatal stress or asphyxia. As in term babies,
source of knowledge and, most importantly, support. Table blood glucose drops after birth in preterm babies, but they are
22-9 illustrates what a mother can expect as she breastfeeds less able to mount a counterregulatory response. In addition, the
her infant. presence of respiratory distress, hypothermia, and other factors

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Chapter 22 The Neonate 483


NEC is the most common acquired GI emergency in the
I. Transient neonatal hypoglycemia neonatal intensive care unit (NICU). This disorder predomi-
A. Preterm and IUGR infants nantly affects premature infants, with higher incidences present
B. Transient hyperinsulinism (IDM)
C. Perinatal stress (hypoxia, RDS)
with decreasing gestational age, although it is seen in term
II. Persistent neonatal hypoglycemia infants with polycythemia, congenital heart disease, and birth
A. Hyperinsulinism asphyxia. The pathogenesis is multifactorial, with intestinal isch-
1. Potassium-ATP channel emia, infection, provision of enteral feedings, and gut maturity
2. Glucokinase hyperinsulinism playing roles to varying degrees in individual patients.54 Recent
3. Glutamate dehydrogenase hyperinsulinism research has suggested a critical role for the neonatal intestinal
4. Beckwith-Wiedemann syndrome microbiome in the pathogenesis of this complication of prema-
B. Counterregulatory hormone deficiency turity. Use of probiotics appears to be a potentially promising
(hypopituitarism) preventative therapy, but data are still insufficient for a general
C. Inborn errors of metabolism recommendation for their use.55 Presumably related to changes
1. Glycogenolysis disorders
2. Gluconeogenesis disorders
in intestinal circulation, tocolysis with indomethacin has
3. Fatty acid oxidation disorders been associated with an increased incidence of NEC, whereas
antenatal betamethasone may decrease the incidence.
ATP, adenosine triphosphate; IDM, infant of a diabetic mother; IUGR, Clinically, the spectrum of disease varies from a mild GI
intrauterine growth restriction; RDS, respiratory distress syndrome. disturbance to a rapid fulminant course characterized by
intestinal gangrene, perforation, sepsis, and shock. The hallmark
symptoms are abdominal distension, ileus, delayed gastric emp-
can increase glucose demand and exacerbate hypoglycemia. SGA tying, and bloody stools. The radiographic findings are bowel
infants are at risk for hypoglycemia resulting from rapidly wall edema, pneumatosis intestinalis, biliary free air, and free
utilized glycogen stores and impaired gluconeogenesis and peritoneal air. Associated symptoms include apnea, bradycardia,
ketogenesis. Onset of hypoglycemia in SGA and preterm hypotension, and temperature instability. Surgical resection of
infants usually occurs at 2 to 6 hours of life. Hyperinsulinemia bowel may be necessary with resulting short bowel syndrome in
occurs in IDMs and in babies with other rare conditions, includ- survivors. In addition, severe NEC has a negative impact on
ing Beckwith-Weidemann syndrome and congenital hyperinsu- neurodevelopmental outcome.56
linism. Onset of hypoglycemia in these infants can be in the
first 30 to 60 minutes after birth. In the case of perinatal as- Neonatal Jaundice
phyxia, hypoglycemia is the result of excessive glucose demand The most common problem encountered in a term nursery
and occasionally transient hyperinsulinism.51,52 Infants with re- population is jaundice. Neonatal hyperbilirubinemia occurs
current hypoglycemia over 3 to 4 days should be evaluated for when the normal pathways of bilirubin metabolism and excre-
endocrine disorders (hyperinsulinism, decreased counterregula- tion are altered. Figure 22-12 demonstrates the metabolism of
tory hormonescortisol, growth hormone, and glucagon) and bilirubin. The normal destruction of circulating red cells accounts
inborn errors of metabolism (Box 22-2). for about 75% of the newborns daily bilirubin production. The
Symptoms of hypoglycemia include jitteriness, seizures, cya- remaining sources include ineffective erythropoiesis and tissue
nosis, respiratory distress, apathy, hypotonia, and eye rolling.50 heme proteins. Heme is converted to bilirubin in the reticulo-
However, many infants, particularly premature infants, are endothelial system with carbon monoxide (CO) produced as a
asymptomatic. Because of the risk of subsequent brain injury, by-product. Unconjugated bilirubin is lipid soluble and is trans-
hypoglycemia should be aggressively treated. However, the ported in the plasma reversibly bound to albumin. Bilirubin
single best treatment is prevention by identifying infants at enters the liver cells by dissociation from albumin in the hepatic
risk, including premature, SGA, IDM, LGA, and stressed sinusoids. Once in the hepatocyte, bilirubin is conjugated with
infants. These newborns should have blood glucose screened glucuronic acid in a reaction catalyzed by uridine diphospho-
with a bedside glucose meter. All values less than or equal to glucuronosyl transferase (UDPGT). The water-soluble conju-
45mg/dL should be confirmed with a laboratory measurement. gated bilirubin is excreted rapidly into the bile canaliculi and
Treatment is initiated by early institution of feedings or an IV into the small intestine. The enzyme -glucuronidase is present
glucose bolus (2mL/kg of D10W solution) followed by a glucose in the small bowel and hydrolyzes some of the conjugated
infusion at a rate of 6mg/kg/min.53 bilirubin. This unconjugated bilirubin can be reabsorbed into
the circulation, adding to the total unconjugated bilirubin
Congenital Gastrointestinal load (enterohepatic circulation). Major predisposing factors of
Surgical Conditions neonatal jaundice are (1) increased bilirubin load because
Several congenital surgical conditions of the GI tract inter- of increased red cell volume with decreased cell survival,
fere with a normal transition to neonatal life. Many of these increased ineffective erythropoiesis, and the enterohepatic
conditions can be diagnosed with antenatal ultrasound to circulation; and (2) decreased hepatic uptake, conjugation,
allow transfer of the mother to a perinatal center for delivery. and excretion of bilirubin. These factors result in the presence
Examples include tracheoesophageal fistula and esophageal atre of clinically apparent jaundice in approximately two thirds of
sia, duodenal atresia, abdominal wall defects (gastroschisis and newborns during the first week of life, and in most it is consid-
omphalocele), and congenital diaphragmatic hernia (CDH). ered physiologic.57 Infants whose bilirubin levels are above
CDH infants are ideally delivered in centers with access the 95th percentile for age in hours and infants in high-risk
to advanced therapies such as extracorporeal membrane groups to develop hyperbilirubinemia require close follow-up
oxygenation (ECMO). (Fig. 22-13 and Box 22-3).58,59

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484 Section IV Postpartum Care

RE system Early peak Pathologic jaundice during the early neonatal period is
Catabolism indirect hyperbilirubinemia, usually caused by overproduc-
Ineffective erythropoiesis
of effete RBC Bone marrow
tion of bilirubin. The leading cause in this group of patients
Tissue heme is hemolytic disease, of which fetomaternal blood group
Heme proteins Liver incompatibilitiesABO, Rh, and other minor antibodiesare
the most common (see Chapter 34). Other causes of hemolysis
Heme 75% 25% include genetic disorders: specifically, hereditary spherocytosis
oxygenase Heme Heme and nonspherocytic hemolytic anemias, such as glucose-6-
RE phosphate dehydrogenase (G6PD) deficiency. Other etiologies
system of bilirubin overproduction include extravasated blood (bruis-
Biliverdin ing, hemorrhage), polycythemia, and exaggerated enterohepatic
reductase circulation of bilirubin because of mechanical GI obstruction or
reduced peristalsis from inadequate oral intake. Disease states
that involve decreased bilirubin clearance must be considered in
and patients in whom no cause of overproduction can be identified.
serum albumin Causes of indirect hyperbilirubinemia in this category include
familial deficiency of UDPGT (Crigler-Najjar syndrome),
Gilbert syndrome, breast milk jaundice, and hypothyroidism.
Smooth Ligandin Mixed and direct hyperbilirubinemia are rare during the first
endoplasmic Glucuronosyl week of life.
reticulum transferase A strong association exists between breastfeeding and neo-
natal hyperbilirubinemia. The syndrome of breast milk jaun-
dice is characterized by full-term infants who have jaundice that
Enterohepatic persists into the second and third weeks of life with maximal
bilirubin bilirubin levels of 10 to 30mg/dL. If breastfeeding is continued,
Bilirubin glucuronide
glucuronidase the levels persist for 4 to 10 days and then decline to normal by
3 to 12 weeks. Interruption of breastfeeding is associated with
a prompt decline in 48 hours. In addition to this syndrome,
breastfed infants as a whole have higher bilirubin levels
over the first 3 to 5 days of life than their formula-fed coun-
terparts (Fig. 22-14). Rather than interrupting breastfeed-
ing, this early jaundice is responsive to increased frequency
of breastfeeding. Suggested mechanisms for breastfeeding-
associated jaundice include decreased early caloric intake, inhibi-
tors of bilirubin conjugation in breast milk, and increased
intestinal reabsorption of bilirubin. In some patients, overlap is
Fecal bilirubin
urobilinogen (minimal) considerable in these described syndromes.
The overriding concern with neonatal hyperbilirubine
FIG 22-12 Neonatal bile pigment metabolism. RBC, red blood cell; RE,
reticuloendothelial. (Modified from Maisels MJ. Jaundice. In Avery
mia is the development of bilirubin toxicity that causes the
GB, Fletcher MA, MacDonald MG, eds. Neonatology: Pathophysiol- pathologic entity of kernicterus, the staining of certain areas
ogy and Management of the Newborn, 5th ed. Philadelphia: Lippin- of the brainbasal ganglia, hippocampus, geniculate bodies,
cott, Williams & Wilkins; 1999:765.) various brainstem nuclei, and cerebellumby bilirubin. Neuro-
nal necrosis is the dominant histopathologic feature at 7 to 10
days of life. The early symptoms of bilirubin encephalopathy
consist of lethargy, hypotonia, and poor feeding that progresses
to a high-pitched cry, hypertonicity, and opisthotonos. Survivors
usually suffer sequelae that include athetoid cerebral palsy, high-
BOX 22-3 RISK FACTORS FOR SIGNIFICANT frequency hearing loss, paralysis of upward gaze, and dental
HYPERBILIRUBINEMIA dysplasia.60,61 The risk of bilirubin encephalopathy is not
Jaundice observed at <24hr well defined except in those infants with Rh isoimmuniza-
Blood group incompatibility with positive direct Coombs tion in whom a level of 20mg/dL has been associated with
test an increased risk of kernicterus. This observation has been
Other hemolytic disease (G6PD deficiency) extended to the management of other neonates with hemolytic
Gestational age <35 to 36wk disease, although no definitive data exist regarding these infants.
Previous sibling needing phototherapy The risk is probably small for term infants without hemolytic
Cephalohematoma, subgaleal blood collection, bruising disease even at levels higher than 20mg/dL. Recent descrip-
Exclusive breastfeeding, especially if it is not going well
East Asian race
tions of bilirubin encephalopathy in breastfed infants, and
in late preterm infants in particular, with dehydration and
Modified from American Academy of Pediatrics Subcommittee on Hyper- hyperbilirubinemia in whom an adequate supply of breast
bilirubinemia. Management of hyperbilirubinemia in the newborn infant milk has not been established mandates close follow-up of
35 or more weeks gestation. Pediatrics. 2004;114:297. all breastfeeding mothers.60 The true risk for nonhemolytic
G6PD, glucose-6-phosphate dehydrogenase.
hyperbilirubinemia to produce brain damage in the preterm

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Chapter 22 The Neonate 485


High-risk zone
95th percentile
Total serum bilirubin (mg/dL)

75th percen
15 k zon
di ate le
rme ercenti
te e 45th p
h in k zon
Hig -ris
10 inte

Low-risk zone

0 12 24 36 48 60 72 84 96 108 120 132 144 156 168

Age (hr)
FIG 22-13 Risk of developing significant hyperbilirubinemia in term and near-term infants based on hour-specific bilirubin determinations. (From
Bhutani VK, Johnson L, Sivieri EM. Predictive ability of a predischarge hour-specific serum bilirubin for subsequent significant hyperbilirubinemia
in healthy term and near-term newborns. Pediatrics. 1999;103:6.)



Breastfed infants
No. of infants

80 Bottle-fed infants




0 2 4 6 8 10 12 14 16 18
Maximum total serum bilirubin concentration (mg/dL)
FIG 22-14 Distribution of maximum serum bilirubin concentrations in white infants who weigh more than 2500g. (Modified from Maisels MJ,
Gifford KL. Normal serum bilirubin levels in the newborn and the effect of breast-feeding. Pediatrics. 1986;78:837.)

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486 Section IV Postpartum Care

infant in the current era of liberal use of phototherapy that TABLE 22-10 ORGAN-RELATED SYMPTOMS
prevents marked elevation of severe bilirubin in these infants is OF HYPERVISCOSITY
unknown. However, most currently available data would suggest
this risk is low.
Central nervous system Irritability, jitteriness, seizures, lethargy
Cardiopulmonary Respiratory distress caused by congestive heart
NEONATAL HEMATOLOGY failure or persistent pulmonary hypertension
Gastrointestinal Vomiting, heme-positive stools, abdominal
Anemia distension, necrotizing enterocolitis
Early hematopoietic cells originate in the yolk sac. By 8 weeks Renal Decreased urine output, renal vein thrombosis
gestation, erythropoiesis is taking place in the liver, which Metabolic Hypoglycemia
Hematologic Hyperbilirubinemia, thrombocytopenia
remains the primary site of erythroid production through the
early fetal period. By 6 months of gestation, the bone marrow
becomes the principal site of red cell development. Normal
hemoglobin levels at term range from 13.7 to 20.1g/dL. In TABLE 22-11 DIFFERENTIAL DIAGNOSIS OF
the very preterm infant, values as low as 12g/dL are accept- NEONATAL THROMBOCYTOPENIA
able. Anemia at birth or appearing in the first few weeks of life DIAGNOSIS COMMENTS
is the result of blood loss, hemolysis, or underproduction of Immune Passively acquired antibody (e.g., idiopathic
erythrocytes.62 Blood loss that results in anemia can occur pre- thrombocytopenic purpura, systemic
natally, at the time of delivery, or postnatally. In utero blood loss lupus erythematosus, drug induced)
can be the result of fetomaternal bleeding, twin-to-twin transfu- Alloimmune sensitization to HPA-1a antigen
sion, or blood loss resulting from trauma (maternal trauma, Infectious Bacterial and congenital viral infections (e.g.,
cytomegalovirus, rubella)
amniocentesis, external cephalic version). The diagnosis of feto- Syndromes Absent radii; Fanconi anemia
maternal hemorrhage significant enough to cause anemia can Giant hemangioma
be made using flow cytometry or the Kleihauer-Betke tech- Thrombosis
nique of acid elution to identify fetal cells in the maternal High-risk infant with Disseminated intravascular coagulation
RDS, pulmonary Isolated thrombocytopenia
circulation. Blood loss at delivery can be caused by umbilical hypertension, and
cord rupture, incision of the placenta during cesarean delivery, so forth
placenta previa, or abruptio placentae. Internal hemorrhage can
HPA-1a, human platelet antigen 1a; RDS, respiratory distress syndrome.
occur in the newborn, often related to a difficult delivery. Sites
include intracranial, cephalohematomas, subgaleal, retroperito-
neal, liver capsule, and ruptured spleen. When blood loss has diagnosis is presented in Table 22-11. The immune thrombo-
been chronic (e.g., fetomaternal), infants will be pale at birth cytopenias have implications for perinatal care. In idiopathic
but well compensated and without signs of volume loss. The thrombocytopenic purpura (ITP), maternal antiplatelet anti-
initial hematocrit will be low. Acute bleeding will present with bodies that cross the placenta lead to destruction of fetal platelets
signs of hypovolemia (tachycardia, poor perfusion, hypoten- (see Chapter 44). However, only 10% to 15% of infants born
sion). The initial hematocrit can be normal or decreased, but to mothers with ITP have platelet counts less than 100,000 per
after several hours of equilibration, it will be decreased. Anemia microliter, and even in infants with severe thrombocytopenia,
caused by hemolysis from blood group incompatibilities is serious bleeding is rare. Alloimmune thrombocytopenia occurs
common in the newborn period. Less common causes of hemo- when an antigen is present on fetal platelets but is not present
lysis include erythrocyte membrane abnormalities, enzyme on maternal platelets. On exposure to fetal platelets, the mother
deficiencies, and disorders of hemoglobin synthesis. Impaired develops antiplatelet antibodies that cross the placenta and cause
erythrocyte production is a rare cause of neonatal anemia. destruction of fetal platelets. In the largest series of cases of
suspected alloimmune thrombocytopenia, the majority were
Polycythemia caused by human platelet antigen 1a (HPA-1a) alloantibodies.
Elevated hematocrits occur in 1.5% to 4% of live births. Because the maternal platelet count is normal, the diagnosis is
Although 50% of polycythemic infants are average for gesta- suspected on the basis of a history of a previously affected preg-
tional age (AGA), the proportion of polycythemic infants is nancy. Intracranial hemorrhage is common with this condition
greater in the SGA and LGA populations. Causes of polycy- (10% to 20%) and can occur in the antenatal or intrapartum
themia include twin-to-twin transfusion, maternal-to-fetal periods.64 Antenatal treatment is guided by the severity of
transfusion, intrapartum transfusion from the placenta associ- thrombocytopenia and presence of intracranial hemorrhage in
ated with fetal distress, chronic intrauterine hypoxia (SGA the previously affected fetus. Treatment options include IV
infants, LGA infants of diabetic mothers), delayed cord clamp- immunoglobulin infusions and corticosteroids given to the
ing, and chromosomal abnormalities. The consequence of poly- mother.64
cythemia is hyperviscosity, which results in impaired perfusion
of capillary beds. Therefore clinical symptoms can be related to Vitamin KDeficiency Bleeding
any organ system (Table 22-10). Reduction of venous hemato- of the Newborn
crit to less than 60% may improve acute symptoms, but it has Vitamin K1 oxide (1mg) should be given intramuscularly to
not been shown to improve long-term neurologic outcome.63 all newborns to prevent hemorrhagic disease caused by a
deficiency in vitamin Kdependent clotting factors (II, VII,
Thrombocytopenia IX, X).65 Babies born to mothers who are on anticonvulsant
Neonatal thrombocytopenia can be isolated or it can occur medication are particularly at risk of having vitamin K defi-
associated with deficiency of clotting factors. A differential ciency. Bleeding occurs in 0.25% to 1.4% of newborns who do

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Chapter 22 The Neonate 487

Vaginal and Rectal GBS Cultures at 35-37 Weeks Gestation

for ALL Pregnant Womena


Previous infant with invasive GBS disease Previous pregnancy with a positive GBS screening
GBS bacteriuria during current pregnancy culture (unless a culture also was positive during the
Positive GBS screening culture during current pregnancy current pregnancy or previous infant with invasive
(unless a planned cesarean delivery is performed in the GBS disease)
absence of labor or membrane rupture) Planned cesarean delivery performed in the absence
Unknown GBS status AND any of the following: of labor or membrane rupture (regardless of GBS
Delivery at 37 weeks gestation culture status)
Membranes ruptured for 18 hours Negative vaginal and rectal GBS screening culture in
Intrapartum fever (temperature 38.0C [100.4F])b late gestation, regardless of intrapartum risk factors

a Exceptions: women with GBS bacteriuria during the current pregnancy or women with a previous infant with invasive GBS
b If chorioamnionitis is suspected, broad-spectrum antimicrobial therapy that includes an agent known to be active against
GBS should replace GBS IAP.
FIG 22-15 Indications for intrapartum antimicrobial prophylaxis to prevent early onset of disease from Group B Streptococcus (GBS) using a
universal prenatal culture screening strategy at 35 to 37 weeks gestation for all pregnant women. IAP, intrapartum antimicrobial prophylaxis.
(From Verani JR, McGee L, Schrag SJ; Division of Bacterial Diseases, National Center for Immunization and Respiratory Diseases, Centers for
Disease Control and Prevention. Prevention of perinatal group B streptococcal diseaserevised guidelines from CDC, 2010. MMWR Recomm
Rep. 2010;59[RR-10]:1-36.)

not receive vitamin K prophylaxis, generally in the first 5 days and other high-risk infants, developmental deficiencies or unfa-
to 2 weeks but sometimes as late as 12 weeks. Oral vitamin K vorable perinatal events hamper a smooth respiratory transi-
has been shown to be effective in raising vitamin K levels, but tion. The presentation of respiratory distress is among the
it is not as effective in preventing late hemorrhagic disease of the most common symptom complexes seen in the newborn and
newborn, which most commonly occurs in breastfed infants may be secondary to both noncardiopulmonary and cardio-
whose courses have been complicated by diarrhea. pulmonary etiologies (Table 22-12). The symptom complex
includes an elevation of the respiratory rate to greater than
60per minute with or without cyanosis, nasal flaring, intercostal
PERINATAL INFECTION and sternal retractions, and expiratory grunting. The retractions
Early-Onset Bacterial Infection are the result of the neonates efforts to expand a lung with poor
The unique predisposition of the neonate to bacterial infection compliance using a very compliant chest wall. The expiratory
is related to defects in both innate and acquired immune grunt is caused by closure of the glottis during expiration in an
responses.66 The incidence of bacterial infection in infants effort to increase expiratory pressure to help maintain FRC. The
younger than 5 days of age is 1 to 2 per 1000 live births. Mater- evaluation of such an infant requires use of history, physical
nal colonization with group B Streptococcus (GBS), rupture examination, and laboratory data to arrive at a diagnosis. It is
of membranes for more than 12 to 18 hours, and the pres- important to consider causes other than those related to the
ence of chorioamnionitis increase the risk of infection.67,68 heart and lungs, because the natural tendency is to focus imme-
Maternal fever from other etiologies (e.g., epidural anesthesia) diately on the more common cardiopulmonary etiologies.
does not increase the risk of neonatal infection and merits only
close observation of the newborn. Irrespective of membrane Cardiovascular Causes
rupture, infection rates are higher in preterm infants. The Cardiovascular causes of respiratory distress in the neonatal
majority of early-onset bacterial infections present on day 1 period can be divided into two major groupsthose with struc-
of life, with respiratory distress the most common presenting tural heart disease and those with persistent right-to-left shunt-
symptom. These infections are most often caused by GBS and ing through fetal pathways and a structurally normal heart. The
gram-negative enteric pathogens. The algorithm for prevention two presentations of serious structural heart disease in the
of early-onset GBS infections is presented in Figure 22-15 with first week of life are cyanosis and congestive heart failure.69
the approach to the newborn shown in Figure 22-16. Other Examples of cyanotic heart disease include transposition of the
etiologies of infection in the newborn are covered in Chapters great vessels, tricuspid atresia, certain types of truncus arteriosus,
52, 53, and 54. total anomalous pulmonary venous return, and right-sided
outflow obstruction including tetralogy of Fallot and pulmonary
stenosis or atresia. Infants with congestive heart failure generally
RESPIRATORY DISTRESS have some form of left-sided outflow obstruction (e.g., hypo-
The establishment of respiratory function at birth is dependent plastic left heart syndrome, coarctation of the aorta). It is now
on expansion and maintenance of air sacs, clearance of lung recommended that all newborns have pulse oximetry screen-
fluid, and adequate pulmonary perfusion. In many premature ing at 24 hours to identify critical heart disease.70

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488 Section IV Postpartum Care

Yes combinations of cyanosis, grunting, nasal flaring, retracting, and

Signs of neonatal sepsis? Full diagnostic evaluation* tachypnea during the first hours after birth. The chest radio-
Antibiotic therapy
No graph is the key to the diagnosis, with prominent perihilar
streaking and fluid in the interlobar fissures. The symptoms
Maternal chorioamnionitis? Limited evaluation generally subside in 12 to 24 hours, although they can persist
Antibiotic therapy longer. The preferred explanation for the clinical features is
delayed reabsorption of fetal lung fluid. Transient tachypnea is
GBS prophylaxis indicated Routine clinical careII seen more commonly in infants delivered by elective cesarean
for mother? section and in the slightly preterm infant (see Mechanics of the
First Breath).
At delivery, the neonate may aspirate clear amniotic fluid or
Mother received intravenous Observation for 48 hoursII, fluid mixed with blood or meconium. MAS occurs in full-term
penicillin, ampicillin, or postmature infants. The perinatal course is often complicated
or cefazolin for 4 hours
before delivery?
by chronic intrauterine hypoxia, fetal distress, and low Apgar
scores. These infants exhibit tachypnea, retractions, cyanosis, an
No overdistended and barrel-shaped chest, and coarse breath sounds.
Yes Chest radiography reveals coarse, irregular pulmonary densities
37 weeks and duration Observation for 48 hoursII,#
of membrane rupture with areas of diminished aeration or consolidation. The inci-
<18 hours? dence of air leaks is high, and many of the infants exhibit per-
sistent pulmonary hypertension.
No The lungs represent the most common primary site of
Either <37 weeks or duration Yes Limited evaluation infection in the neonate. Both bacterial and viral infections can
of membrane rupture Observation for 48 hoursII be acquired before, during, or after birth. The most common
18 hours? route of infection, particularly for bacteria, is ascending from
the genital tract before or during labor. Infants with congenital
* Full diagnostic evaluation includes a blood culture, a complete pneumonia present with respiratory distress very early in life.
blood count (CBC) including white blood cell differential and The chest radiograph pattern is often indistinguishable from
platelet counts, chest radiograph (if respiratory abnormalities are
present), and lumbar puncture (if patient is stable enough to tolerate
other causes of respiratory distress, particularly hyaline mem-
procedure and sepsis is suspected). brane disease (HMD).

Antibiotic therapy should be directed toward the most common Spontaneous pneumothorax occurs in 1% of all deliveries,
cause of neonatal sepsis, including intravenous ampicillin for GBS but a much lower percentage results in symptoms. The risk is
and coverage for other organisms (including Escherichia coli and increased by manipulations such as positive-pressure ventila-
other gram-negative pathogens) and should take into account local
antibiotic resistance patterns. tion. Respiratory distress is usually present from shortly after

Consultation with obstetric providers is important to determine the birth, and breath sounds may be diminished on the affected side.
level of clinical suspicion for chorioamnionitis. Chorioamnionitis is The majority of these air leaks resolve spontaneously without
diagnosed clinically and some of the signs are nonspecific. specific therapy.

Limited evaluation includes blood culture (at birth) and CBC with
differential and platelets (at birth and/or at 6-12 hours of life).
HMD remains the most common etiology for respiratory
If signs of sepsis develop, a full diagnostic evaluation should be distress in the neonatal period. Initial reports of Avery and
conducted and antibiotic therapy initiated. Mead72 demonstrated a high surface tension in extracts of lungs

If 37 weeks gestation, observation may occur at home after 24 from infants dying of RDS, which led to the present understand-
hours if other discharge criteria have been met, access to medical ing of the role of surfactant in the pathogenesis of HMD. The
care is readily available, and a person who is able to comply fully
with instructions for home observation will be present. If any of deficiency of surfactant in the premature infant increases alveolar
these conditions is not met, the infant should be observed in the surface tension and, according to LaPlaces law (see Fig. 22-2),
hospital for at least 48 hours and until discharge criteria are achieved. increases the pressure necessary to maintain patent alveoli. The
Some experts recommend a CBC with differential and platelets at end result is poor lung compliance, progressive atelectasis, loss of
age 6-12 hours.
FRC, alterations in ventilation-perfusion mismatch, and uneven
FIG 22-16 Algorithm for secondary prevention of early-onset Group B distribution of ventilation. HMD is further complicated by
streptococcal disease among newborns. (From Verani JR, McGee L, the weak respiratory muscles and compliant chest wall of the
Schrag SJ; Division of Bacterial Diseases, National Center for Immu-
nization and Respiratory Diseases, Centers for Disease Control and
premature infant. Hypoxemia and respiratory and metabolic
Prevention. Prevention of perinatal group B streptococcal disease acidemia contribute to increased pulmonary vascular resis-
revised guidelines from CDC, 2010. MMWR Recomm Rep. 2010; tance, right-to-left ductal shunting, and worsening ventilation-
59[RR-10]:1-36.) perfusion mismatch that exacerbate hypoxemia. Hypoxemia and
hypoperfusion result in alveolar epithelial damage with increased
capillary permeability and leakage of plasma into alveolar spaces.
Pulmonary Causes Leakage of protein into airspaces serves to inhibit surfactant
Of the causes of respiratory distress related to the airways and function, which exacerbates the disease process. The materials
pulmonary parenchyma listed in Table 22-12, the differential in plasma and cellular debris combine to form the charac-
diagnosis in a term infant includes transient tachypnea, teristic hyaline membrane seen pathologically. The recovery
aspiration syndromes, congenital pneumonia, and spontane- phase is characterized by regeneration of alveolar cells, including
ous pneumothorax.71 The syndrome of transient tachypnea type II cells, with an increase in surfactant activity.
presents as respiratory distress in nonasphyxiated term infants Clinically, neonates with HMD demonstrate tachypnea, nasal
or slightly preterm infants. The clinical features include various flaring, subcostal and intercostal retractions, cyanosis, and

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Chapter 22 The Neonate 489


Hypothermia or hyperthermia Left-sided outflow obstruction Upper airway obstruction
Hypoglycemia Hypoplastic left heart Choanal atresia
Metabolic acidosis Aortic stenosis Vocal cord paralysis
Drug intoxications, withdrawal Coarctation of the aorta Meconium aspiration
Polycythemia Cyanotic lesions Clear fluid aspiration
Central nervous system insult Transposition of the great vessels Transient tachypnea
Asphyxia Total anomalous pulmonary venous return Pneumonia
Hemorrhage Tricuspid atresia Pulmonary hypoplasia
Neuromuscular disease Right-sided outflow obstruction Primary
Werdnig-Hoffman disease Secondary
Myopathies Hyaline membrane disease
Phrenic nerve injury Pneumothorax
Skeletal abnormalities Pleural effusions
Asphyxiating thoracic dystrophy Mass lesions
Lobar emphysema
Cystic adenomatoid malformation

FIG 22-17 A, Chest radiograph demonstrates findings consistent with hyaline membrane disease (respiratory distress syndrome) including exten-
sive atelectasis with homogeneous ground-glass appearance to the lung fields and air bronchograms and elevated diaphragm. B, Chest radio-
graphs demonstrate changes consistent with bronchopulmonary dysplasia, including heterogeneous areas of atelectasis and hyperlucency.

expiratory grunting. The radiologic appearance of the lungs is includes bronchopulmonary dysplasia and significant neu-
consistent with an extensive atelectatic process (Fig. 22-17). The rologic impairment. The incidence is especially high in infants
infiltrate is diffuse and has a ground-glass appearance, and major born at less than 800g. The severity is variable and ranges from
airways are air filled and contrast with the atelectatic alveoli to very mild pulmonary insufficiency to severe disease with pro-
create the appearance of air bronchograms. The diaphragm is longed mechanical ventilation, frequent readmissions for respira-
elevated because of profound hypoexpansion. Acute complica- tory exacerbations after nursery discharge, and a higher incidence
tions of HMD include infection, air leaks, and persistent patency of neurodevelopmental sequelae compared with VLBW controls.
of the ductus arteriosus. Although pulmonary function improves over time and most chil-
Of more concern than acute complications are the long- dren do well, long-term pulmonary sequelae are evident. Factors
term sequelae suffered by infants with HMD. The major involved in the etiology of CLD are gestational age, elevated
long-term consequences are chronic lung disease (CLD) inspired oxygen concentration, ventilator volutrauma, sever-
that requires prolonged ventilator and oxygen therapy and ity of underlying disease, inflammation, and infection.

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490 Section IV Postpartum Care

TABLE 22-13 CLASSIFICATION OF obstetric and neonatal care, the therapeutic focus continues to
INTRAVENTRICULAR HEMORRHAGE be on strategies to prevent this complication of prematurity.
Both antenatal and postnatal approaches have been developed.
For the most part, postnatal pharmacologic strategies have not
I Subependymal hemorrhage had a major effect in decreasing the incidence, severity, and
II Intraventricular hemorrhage without ventricular dilatation
III Intraventricular hemorrhage with ventricular dilatation
neurodevelopmental outcomes of IVH. Because IVH and PVL
IV Intraventricular hemorrhage with associated parenchymal are likely perinatal events, antenatal prevention holds the
hemorrhage most promise. Although not used specifically to decrease the
Modified from Papile LA, Burstein J, Burstein R, Koffler H. Incidence and evolution of
incidence of IVH and PVL, antenatal corticosteroids decrease
subependymal and intraventricular hemorrhage: a study of infants with birth weights less the frequency of these complications and likely represent the
than 1500g. J Pediatr. 1978;92:529. most important antenatal strategy to prevent intracranial
hemorrhage.5 Furthermore, antenatal magnesium sulfate also is
used for neuroprotection of the newborn prior to preterm deliv-
ery, although long-term benefits are unclear.79,80
Intraventricular Hemorrhage and CLASSIFICATION OF NEWBORNS BY
Periventricular Leukomalacia GROWTH AND GESTATIONAL AGE
Periventricular/intraventricular hemorrhage (PVH/IVH) In assessing the risk for mortality or morbidity in a given
and periventricular leukomalacia (PVL) are the most com- neonate, evaluation of birthweight and gestational age
mon neurologic complications of prematurity. The overall together provide the clearest picture. When large populations
incidence of PVH/IVH is 20% to 30% in infants weighing less are considered, maternal dates remain the single best determi-
than 1500g or at less than 31 weeks gestation with severe bleeds nant of gestational age. Early obstetric ultrasound is a very useful
(grades 3 and 4) at 10%. The highest incidence is observed in adjunct (see Chapter 9). However, in the individual neonate,
babies of the lowest gestational age and birthweight; nearly 50% especially when dates are uncertain, a reliable postnatal assess-
and 25%, respectively, of all IVH and severe bleeds are seen in ment of gestational age is necessary. A scoring system that
babies born at less than 700g.73 Bleeds are graded according to appraises gestational age on the basis of physical and neurologic
severity as indicated in Table 22-13, and diagnosis is confirmed criteria was developed by Dubowitz and colleagues and later
with ultrasound. PVL is reported in about 2% to 4% of infants simplified and updated by Ballard and associates (Fig. 22-18).81
younger than 32 weeks gestation,73 but the cystic PVL reported The Ballard examination is less accurate before 28 weeks gesta-
likely underestimates the full spectrum of PVL. tion, but additional features can be examined to aid in the
Cystic PVL comprises multifocal areas of necrosis with cyst determination of an accurate gestational age. The anterior vas-
formation in deep periventricular white matter. It has been well cular capsule of the lens reveals complete coverage of the lens by
characterized by ultrasound, and the expanded use of MRI scans vessels at 27 to 28 weeks. Foot length (from the heel to the tip
in preterm infants has identified infantsespecially among of the largest toe) is 4.5cm at 25 weeks and increases by
those of lower gestational agewith diffuse white matter injury 0.25cm/wk. Using growth parameters and gestational age,
often accompanied by ventricular dilation. These findings are far infants can then be classified by means of intrauterine growth
more common in the preterm population than cystic PVL and curves such as those developed by Lubchenco and colleagues
represent part of the spectrum of PVL. The other important (Fig. 22-19).82 Infants born between 37 and 42 weeks are
clinical correlate with PVL is maternal chorioamnionitis and classified as term infants; less than 37 weeks is preterm;
neonatal infection. and greater than 42 weeks is postterm (see Chapter 36). In
The neurodevelopmental outcome of infants with IVH is each grouping, infants are then identified according to growth;
related to the severity of the original bleed, development of AGA if birthweight falls between the 10th and 90th percentiles,
posthemorrhagic hydrocephalus, and the degree of associ- SGA if birthweight is below the 10th percentile, and LGA if
ated parenchymal injury. Although cranial ultrasound is the birthweight is above the 90th percentile. Knowledge of a babys
primary modality used to diagnose IVH and PVL, it is not a birthweight in relation to gestational age is helpful in anticipat-
sensitive predictor of outcome. In extremely low-birthweight ing neonatal problems.
infants with no abnormalities on cranial ultrasound, nearly one The causes of growth restriction are numerous (see Chapter
third will have some degree of neurodevelopmental handicap 33). Those operative early in pregnancy such as chromosomal
(cerebral palsy or cognitive delays).74 Infants with grade I or II aberrations, congenital viral infections, and some drug exposures
IVH are at slightly greater risk for handicap.75 School-aged chil- induce symmetric restriction of weight, length, and head cir-
dren who had mild IVH display a variety of neurologic and cumference. In most cases, the phenomenon occurs later in
cognitive abnormalities, including motor incoordination, hyper- gestation and leads to more selective restriction of birthweight
activity, attention and learning deficits, and visual motor diffi- alone. Such factors include hypertension or other maternal
culties.76 Infants with progressive ventricular dilatation (grade vascular disease and multiple gestation. Neonatal problems in
III) or periventricular hemorrhagic infarction (grade IV) are at addition to chromosomal abnormalities and congenital viral
higher risk for major neurodevelopmental handicap as well as infections common in SGA infants include birth asphyxia,
less severe neurologic and cognitive disabilities.77,78 The presence hypoglycemia, polycythemia, and hypothermia. In addition,
of severe cystic PVL carries a guarded prognosis with a high risk congenital malformations are seen more frequently among
of cerebral palsy and associated cognitive deficit. undergrown infants.83
Although the incidence and severity of intracranial hemor- The most common identifiable conditions that lead to exces-
rhage have progressively decreased as a result of advances in both sive infant birthweight are maternal diabetes and maternal

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Chapter 22 The Neonate 491

Neuromuscular Maturity

1 0 1 2 3 4 5


>90 90 60 45 30 0

Arm Recoil
180 140180 110140 90110 <90

180 160 140 120 100 90 <90

Scarf Sign

Heel to Ear

Physical Maturity Maturity Rating

superficial parchment,
sticky, gelatinous, cracking leathery, Score Weeks
smooth pink, peeling deep,
Skin friable, red, pale areas, cracked,
visible veins and/or rash, cracking,
transparent translucent rare veins wrinkled 10 20
few veins no vessels
5 22
bald mostly
Lanugo none sparse abundant thinning
areas bald
0 24

heel-toe >50 mm, anterior creases 5 26

Plantar faint creases
40-50 mm: 1 no transverse over
Surface red marks ant. 2/3
<40 mm: 2 crease crease only entire sole 10 28

stippled raised full areola, 15 30

barely flat areola
Breast imperceptible areola, areola, 5-10 mm
perceptible no bud
1-2 mm bud 3-4 mm bud bud 20 32

lids fused lids open, slight curved well-curved formed thick 25 34

Eye/Ear loosely: 1 pinna flat and pinna, soft, pinna, soft but and firm, cartilage,
tightly: 2 stays folded slow recoil ready recoil instant recoil ear stiff 30 36

scrotum scrotum testes in testes testes down, testes 35 38

flat, empty, upper canal, descending, good pendulous,
smooth faint rugae rare rugae few rugae rugae deep rugae 40 40
prominent majora
clitoris prominent majora 45 42
Genitals clitoris, and minora majora large,
prominent, clitoris, small cover clitoris
Female enlarging equally minora small
labia flat labia minora and minora 50 44
minora prominent
FIG 22-18 Assessment of gestational age. ant., anterior. (From Ballard JL, Khoury JC, Wedig K, etal. New Ballard Score, expanded to include
extremely premature infants. J Pediatr. 1991;119:417.)

obesity. Other conditions associated with macrosomia are eryth- NURSERY CARE
roblastosis fetalis, other causes of fetal hydrops, and Beckwith- Nurseries are classified on the basis of the level of care provided
Wiedemann syndrome. LGA infants are at risk for hypoglycemia, (Box 22-4). Level I nurseries care for infants presumed
polycythemia, congenital anomalies, cardiomyopathy, hyperbili- healthy, with an emphasis on screening and surveillance.
rubinemia, and birth trauma. Level II nurseries can care for infants at more than 32 weeks

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492 Section IV Postpartum Care

24 25 26 27 28 29 30 31 32 33 34 35 36 37 38 39 40 41 42 43 24 25 26 27 28 29 30 31 32 33 34 35 36 37 38 39 40 41 42 43
cm cm
53 90% 37 Intrauterine head growth
52 Intrauterine length chart, 36 90%
both sexes 75% 35 75%
51 both sexes
50 34 50%
49 33 25%
48 25% 32 10%
47 31
46 10% 30
45 29
44 28
43 27
42 26
41 25
40 24
39 23
38 22
37 0
35 Grams
34 4200 3.50
33 4000 3.40 Intrauterine weight/length ratio:
90% 3800
32 3.30 100 w grams/L3 centimeters,
31 75% 3600 3.20 both sexes
30 3400 3.10 90%
Intrauterine weight chart, 50%
0 both sexes 3200 3.00
25% 3000 2.90
2800 2.80
Grams 2600 2.70
2400 2.60 50%
2200 2.50
2000 2.40
1800 2.30
1600 2.20
1400 2.10
1200 2.00
1000 1.90
800 1.80
600 1.70
400 1.60
0 0
24 25 26 27 28 29 30 31 32 33 34 35 36 37 38 39 40 41 42 43 24 25 26 27 28 29 30 31 32 33 34 35 36 37 38 39 40 41 42 43
Week of gestation Week of gestation
FIG 22-19 Intrauterine growth curves for weight, length, and head circumference for singleton births in Colorado. 100w grams/L3 centimeters,
weight in grams divided by 100, with the quotient divided by the length cubed. (From Lubchenco LO, Hansman C, Boyd E. Intrauterine growth
in length and head circumference as estimated from live births at gestational ages from 26 to 42 weeks. Pediatrics. 1966;37:403.)


Level 1: A nursery with personnel and equipment to perform Level 3: Provides care for the sickest and most complex
neonatal resuscitation, evaluate and provide newborn care infants.
for healthy infants, stabilize and provide care for infants born 3A: Provides care for infants beyond 28 weeks and
at 35 to 37 weeks gestation who remain physiologically 1000g who are in need of conventional mechanical
stable, and stabilize ill infants and those at less than 35 ventilation.
weeks gestation before transport to a higher-level facility. 3B: Can provide care for infants at less than 28 weeks
Level 2: A facility able to provide care to infants born at and 1000g, including high-frequency ventilation,
more than 32 weeks gestation weighing more than 1500g inhaled nitric oxide, on-site subspecialists, advanced
who have physiologic immaturity, are moderately ill with imaging, on-site or nearby pediatric surgeons, and
problems expected to resolve quickly, and do not need anesthesiologists.
urgent subspecialty care; and they can provide convalescent 3C: Can provide ECMO and repair of complex congenital
care for infants after intensive care. heart disease.
2A: Does not do mechanical ventilation or nasal CPAP
2B: Can do short-term (<24hr) ventilation.

Modified from the American Academy of Pediatrics Committee on Fetus and Newborn. Levels of neonatal care. Pediatrics. 2004;114:1341.
CPAP, continuous positive airway pressure; ECMO, extracorporeal membrane oxygenation.

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Chapter 22 The Neonate 493

gestation who weigh at least 1500g but who require special Care of the Parents
attention but will probably not need subspecialty services. Klaus and Kennell89 have outlined the steps in maternal-
Level III nurseries care for all newborn infants who are criti- infant attachment: (1) planning the pregnancy; (2) confirm-
cally ill regardless of the level of support required.84 A peri- ing the pregnancy; (3) accepting the pregnancy; (4) noting
natal center encompasses both high-risk obstetric services fetal movement; (5) accepting the fetus as an individual;
and level III nursery services. Survival for VLBW infants is (6) going through labor; (7) giving birth; (8) hearing and
improved with delivery at centers with a higher volume (>100) seeing the baby; (9) touching, smelling, and holding the
of VLBW deliveries per year and a higher-level nursery.85 This baby; (10) caretaking; and (11) accepting the infant as a
survival advantage may extend to moderately preterm newborns separate individual. Numerous influences can affect this
as well.86 process. A mothers and fathers actions and responses are derived
Care of the normal newborn involves observation of transi- from their own genetic endowment and their own interfamily
tion from intrauterine to extrauterine life, establishing breast or relationships, cultural practices, past experiences with this or
bottle feedings, noting normal patterns of stooling and urina- previous pregnancies, and, most important, how they were
tion, and surveillance for neonatal problems. Signs suggestive of raised by their parents. Also critical is the in-hospital experience
illness include temperature instability, change in activity, refusal surrounding the birthhow doctors and nurses act, separation
to feed, pallor, cyanosis, jaundice, tachypnea and respiratory from the baby, and hospital practices.
distress, delayed (>24hr) passage of the first stool or void, and The 60- to 90-minute period after delivery is a very impor-
bilious vomiting. In addition, the following laboratory screens tant time. The infant is alert, active, and able to follow with his
should be performed: (1) blood type and direct and indirect or her eyes, allowing meaningful interaction to transpire between
Coombs test on infants born to mothers with type O or Rh- infant and parents. The infants array of sensory and motor abili-
negative blood; (2) glucose screen in infants at risk for hypogly- ties evokes responses from the mother and initiates communica-
cemia; (3) hematocrit in infants with signs and symptoms of tion that may be helpful for attachment and induction of
anemia or polycythemia; and (4) mandated screening for inborn reciprocal actions. Whether a critical period for these initial
errors of metabolism, such as phenylketonuria (PKU) and galac- interactions exists is unclear, but improved mothering behavior
tosemia, sickle cell disease, hypothyroidism, cystic fibrosis, does seem to occur with increased contact over the first 3 post-
and congenital adrenal hyperplasia. Many states now mandate partum days. The practical implications of this information
or offer expanded newborn screening by tandem mass spectros- are that labor and delivery should pose as little anxiety as
copy that looks for a variety of other inborn metabolic errors. possible for the mother, and parents and baby should have
All newborns should also have an initial hearing screen per- time together immediately after delivery if the babys medical
formed before discharge. Finally, babies routinely receive 1mg condition permits.
of vitamin K intramuscularly to prevent vitamin Kdeficient Mothers with high-risk pregnancies are at increased risk
hemorrhagic disease of the newborn, and erythromycin oint- for subsequent parenting problems. It is important for both
ment is used to prevent gonococcal ophthalmia neonatorum. obstetrician and pediatrician alike to be involved prenatally to
Hepatitis B vaccine should be given to all newborns, and hepa- allow time to prepare the family for anticipated aspects of the
titis B immunoglobulin is also administered to infants born to babys care and to provide reassurance that the odds are heavily
HBsAg-positive mothers (see Chapter 52). Infants should be in favor of a live baby who will ultimately be healthy. If it is
positioned supine for sleep to minimize the risk of sudden infant possible before birth to anticipate the need for neonatal intensive
death syndrome (SIDS).87 care, such as with a known congenital anomaly or with refrac-
Discharge of the normal newborn is safe provided all criteria tory premature labor, maternal transport to a center with a unit
are met in Box 22-5. The initial follow-up visit needs to occur that can care for the baby should be planned. Before delivery, it
48 to 72 hours after discharge.88 is also very helpful to allow the parents to tour the unit their
Circumcision is an elective procedure to be performed baby will occupy.
only in healthy, stable infants. The procedure probably has The basic principle in dealing with parents of a sick infant
medical benefits that include prevention of phimosis, paraphi- is to provide essential information clearly and accurately
mosis, and balanoposthitis as well as a decreased incidence of to both parents, preferably when they are together. With
cancer of the penis, cervical cancer in partners of circumcised improved survival rates, especially in premature infants, most
men, sexually transmitted diseases (including HIV), and urinary babies will do well despite early problems. Therefore it is rea
tract infection in male infants. Most parents, however, make the sonable in most circumstances to be positive about the out
decision regarding circumcision for nonmedical reasons. The come. There is also no reason to emphasize problems that might
risks of the procedure include local infection, bleeding, removal occur in the future or to deal with individual worries of the
of too much skin, and urethral injury. The combined incidence physician. If asked, questions need to be answered honestly,
of these complications is less than 1%. Local anesthesia (dorsal but the list of parents worries does not need to be voluntarily
penile nerve block or circumferential ring block) with 1% lido- increased.
caine without epinephrine is safe and effective and should Before the parents initial visit to the unit, a physician or nurse
always be used. Techniques that allow visualization of the glans should describe what the baby and the equipment look like.
throughout the procedure (Plastibell and Gomco clamp) are When they arrive in the nursery, this can again be reviewed in
preferred to a blind technique (Mogen clamp) because of detail. If a baby must be moved to another hospital, the mother
occasional amputation of the glans with the latter. Circumcision should be given time to see and touch her infant before the
is contraindicated in infants with genital abnormalities. In transfer. The father should be encouraged to meet the baby at
infants with a family history of bleeding disorders, appropri- the receiving hospital so he can become comfortable with the
ate laboratory evaluation should be performed before the intensive care unit. He can serve as a link between baby and
procedure. mother with information and photographs.

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494 Section IV Postpartum Care


1. The newborn is term, defined as an infant born Cord, skin, and genital care for the infant, including
between 37 and 41 completed weeks of gestation. circumcision care
2. No abnormalities are present that require continued The ability to recognize signs of illness and common
hospitalization. infant problems, particularly jaundice
3. Vital signs are documented as being within normal Infant safety (such as use of an appropriate car
ranges with appropriate variations based on safety seat, supine positioning for sleeping,
physiologic state and stable for the 12 hours preceding maintaining a smoke-free environment, and room
discharge. sharing)
4. The infant has urinated regularly and has passed stool 13. Family, environmental, and social risk factors have
spontaneously. been assessed, and the mother and her other family
5. The infant has completed at least two successful members have been educated about safe home
consecutive feedings. environment. These risk factors include but are not
6. No significant bleeding is present at the circumcision limited to:
site. Untreated parental substance abuse or positive urine
7. The clinical risk of development of subsequent toxicology results in the mother or newborn
hyperbilirubinemia has been assessed, and appropriate History of child abuse or neglect
management and/or follow-up plans have been Mental illness in a parent who is in the home
instituted. Lack of social support, particularly for single and
8. The infant has been adequately evaluated and first-time mothers
monitored for sepsis on the basis of maternal risk Mothers who live in a shelter, a rehabilitation home,
factors and in accordance with current guidelines for or on the street
prevention of perinatal Group B streptococcal disease. History of domestic violence, particularly during this
9. Maternal blood test and screening results are available pregnancy
and have been reviewed, including those for maternal Communicable illness in a parent or other members
syphilis, hepatitis B surface antigen status, and a test of the household
for HIV in accordance with state regulations. Adolescent mother, particularly if other above-listed
10. Infant blood tests are available and have been conditions apply
reviewed, such as cord or infant blood type and direct 14. A medical home for continuing medical care for the
Coombs test results as clinically indicated. infant has been identified, and a plan for timely
11. Newborn metabolic and hearing screenings have communication of pertinent clinical information to the
been completed per hospital protocol and state medical home is in place. For newborns discharged
regulations. less than 48 hours after delivery, an appointment
12. The mothers knowledge, ability, and confidence to should be made for the infant to be examined by a
provide adequate care for her infant have been licensed health care professional, preferably within 48
assessed for competency regarding: hours of discharge based on risk factors but no later
Breastfeeding or bottle feeding (the breastfeeding than 72 hours in most cases.
mother and infant should be assessed by trained 15. Barriers to adequate follow-up care for the newborn
staff regarding breastfeeding position, latch-on, and such as lack of transportation to medical care services,
adequacy of swallowing) lack of easy access to telephone communication, and
The importance and benefits of breastfeeding for nonEnglish-speaking parentshave been assessed
both mother and infant and, whenever possible, assistance has been given to
Appropriate urination and defecation frequency for the family to make suitable arrangements to address
the infant them.

The birth of an infant with a congenital malformation death and then several months later to review the findings of the
provides another situation in which staff support is essen- autopsy, answer questions, and see how the family is doing.
tial. Parents reactions to the birth of a malformed infant
follow a predictable course. For most, there is initial shock and Kangaroo Care
denial, a period of sadness and anger, gradual adaptation, and As a babys course proceeds, the nursery staff can help the parents
finally an increased satisfaction with and the ability to care for become comfortable with their infant. This can include partici-
the baby. The parents must be allowed to pass through these pation in caretaking as well as skin-to-skin contact with the
stages and, in effect, to mourn the loss of the anticipated infant (kangaroo maternal care [KMC]). In addition to benefits
normal child. for thermoregulation, in the LBW population (<2500g),
The death of an infant or a stillborn is a highly stressful KMC improves rates of mortality, nosocomial infection/
family event. This fact has been emphasized by Cullberg,90 who sepsis, and length of hospital stay. A benefit also may exist for
found that psychiatric disorders developed in 19 of 56 mothers infant growth and breastfeeding rates.44 Individualized develop-
studied 1 to 2 years after the deaths of their neonates. One of mentally based care has also shown some benefit for high-risk
the major predispositions was a breakdown of communication infants.91 It is also important for the staff to discuss among
between parents. The health care staff needs to encourage the themselves any problems that parents may be having as well as
parents to talk with each other, discuss their feelings, and display to keep a record of visits and phone calls. This approach will
emotion. The staff should talk with the parents at the time of allow early intervention to deal with potential problems.

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Chapter 22 The Neonate 495

survivors from 1000 to 1500g. The number increases from

OUTCOME OF NEONATAL INTENSIVE CARE 10% to 25% in infants of extremely low birthweight (<1000g)
AND THRESHOLD OF VIABILITY and is particularly troubling for infants born at less than 25
More sophisticated neonatal care has resulted in improved sur- weeks gestation. In these infants, approximately half of the
vival of VLBW (<1500g) infants, in particular those less than survivors have moderate or severe neurosensory disability (Fig.
1000g (Fig. 22-20). Current survival rates are 90% or greater 22-21).92 In addition to the increase in severe disability,
for infants greater than 1000g and 28 weeks gestation, 85% these infants have an increased rate of lesser disabilities
at 800 to 1000g and 26 to 27 weeks gestation, and nearly that include deficits in academic achievement, behavior
70% to 75% for infants at 700 to 800g and 25 weeks gestation, and attention problems, and the need for special education
with a considerable drop in survival below 700g and at less in school (see Fig. 22-20).94-96 Finally, recent information has
than 25 weeks.92,93 Predictions of survival can be signifi- begun to demonstrate an increase in autism spectrum disor-
cantly improved by consideration of clinical data in addition ders in preterm infant survivors.97 Risk factors for neurologic
to birthweight and gestational age. These data include an morbidity include seizures, major intracranial hemorrhage or
appropriate course of antenatal steroids, sex of the baby, and PVL, severe intrauterine growth restriction (IUGR), NEC,
whether the pregnancy is a singleton gestation. It is important chorioamnionitis in the mother, neonatal infection, need for
to note that survival in terms of best obstetric estimate is greater mechanical ventilation, chronic lung disease (CLD), poor early
at very low gestational ages than survival in terms of postnatal head growth, retinopathy of prematurity, and low socioeco-
assessment of gestational age. The numbers in terms of best nomic class.
obstetric estimate based on data at the institution of birth In addition, other morbidities need to be considered. Because
should be referred to for antenatal counseling. Alternatively, the number of survivors weighing less than 1000g has increased,
data from the National Institute of Child Health and Human a reemergence of retinopathy of prematurity has been seen.
Development (NICHD) can be referenced as well. It is criti- This disorder is caused by retinal vascular proliferation that leads
cally important when making decisions at the thresholds of to hemorrhage, scarring, retinal detachment, and blindness. It
viability that a shared understanding is reached among neonatol- is triggered by low concentrations of insulin-like growth factor
ogy, obstetrics, and the family. Paramount to that discussion is 1 (IGF-1) and relative hyperoxia in the early postnatal period,
that improved survival comes with a price, because a variety which leads to delayed retinal vessel growth. Later increases in
of morbidities are seen in these infants. The rate of severe IGF-1 allow vascular endothelial growth factor (VEGF)induced
neurologic disability is fairly constant at 10% of all VLBW angiogenesis and result in an abnormal vascular proliferation.98

140 n= n= n= n= n= n=
555 941 1208 1144 1095 1147
130 100%
100 80%
Cognitive score

50 40%
0 0%
Boys Girls Boys Girls Boys Girls Boys Girls
(n7) (n17) (n37) (n36) (n78) (n66) (n71) (n89) 500 501- 601- 701- 801- 901-
600 700 800 900 1000
23 wk 24 wk 25 wk Comparison
group Birthweight (g)
Gestational age (complete wk)
FIG 22-20 Cognitive scores according to sex and completed weeks of Incomplete FU
gestation at birth for 241 extremely preterm children and 160 age- Lost to FU
matched classmates who were full term at birth. The scores are Died
the Kaufman Assessment Battery for Children scores for the Mental Impaired
Processing Composite or developmental scores according to the Mild
Griffiths Scales of Mental Development and NEPSY (a developmental Unimpaired
neuropsychological assessment). Bars indicate mean scores, and the
dashed line is the mean of a standardized population. (From Marlow FIG 22-21 Outcomes at 18 and 22 months by birthweight in extremely-
N, Wolke D, Bracewell MA, etal: Neurologic and developmental dis- low-birthweight infants. FU, follow-up. (From Gargus RA, Vohr BR,
ability at six years of age after extremely preterm birth. N Engl J Med. Tyson JE, etal. Unimpaired outcomes for extremely low birth weight
2005;352:9.) infants at 18 to 22 months. Pediatrics. 2009;124:112.)

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496 Section IV Postpartum Care

Incidence of acute proliferative retinopathy by birthweight is less complications. Discharge of these babies should be delayed
than 10% in infants who weigh more than 1250g, 20% in those until they have demonstrated reliable oral intake and resolution
1000 to 1250g, 50% to 60% in those 750 to 1000g, and 70% of any acute neonatal problems. The initial outpatient follow-up
in those less than 750g.73 Severe retinopathy is evident in 5% visit should occur within 48 to 72 hours of discharge.
of the infants 1000 to 1250g, in 10% of infants 750 to 1000g,
and in 25% to 40% of infants less than 750g. Of the infants
with severe retinopathy, 10% (4% of the total population) will KEY POINTS
go on to have severe visual problems. The other major neuro-
sensory morbidity is hearing loss, which occurs in 2% of NICU Surfactant maintains lung expansion on expiration by
survivors. Other sequelae of neonatal intensive care include lowering surface tension at the air-liquid interface in the
CLD, growth failure, short gut, and need for postdischarge alveolus.
rehospitalization. Respiratory distress syndrome in premature infants is in
The information presented earlier on outcome is relevant to part caused by a deficiency of surfactant and can be
discussions about obstetric and neonatal intervention at the treated with surfactant replacement therapy.
threshold of viability. If the end point of survival without Antenatal corticosteroids accelerate fetal lung matura-
major disability is considered, this occurs in 0% at 22 weeks, tion and decrease neonatal mortality and respiratory
less than 10% at 23 weeks, approximately 20% to 25% at 24 distress syndrome in preterm infants. In addition, cor-
weeks, and approximately 45% to 50% at 25 weeks.92,93 With ticosteroids are associated with a decrease in intracranial
this information in mind, most neonatologists believe that care hemorrhage and necrotizing enterocolitis.
is clearly beneficial beyond 25 completed weeks, whereas less Transition from intrauterine to extrauterine life requires
than half believe that care is beneficial at 24 to 24 6/7 weeks, removal of fluid from the lungs, switching from fetal to
and even fewer feel care is beneficial at less than 24 completed neonatal circulation, and establishment of a normal
weeks. That said, more than half would intervene on behalf of neonatal lung volume.
an infant beyond 23 weeks gestation. These discussions need to The most important step in neonatal resuscitation is to
be modified depending on circumstances. For instance, morbid- achieve adequate expansion of the lungs.
ity and mortality would increase in the face of overt infection Meconium aspiration syndrome is likely the result of
or severe IUGR. A reasonable approach would seem to be to intrauterine asphyxia with mortality related to associ-
encourage interventions on behalf of a fetus or newborn ated persistent pulmonary hypertension.
beyond 25 completed weeks gestation and to not intervene The best predictor of neurologic sequelae of birth
at less than 23 weeks gestation. The range between 23 and asphyxia is the presence of hypoxic ischemic encepha-
25 weeks should be evaluated on a case-by-case basis. lopathy in the neonatal period. The neurologic sequelae
of birth asphyxia is cerebral palsy. However, the great
majority of cerebral palsy is of unknown origin or has
LATE PRETERM INFANT some etiology other than perinatal asphyxia.
The rate of preterm births in the United States has been increas- The major neurologic complications seen in premature
ing, especially for births between 34 0/7 and 36 6/7 weeks, infants are periventricular hemorrhage/intraventricular
which now make up 70% of all preterm births. Of these births, hemorrhage and periventricular leukomalacia.
as many as 23% had no recorded indication for early delivery Hypoglycemia is a predictable and preventable compli-
noted on the birth certificate.99 Compared with term infants, cation in the newborn.
late preterm infants have a higher mortality and prevalence With improved methods of neonatal intensive care, sur-
of acute neonatal problems that include respiratory distress, vival has increasedin particular for infants weighing
temperature instability, hypoglycemia, apnea, jaundice, and less than 1000gbut it comes at the price of medical
feeding difficulties.97 The respiratory issues are caused by and neurodevelopmental sequelae.
delayed clearance of fetal lung fluid, surfactant deficiency, or
both and can on occasion progress to respiratory failure. Feeding
issues are caused by poor coordination of suck and swallow,
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Chapter 22 The Neonate 498.e1

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