You are on page 1of 20

Pediatr Clin N Am 51 (2004) 599 – 618

Discharge criteria for the term newborn


Michael A. Friedman, MD*, Alan R. Spitzer, MD
Division of Neonatology, Department of Pediatrics, State University of New York at Stony Brook,
Health Sciences Center T11-060, Stony Brook, NY 11794-8111, USA

The birthing process represents a traumatic eviction from the warm, quiet
womb with a constant supply of food to the cold, bright world with nothing
to eat. Tremendous physiologic strains are suddenly placed on the newborn
infant. In a time frame of a few days, the neonate must transition successfully
to extrauterine life, and the family must be prepared for the care of their new-
born at home. As defined by the American College of Obstetricians (ACOG)
and the American Academy of Pediatrics (AAP) in the joint publication
‘‘Guidelines for Perinatal Care,’’ the purpose of postpartum care is ‘‘to identify
maternal and neonatal complications, and to provide professional assistance
during the time when the mother is likely to need support and care’’ [1].
The length of postpartum hospitalization, however, has decreased dramati-
cally over the last several decades [2], which makes it increasingly difficult
to achieve these goals. This article reviews the physiologic and social issues
that face the newborn and mother, discusses the specific issues created by
early discharge, and provides suggested criteria for the timing of discharge of
the well term neonate.

Neonatal transition to extrauterine life


The process of transforming from a fetus to a neonate is neither simple
nor quick. Physiologically, it is a dynamic period in which many congenital
disorders may present and in which disruption of the transition process can
manifest as serious neonatal disease. Ideally, the newborn should not be dis-
charged until transition is complete. Recognizing and anticipating problems of
transition and the proper timing of discharge can be determined only from
an understanding of normal transitional events.

* Corresponding author.
E-mail address: michael.friedman@stonybrook.edu (M.A. Friedman).

0031-3955/04/$ – see front matter D 2004 Elsevier Inc. All rights reserved.
doi:10.1016/j.pcl.2004.01.011
600 M.A. Friedman, A.R. Spitzer / Pediatr Clin N Am 51 (2004) 599–618

Cardiopulmonary events

Transitional circulation
The hallmark of fetal circulation is high pulmonary vascular resistance
(PVR) with low pulmonary blood flow. These circumstances promote right-to-
left shunting through the ductus arteriosus and the foramen ovale, with most
of the cardiac output bypassing the lungs. After the umbilical cord is cut,
the placenta no longer provides oxygen to the neonatal blood supply, and the
PVR must fall dramatically to allow blood flow to the infant’s lungs. The
mechanical act of ventilation, a fall in the partial pressure of carbon dioxide
(PCO2), and an increase in the partial pressure of oxygen (PO2) are all impor-
tant immediate postnatal stimulators for the normal decline in PVR [3 – 7].
Exposure to light and changes in circulating vasoactive agents also seem to
mediate this process. The largest decrease in PVR occurs during the first 12 to
24 hours of life and is related to the production of vasodilators, such as
prostacyclin and nitric oxide [8,9]. Further reduction in PVR occurs over
days to months and involves the remodeling of the pulmonary vascular muscu-
lature [10].
Alterations in the normal decline of PVR result in the disorder known as
persistent pulmonary hypertension of the newborn, in which postnatal eleva-
tions in PVR result in the continuation of fetal-type circulation with right-
to-left shunting and resulting cyanosis. Hypoxia, acidosis, hypercarbia, and
inflammatory mediators are believed to precipitate pulmonary vasoconstriction
and lead to persistent pulmonary hypertension of the newborn in the presence
of parenchymal lung disease. Diseases such as meconium aspiration syndrome,
respiratory distress syndrome, and pneumonia fall into this category [11– 13].
Because of a different mechanism, chronic intrauterine hypoxia also can lead
to persistent pulmonary hypertension of the newborn after birth, secondary to
the development of an abnormal pulmonary vascular bed, with thickened,
abnormal muscularization of the pulmonary vessels [14]. In addition to abnor-
mal muscularization, neonates with hypoplastic lungs, such as those with
congenital diaphragmatic hernia, have an associated hypoplasia of the pulmo-
nary vascular bed that is believed to contribute to their elevated PVR [15].

Fetal lung fluid


Driven by lung inflation and a large increase in pulmonary blood flow,
absorption of fetal lung fluid occurs in the first hours after birth. Lung fluid
is absorbed via the pulmonary vascular bed and, to a lesser extent, through
the pulmonary lymphatic vessels. The common condition known as transient
tachypnea of the newborn is believed to occur when the normal absorption of
fetal lung fluid is disrupted [16]. This disorder of transition is most common
after elective cesarean section and may be caused by a lack of catecholamine
surge and absence of physical compression of the thorax that occurs during
labor and vaginal delivery [17].
M.A. Friedman, A.R. Spitzer / Pediatr Clin N Am 51 (2004) 599–618 601

Breathing pattern
In utero, fetal breathing is intermittent. After delivery, this irregular pattern
must become substantially more continuous to avoid apnea and hypoventila-
tion. The driving forces responsible for this postnatal adaptation in the respira-
tory pattern are unclear, and a mildly irregular breathing pattern in the first week
of life may be considered normal [18]. Pauses in breathing that are prolonged
( >20 seconds), associated with bradycardia, or accompanied by cyanosis
should be considered pathologic and prompt investigation for an underlying
cause, such as sepsis, electrolyte imbalance, intracranial bleeding, maternal
drug use (including magnesium sulfate administration), and congenital neuro-
logic disorders.

Thermal regulation
After delivery, the neonate experiences enormous heat loss. Some degree of
cold stress may be a stimulant for the initiation of nonshivering thermogenesis
and other transitional processes not related to heat production. Upon parturition,
a norepinephrine-mediated response ensues, which causes peripheral vaso-
constriction to conserve heat and the initiation of heat production via non-
shivering thermogenesis in the brown adipose tissue [19]. The surge in thyroid
hormone seen after birth also may be permissive in this process [20]. Small-
for-gestational-age and premature neonates often lack brown fat and are par-
ticularly vulnerable to impaired thermal regulation in the first days of life.
Inability to maintain normal core temperature (36.5 – 37C) also can represent a
pathologic condition, such as sepsis, or a central nervous system disorder and
should be investigated when appropriate.

Glucose homeostasis
The fetal supply of glucose comes solely from the mother, and there is a di-
rect relationship between maternal and fetal glucose levels. Upon delivery,
there is an abrupt cessation of glucose, and the newborn must maintain blood
glucose levels independently. The catecholamine surge after birth, along with
an increase in glucagon levels, stimulates hepatic glycogenolysis and gluco-
neogenesis [21]. Particularly in breastfed babies, dietary carbohydrate intake is
low for several days and the neonate depends on these pathways to maintain
normoglycemia. Additional mechanisms for compensation in healthy infants
with low glucose intake include changes in cerebral blood flow to increase glu-
cose delivery to the brain [22] and the use of alternative fuels, such as ketone
bodies [23]. Ketone body production appears as a normal part of adaptation
in term babies during the first 3 postnatal days. There is also evidence that
breastfeeding activates ketogenesis because of low energy content of breast
milk in the first days of life [24].
One problem in determining normoglycemia is the lack of consensus regard-
ing the definition of hypoglycemia. In 1988, Koh et al [25] reported signifi-
602 M.A. Friedman, A.R. Spitzer / Pediatr Clin N Am 51 (2004) 599–618

cant variation in the definition of hypoglycemia among textbooks, medical


centers, and physicians within centers. In the 1980s, two reports of serial
plasma values of glucose were published in an attempt to define hypoglycemia.
Srinivasan et al [26] measured values in 344 term, appropriate-for-gestational-
age infants. Heck and Erenberg [27] measured values in 114 term infants but
included large-for-gesational-age and small-for-gestational-age infants. There
was also a higher percentage of breastfed infants in the study by Heck and
Erenberg. Both studies reported plasma glucose values and suggested defini-
tions of hypoglycemia (Table 1).
Separate complicating factors are the means and methods used to screen
for hypoglycemia. Whole blood glucose values used in bedside techniques are
12% to 15% lower than plasma values [28]. Falsely low values also may result
from erythrocyte use of glucose if there is a delay in specimen processing.
The source of the blood sample is also a factor, with glucose values from arterial
blood being greater than capillary samples, which are, in turn, higher than venous
samples [29]. Isopropyl alcohol used to prepare skin for blood drawing can
cause falsely high readings if the skin is not allowed to dry completely [30].
Bedside glucometers also are designed for hyperglycemia, and results may not
be as accurate at low levels.
Problems with attaining euglycemia in the immediate postnatal period can
reflect maternal or neonatal metabolic conditions. Maternal diabetes causes
transient hyperinsulinemia in the neonate with resultant hypoglycemia. Ma-
ternal administration of dextrose-containing intravenous fluids [31], b-sympatho-
mimetic tocolytics [32], or oral hypoglycemics [33] can cause neonatal
hypoglycemia. Small-for-gestational-age infants may be hypoglycemic from
low levels of glycogen stores [34]. Perinatally stressed newborns also may
have depleted hepatic glycogen stores secondary to prolonged catecholamine
exposure. Septic and polycythemic infants also may be hypoglycemic, although
the mechanism in these instances is unclear. In evaluating the newborn during
the immediate postnatal period, any hypoglycemia that is persistent should
not be considered simply an alteration of transition and should prompt an
investigation for inborn errors of metabolism and endocrine disorders.

Table 1
Proposed definitions of hypoglycemia
Age Srinivasan et al Heck et al
<24 h <40 mg/dL <30 mg/dL
>24 h <45 mg/dL <40 mg/dL
Data from Srinivasan G, Pildes RS, Cattamanchi G, Voora S, Lilien LD. Plasma glucose values in
normal neonates: a new look. J Pediatr 1986;109(1):114 – 7; Heck LJ, Erenberg A. Serum glucose
levels in term neonates during the first 48 hours of life. J Pediatr 1987;110(1):119 – 22.
M.A. Friedman, A.R. Spitzer / Pediatr Clin N Am 51 (2004) 599–618 603

Hematologic adaptations
The fetus lives in an hypoxemic environment with an arterial oxygen ten-
sion of approximately 35 mm Hg. This stimulates the production of erythro-
poietin and is reflected in the high red blood cell mass in the neonate, with
an average hemoglobin level of approximately 16.8 g/dL [35]. Depending on
the position of the baby relative to the placenta and the timing of cord
clamping at delivery, the baby may receive a placental transfusion [36]. This
process further increases the hematocrit and enhances the potential for poly-
cythemia and hyperbilirubinemia during the transition period. Other causes for
polycythemia include twin-twin transfusion, maternal diabetes, intrauterine
growth restriction, maternal-fetal transfusion, fetal hypoxia, and chromosomal
abnormalities. The infant is usually plethoric and may have signs or symptoms
of hyperviscosity syndrome, such as respiratory distress, hypoglycemia, oliguria,
abnormal cry, and even seizures. Any hematocrit of more than 65%, particu-
larly in a symptomatic infant, should be repeated with a central venous or
arterial specimen, because capillary specimens often give falsely high readings.
Neonatal anemia also may be seen in the transition period. Causes include
placental hemorrhage (eg, abruptio placentae, placenta previa), neonatal bleeding
after birth trauma (subgaleal, intracranial, intra-abdominal), fetal-maternal trans-
fusion, twin-twin transfusion, and hemolytic disease [8]. Often the cause can be
ascertained based on the presence of hypovolemia with acute blood loss, pallor
without hypovolemia with more chronic processes, and the presence of early
jaundice with hemolytic disease.
The clotting system of the newborn is essentially intact except for a defi-
ciency in vitamin K-dependent clotting factors. Vitamin K production depends
on bacterial colonization of the gut, which takes several days to establish in
the neonate [37]. The risk is the development of hemorrhagic disease of the
newborn, which is exceedingly rare in the United States because of the ad-
ministration of prophylactic vitamin K shortly after birth.
White blood cells also undergo changes in the first days of life. There is a
normal rise in the neutrophil count in the first 24 hours of life, with the ratio
of immature to mature cells remaining less than 0.2 [38]. Any type of intra-
partum stress can raise the absolute neutrophil count and the immature-to-
mature-cell ratio, which makes the white blood cell count difficult to interpret
when used as a screening device for neonatal infection. The presence of
neutropenia is much more likely to represent a newborn pathologic condition
in this situation.

Renal adaptations
The passage of urine in utero contributes to the amniotic fluid. The pla-
centa, not the fetal kidney, is responsible for fluid and electrolyte homeostasis.
After birth, renal blood flow and glomerular filtration increase. Standardized
for body surface area, this increase continues into the third year of life [39].
604 M.A. Friedman, A.R. Spitzer / Pediatr Clin N Am 51 (2004) 599–618

Most infants (97%) pass urine in the first 24 hours of life, with essentially
100% voiding in the first 48 hours of life [40]. The possibility of either renal
or urinary tract pathology should be considered with a delay in urine passage
after 24 hours.

Gastrointestinal adaptations
In the transition from intrauterine to extrauterine life, the neonate must
transition from an intravenous continuous feeder supplied by the maternal/
placenta unit to an intermittent enteral feeder that depends on its own sucking,
swallowing, and digestive capabilities. Coordination of sucking and swallow-
ing is almost always established during the first day of life [41]. Initial feedings
stimulate the release of digestive hormones [42] and an increase in gut motility,
which leads to the passage of stool. Nearly all infants pass stool in the first
48 hours of life [40]. Delay in stool passage should prompt an investigation for
anatomic or functional gastrointestinal obstruction.

Maternal transition
The initial days after birth are also a time of dynamic physiologic and
psychosocial change for the mother. Coping with these changes has a direct
impact on the framework of the developing mother-baby relationship. Maternal
medical issues, including postoperative recovery from a cesarean section, can
disrupt this bonding and learning period. Being a primigravid or first-time
breastfeeding mother also makes the transition to caregiver more difficult.

Breastfeeding
In the first days after birth, the mother must transition from providing pla-
cental feeding to becoming a breast milk supplier. A tremendous increase in
prolactin and oxytocin after parturition stimulates milk production [43]. Nursing
itself further stimulates this process with a change in the composition of the
milk from colostrum to mature breast milk by 5 days postpartum. Breastfeeding
success is enhanced with teaching and support during this critical transition
period. Measures such as rooming-in, no separation after birth, early nursing,
frequent on-demand feedings, and exclusive breastfeeding all enhance the
chances for success [44]. In these times of decreased hospital staffing and
shorter hospital stays, it is increasingly important to provide the family-centered
environment needed to support successful breastfeeding.

Maternal education
Ideally, teaching the mother and family to care for their newborn should be
an ongoing process that begins before birth. After a vaginal delivery, the time
for teaching is particularly limited. In addition to general care issues such as
bathing, umbilical cord care, and taking a temperature, knowledge of infant
M.A. Friedman, A.R. Spitzer / Pediatr Clin N Am 51 (2004) 599–618 605

safety and signs of neonatal illness also must be taught. Providing information on
safety issues, such as ‘‘back to sleep’’ and proper car seat use, is vital. Several
disorders of the newborn, such as jaundice, infection, and heart disease, may
present after 48 hours of life, when many families already have been dis-
charged, which makes education on the recognition of these problems poten-
tially lifesaving.

Early discharge

History
The trend toward shorter postpartum hospitalization has been an ongoing
process since the 1960s [2]. The initial driving force for early discharge evolved
from the desire to make the childbirth process less ‘‘medical’’ and more in the
control of the mother and family [45]. As medicine entered the 1980s, how-
ever, economic issues became the stimulus for the continued downward trend
in length of stay. The introduction of managed care and capitated payment cre-
ated a system in which hospitals could be more profitable if they discharged
patients earlier [46]. With this system, early discharge translated into huge
savings for hospitals, because childbirth is the most common reason for
hospitalization in the United States. Based on figures from the Centers for
Disease Control and Prevention, the average length of postpartum stay for a
vaginal delivery dropped from 3.9 days in 1970 to 2.1 days in 1992 (Fig. 1)
[2]. The downward trend continued during the 1990s to a point at which many
infants were discharged at or before 24 hours of life after a vaginal delivery. The
question of early discharge received national attention—both in the lay and
medical community—with reports of adverse outcomes and general dissatisfac-
tion expressed by consumers and providers [47 – 50]. The outcry culminated in
the Newborns’ and Mothers’ Health Protection Act, which went into effect on

Fig. 1. Average length of stay for hospital deliveries, by delivery method: United States, 1970 – 1992.
(From Centers for Disease Control. Trends in length of stay for hospital deliveries: United States,
1970 – 1992. MMWR Morb Mortal Wkly Rep 1995;44(17):335 – 7.)
606 M.A. Friedman, A.R. Spitzer / Pediatr Clin N Am 51 (2004) 599–618

January 1, 1998. This legislation guaranteed payment for at least a 48-hour


postpartum stay after a vaginal birth and a 96-hour stay after a cesarean section.

Benefits of early discharge


In light of the negativism toward early discharge, there are several benefits
to early discharge that should not be discounted in an appropriate situation.
‘‘Demedicalizing’’ the transition period after birth and placing the mother and
infant in a home environment in a timely manner can promote a more positive
experience for the family. A more comfortable, relaxed environment promotes
breastfeeding success and ongoing maternal-infant bonding during this critical
period of change. When combined with a home nursing visit and early medi-
cal follow-up, early discharge may be a more desirable and safe option, par-
ticularly for educated families with prior experience in child rearing. Although
economics never should be the primary concern, selective early discharge in
appropriate situations has the added benefit of reducing the cost of health care.

Discharge dilemmas
The following situations can be problematic for any newborn but are often
exacerbated when babies are discharged before 48 hours of life.

Missed newborn screening


Mandatory newborn screening to detect metabolic diseases was first intro-
duced in Massachusetts and Oregon in the early 1960s [51]. Although screen-
ing varies by state with respect to the disorders that are tested, all 50 states
have newborn screening programs. Some disorders are detectable at birth,
whereas others require the accumulation of a byproduct secondary to the
metabolic defect. The timing of the sample is critical for preventing false nega-
tive results. In one study by McCabe et al [52], the authors determined that
48 to 72 hours was the best time to screen for phenylketonuria. This has led all
states to require a repeat newborn screen as an outpatient if the newborn is
discharged at less than 24 hours of life. Clearly, this reliance on patients,
health care providers, and adequate follow-up may result in a failure to have a
test repeated, and potentially treatable diseases may be missed [53]. Even for
infants not discharged early, it is imperative for families to be educated about
the importance of newborn screening, and the primary physician designated on
the specimen also should be the physician who sees the baby after discharge.
With a significant proportion of missed cases caused by inadequate follow-up
of an abnormal screen result, strict attention and sound procedures to ensure
postdischarge follow-up are vital.

Hyperbilirubinemia
Hyperbilirubinemia is a normal part of transition, with approximately half
of all babies demonstrating clinical jaundice [54]. Bilirubin-induced neurologic
M.A. Friedman, A.R. Spitzer / Pediatr Clin N Am 51 (2004) 599–618 607

dysfunction, particularly kernicterus, is seen more often when jaundice is caused


by hemolytic disease, severe illness, or hepatic dysfunction [55]. Coinciding with
the decrease in postpartum stay, there has been an increase in kernicterus in
apparently healthy newborns [56]. Proper surveillance and management of
jaundice during the postpartum hospitalization and in the days after discharge
essentially should eradicate kernicterus in this group of healthy term babies.
With most babies discharged from the hospital at approximately 36 hours of
age, their peak bilirubin level occurs at home. Predicting which infants will
develop significant hyperbilirubinemia remains a challenge that is exacerbated
by earlier discharge. Current guidelines rely on visual assessment to determine
which infants require measurement of a total serum bilirubin. Estimating the
total serum bilirubin level based on visual inspection is limited and often
inaccurate, particularly in our multiethnic society with its wide range of skin
pigmentation [54,57,58]. Discharge of a jaundiced newborn with reliance on
outpatient follow-up and parental observation potentially leads to missed oppor-
tunities to prevent bilirubin-induced neurologic dysfunction, because appoint-
ments may be missed or the severity of jaundice may be misjudged by families
and health care professionals. It has been suggested that universal bilirubin
screening before discharge can identify accurately infants at risk for significant
hyperbilirubinemia after discharge and infants in need of closer follow-up [59].
The AAP is currently examining the potential benefits of adopting this approach.
Bhutani et al [59] demonstrated the predictive value of an hour-specific
total serum bilirubin performed at the time of routine metabolic screening.
Based on predischarge and postdischarge total serum bilirubin levels, they de-
veloped a nomogram that classifies infants as high risk, intermediate risk, or
low risk for ultimately developing significant hyperbilirubinemia (17 mg/dL)
(Fig. 2). The nomogram was most predictive for total serum bilirubin levels in
the low-risk zone (less than fortieth percentile), with none of these newborns
jumping to the high-risk zone (more than ninety-fifth percentile) and no sub-
sequent measurable risk for significant hyperbilirubinemia. Infants in the inter-
mediate-risk zone had a small but clinically significant chance to jump to the
high-risk zone, with 6.4% changing zones. Universal bilirubin screening could
be a simple tool for providing more rational and targeted follow-up. The use of
transcutaneous bilirubin measurements may make universal screening more fea-
sible. Taken together with an assessment of the demographic risk factors of each
infant, the hour-specific total serum bilirubin level can provide the physician with
a more concrete assessment of risk and subsequent need for further follow-up,
including the implementation of AAP recommendations for treatment.

Breastfeeding issues
Breastfeeding is beneficial for the mother and infant. Breast milk is immu-
nogenic, and it offers the nursing baby protection from disease [60 – 63]. It is
more easily digested than cow’s milk, and infants are never allergic to their
mother’s milk [64]. For the mother, breastfeeding stimulates oxytocin release
and promotes uterine involution, less postpartum bleeding [65], and a faster re-
608 M.A. Friedman, A.R. Spitzer / Pediatr Clin N Am 51 (2004) 599–618

Fig. 2. Risk designation of term and near-term well newborns based on their hour-specific serum
bilirubin values. (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(1):6 – 14, with permission.)

turn to prepregnancy weight [66]. Nursing mothers also have a decreased risk
of breast [67] and ovarian cancer [68]. Breastfeeding is convenient and eco-
nomic, with the mother providing a continuous supply of free nourishment for
her baby. Although difficult to measure, there are clearly psychosocial benefits
from the intimate interaction between mother and baby that occur during nurs-
ing. With all these benefits to the mother-baby dyad and to society as a
whole, providing substantial resources toward the promotion of breastfeeding
seems prudent.
After a vaginal delivery, abundant milk production is not often present
until after discharge. Breastfeeding problems, such as improper latching on,
poor milk supply, and painful cracked nipples, often present at home and can
lead to an early cessation of nursing [69]. Medical problems, such as hyper-
bilirubinemia [70] and hypernatremic dehydration [71], are more common in
breastfed infants, and they often present after discharge. Particularly in light
of early discharge practices, predischarge maternal education and the availability
of good follow-up services are vital for successful and safe breastfeeding.
A supportive environment in the hospital during the initiation of breastfeed-
ing is important for success, particularly for the first-time breastfeeding mother.
To promote breastfeeding globally, the United Nations Children’s Fund and
M.A. Friedman, A.R. Spitzer / Pediatr Clin N Am 51 (2004) 599–618 609

the World Health Organization introduced ‘‘he Baby-Friendly hospital initiative’’


in 1991 [72]. The program advocates early initiation of breastfeeding, no bottles
or supplementation, rooming-in, and no pacifiers. The program also promotes
in-hospital education and postdischarge services and support. A cornerstone to
the initiative is a hospital environment and policy conducive to breastfeeding
and a supportive staff well trained in lactation.
Once discharged from the hospital, early personal contact with a health care
professional (eg, physician, nurse, or lactation consultant) can be vital to
breastfeeding success. An infant who was apparently breastfeeding well in the
hospital can begin to have problems after discharge as the milk supply increases.
Problems during this vital period can lead to decreased nutrition, decreased
maternal milk production, and, ultimately, early cessation of nursing [73]. With
an early visit in the first 24 to 72 hours after discharge, many problems of
breastfeeding can be remedied and potential health problems, such as dehydra-
tion and hyperbilirubinemia, can be avoided.

Congenital anomalies
Congenital malformations may not always be apparent at birth. They may
present at various times during the transitional period, with some presenting
after discharge. All discharge guidelines require adequate feeding intake and
passage of stool and urine, identifying most malformations of the gastrointesti-
nal and urogenital systems. Of particular concern, however, are cardiac anom-
alies that may present during the first weeks of life after discharge.
The complete transition of the cardiovascular system after birth takes several
weeks. Several cardiac anomalies can present after many newborns are at home,
which makes recognition and timely treatment a challenge [74]. Disorders that
depend on ductal patency for systemic blood flow, such as the hypoplastic
left heart syndrome and ductal-dependent coarctation of the aorta, may not
show cardiovascular collapse until ductal closure occurs [75,76]. In infants with
tetralogy of Fallot and pulmonary artery stenosis or atresia, pulmonary blood
flow also may be ductal-dependent, with cyanosis becoming apparent only after
ductal closure. When there is a ventricular septal defect, as with tetralogy of
Fallot, these disorders of decreased pulmonary blood flow may take even longer
to detect. Babies with transposition of the great arteries often present in the first
24 hours of life with cyanosis, but the presence of an accompanying ventricular
septal defect can create adequate mixing between the two sides of the heart so
that the baby’s condition may go undetected before discharge.
Recently, it has been suggested that pulse oximetry measurement of oxygen
saturation before discharge may be an effective screening tool to detect cyanotic
congenital heart disease [77]. Although this may be a promising, low-cost,
noninvasive tool, its use in screening a large neonatal population requires further
study. Careful observation and examination while the baby is hospitalized,
parental education with respect to signs of illness, and frequent close follow-up
of any abnormal findings, such as murmurs, are the best means for timely
identification of cardiac anomalies.
610 M.A. Friedman, A.R. Spitzer / Pediatr Clin N Am 51 (2004) 599–618

Healthy newborn at risk for sepsis


The confusion over the treatment of possible sepsis in the apparently healthy
term newborn is dramatically illustrated by a group of 687 infants from the
Paidos health management services’ database who were treated for suspected
sepsis [78]. All the infants were in room air and on enteral feeds within 1 day
of birth and had negative blood culture results. Data collected from the Paidos
database showed a wide variation in length of antibiotic treatment, with 19% of
newborns being treated for 4 to 6 days, which appears too long if sepsis has
been ruled out for an infant and too short if one truly believes that an infant is
infected. The management of the apparently healthy term newborn who is at
risk for sepsis remains controversial and lacks consistency.
The leading cause of early neonatal sepsis is group B streptococcus (GBS),
which has a mortality rate of approximately 15% [79,80]. In the mid-1990s,
the ACOG, the AAP, and the Centers for Disease Control and Prevention issued
recommendations for preventing neonatal GBS disease that involved screening
of mothers for GBS at 35 to 37 weeks’ gestation, intrapartum antibiotic pro-
phylaxis (IAP) of mothers who tested positive during labor, and subsequent
management of newborns born to GBS-positive mothers [81]. The initial guide-
lines suggested the use of either a risk-based or culture-based screening ap-
proach to IAP. The guidelines were revised in 2002 [82], and they recommended
universal GBS screening of all mothers, abandoning the option of the risk-
based approach. These recommendations on the management of an infant born
to a GBS-positive mother directly affect the timing of discharge.
Initial management guidelines recommended 48 hours of observation in
term newborns delivered to a GBS-positive mother who received adequate IAP
(4 hours before delivery). In a study of the impact that IAP had on the clini-
cal presentation of sepsis, researchers determined that the clinical onset was
not delayed and it occurred in more than 90% of infants in the first 24 hours of
life. Discharge at 24 hours of life in a term (38 weeks) newborn whose
GBS-positive mother received adequate IAP is allowable. For infants whose
GBS-positive mothers received inadequate IAP, the guidelines have not
changed, and they suggest a limited evaluation and at least 48 hours of obser-
vation. Also impacting time of discharge is the recommendation that all infants
born to mothers who are given intrapartum antibiotics for suspected chorioam-
nionitis should receive an evaluation for sepsis and empiric antibiotic therapy
regardless of the clinical condition of the baby. One last issue that creates
some confusion for persons who care for newborns is the recommendation that
GBS-positive women who undergo planned cesarean section in the absence of
labor or rupture of membranes do not require IAP and thus this situation does
not represent inadequate IAP.

The drug-exposed newborn


Along with possible medical problems, myriad psychosocial issues complicate
the management of infants born to mothers with a history of substance abuse.
Medical issues include recognition of neonatal abstinence syndrome and proper
M.A. Friedman, A.R. Spitzer / Pediatr Clin N Am 51 (2004) 599–618 611

screening for infectious diseases (eg, HIV, hepatitis B, hepatitis C, syphilis,


gonorrhea, and chlamydia). In infants with a history of maternal opiate use,
the baby should be observed for at least 48 hours for signs of withdrawal
[83]. The timing of discharge, however, often depends on family, social, and
treatment issues surrounding the mother. Involvement of social workers and,
when appropriate, child protective agencies is key in helping a physician assess
the home environment and whether it is safe to discharge the infant. A non-
judgmental, supportive atmosphere may help to ensure future compliance with
pediatric follow-up and any maternal rehabilitation that may be required.

Guidelines for discharge

History
The management of newborns in the hospital was first addressed by the AAP
in the 1940s. The Committee on Fetus and Newborn published a manual,
followed by the first edition of ‘‘Standards and Recommendations for Hospital
Care of Newborn Infants’’ in 1948 [84]. Although initial editions of this
publication addressed general care, social, and follow-up issues, the timing of
discharge was not mentioned specifically until the sixth edition in 1977 [85].
This edition suggested a 72- to 96-hour length of stay. In 1983, the AAP and
the ACOG jointly published the first edition of ‘‘Guidelines for Perinatal Care,’’
in which the intent of the postpartum hospitalization was clearly defined as a
period in which the baby and mother could be observed for medical complica-
tions and the family could be prepared for their role as caregivers [86]. A
1995 policy statement by the AAP laid out specific minimum criteria for
discharge [87], and it stressed that meeting these criteria is not likely to occur
in less than 48 hours. Another key point to the policy statement was the
requirement that a follow-up visit occur within 48 hours of any infant dis-
charged early (<48 hours) and that the visit be reimbursed separately from
the hospital stay.

Minimum criteria for discharge


The discharge criteria laid out in the 1995 AAP policy statement have
been incorporated into the latest editions of ‘‘Guidelines for Perinatal Care’’
[1] and include the following recommendations.

 The antepartum, intrapartum, and postpartum courses for the mother and
the neonate are uncomplicated.
 Delivery was vaginal.
 The neonate is a single birth at 38 to 42 weeks’ gestation, and birth weight
is appropriate for gestational age according to appropriate intrauterine
growth curves.
612 M.A. Friedman, A.R. Spitzer / Pediatr Clin N Am 51 (2004) 599–618

 The neonate’s vital signs are documented to be normal and stable for
the 12 hours before discharge, including a respiratory rate of fewer than
60 breaths/min, a heart rate of 100 to 160 beats/min, and an axillary
temperature of 36.1 to 37C (97 –98.6F) in an open crib with appro-
priate clothing.
 The neonate has urinated and has passed at least one stool.
 The neonate has completed at least two successful feedings, and doc-
umentation has been made that the neonate is able to coordinate suck-
ing, swallowing, and breathing while feeding. If breastfeeding, an actual
feeding should be observed by a caregiver knowledgeable in breastfeed-
ing, and documentation of latch, milk transfer, maternal pain, maternal
comments, and infant satiety should be made in the medical record.
 Physical examination reveals no abnormalities that require continued hos-
pitalization.
 There is no evidence of excessive bleeding at the circumcision site for at
least 2 hours.
 There is no evidence of significant jaundice in the first 24 hours of
life (noninvasive means of detecting jaundice may be useful).
 The mother’s (or, preferably, both parents’) knowledge, ability, and con-
fidence to provide adequate care for the neonate are documented by the fact
that the following training and information has been received:
Condition of the neonate.
The breastfeeding mother-neonate dyad should be assessed by trained
staff regarding nursing position, latch-on, adequacy of swallowing,
and woman’s knowledge of urine and stool frequency.
Umbilical cord, skin, and newborn genital care and temperature
assessment and measurement with a thermometer should be reviewed.
The mother should be able to recognize signs of illness and common new
born problems, particularly jaundice.
Instruction in proper newborn safety (eg, proper use of a car seat and
positioning for sleeping) should be provided.
 Family members or other support persons, including health care providers
such as the family pediatrician or his or her designees, who are familiar
with newborn care and are knowledgeable about lactation and the recog-
nition of jaundice and dehydration are available to the mother and the
neonate for the first few days after discharge.
 Laboratory data are available and have been reviewed, including:
Maternal syphilis, hepatitis B virus surface antigen (HbsAg), and HIV
status.
Umbilical cord or newborn blood type and direct Coombs’ test result, as
clinically indicated.
 Screening tests have been performed in accordance with state requirements.
If a test was performed before 24 hours of milk feeding, a system for
repeating the test during the follow-up visit must be in place in accord-
ance with local or state policy.
M.A. Friedman, A.R. Spitzer / Pediatr Clin N Am 51 (2004) 599–618 613

 Initial hepatitis B vaccine has been administered or an appointment has


been scheduled for its administration, and the importance of maintaining
newborn immunization has been stressed.
 A physician-directed source of continuing medical care for the mother
and the neonate has been identified. For newborns discharged before
48 hours after delivery, an appointment has been made for the neonate to
be examined within 48 hours of discharge. The follow-up visit can take
place in a home or clinic setting, as long as the personnel who examine
the neonate are competent in newborn assessment and the results of the
follow-up visit are reported to the neonate’s physician or designees on
the day of the visit.
 Family, environmental, and social risk factors have been assessed. When
risk factors are present, the discharge should be delayed until they are
resolved or a plan to safeguard the newborn is in place. Such factors
may include, but are not limited to:
Untreated parental substance use or positive urine toxicology test results
in the mother or the newborn.
History of child abuse or neglect.
Mental illness in a parent who is in the home.
Lack of social support, particularly for single, first-time mothers.
No fixed home.
History of untreated domestic violence, particularly during this preg-
nancy.
Adolescent mother, particularly if other risk factors are present.

(From American Academy of Pediatrics and the American College of


Obstetricians and Gynecologists. Care of the neonate. In: Guidelines for peri-
natal care. 5th edition. Elk Grove Village (IL) and Washington, DC: AAP/ACOG;
2002. p. 187 – 235, with permission.)

Follow-up for discharge in less than 48 hours


The ‘‘Guidelines for Perinatal Care’’ also state that for infants discharged
at less than 48 hours after delivery, it is essential that they be examined by
‘‘experienced health care providers within 48 hours of discharge’’ [1]. If this
visit cannot be assured, then the discharge should be delayed. The purpose of
this postdischarge visit is to perform the following assessments:

 Assess the newborn’s general health, hydration, and degree of jaundice


and identify any new problems.
 Review feeding pattern and technique, including observation of breast-
feeding for adequacy of position, latch-on, and swallowing.
 Assess historical evidence of adequate stool and urine patterns.
 Assess quality of maternal-neonate interaction and details of newborn
behavior.
614 M.A. Friedman, A.R. Spitzer / Pediatr Clin N Am 51 (2004) 599–618

 Reinforce maternal or family education in neonatal care, particularly re-


garding feeding and sleep position.
 Review results of laboratory tests performed at discharge.
 Perform screening tests in accordance with state regulations and other
tests that are clinically indicated.
 Identify a plan for health care maintenance, including a method for obtain-
ing emergency services, preventive care and immunizations, periodic eval-
uations and physical examinations, and necessary screening.

(From American Academy of Pediatrics and the American College of Obste-


tricians and Gynecologists. Care of the neonate. In: Guidelines for perinatal
care. 5th edition. Elk Grove Village (IL) and Washington, DC: AAP/ACOG;
2002. p. 187– 235, with permission.)
Not all states require insurance companies to pay for an early follow-up visit,
which further complicates early discharges even in appropriate situations.

Summary
Guidelines in medicine never should be mistaken for strict edicts. They
should provide a framework to direct the physician in his or her decision
making. In determining the timing of postnatal discharge, each mother-baby
pair must be evaluated in the context of the guidelines summarized in this
article as proposed by the AAP and the ACOG. In addition to these guidelines,
many factors must be considered, including medical risk factors in the neonate
and mother, previous experience with childbearing (including breastfeeding),
psychosocial and financial state of the family, the ability of the family to care
for the infant, and the availability of follow-up care. Only after a multifac-
torial analysis is made can the length of stay for each neonate be determined.
Although costs and third-party payer considerations cannot be ignored, the
timing of discharge must be between the physician and the family and must
be free of financial pressures. When done correctly and efficiently, the postnatal
hospitalization can ensure the immediate health and well-being of the new-
born during transition and prepare the family for their vital role in the future
health and well-being of their baby.

References
[1] American Academy of Pediatrics and the American College of Obstetricians and Gynecologists.
Care of the neonate. In: Gilstrap LC, Oh W, editors. Guidelines for perinatal care. 5th edition. Elk
Grove Village: AAP/ACOG; 2002. p. 187 – 235.
[2] Centers for Disease Control. Trends in length of stay for hospital deliveries: United States,
1970 – 1992. MMWR Morb Mortal Wkly Rep 1995;44(17):335 – 7.
[3] Permutt S, Riley KL. Hemodynamics of collapsible vessels with tone: the vascular waterfall.
J Appl Physiol 1963;18:924 – 32.
M.A. Friedman, A.R. Spitzer / Pediatr Clin N Am 51 (2004) 599–618 615

[4] Assali NS, Kirschbaum TH, Dilts PV. Effects of hyperbaric oxygen on uteroplacental and fetal
circulation. Circ Res 1968;22:573 – 88.
[5] Cassin S, Dawes GS, Mott JC, Ross BB, Strang LB. The vascular resistance of the foetal and
newly ventilated lung of the lamb. J Physiol 1964;171:61 – 79.
[6] Heymann MA, Rudolph AM, Nies AS, Melmon KL. Bradykinin production associated with
oxygenation of the fetal lamb. Circ Res 1969;25:521 – 34.
[7] Morin III FC, Egan EA. Pulmonary hemodynamics in fetal lambs during development at normal
and increased oxygen tension. J Appl Physiol 1992;73(1):213 – 8.
[8] Britton JR. The transition to extrauterine life and disorders of transition. Clin Perinatol 1998;
25(2):271 – 94.
[9] Ziegler JW, Ivy DD, Kinsella JP, Abman SH. The role of nitric oxide, endothelin, and prosta-
glandins in the transition of the pulmonary circulation. Clin Perinatol 1995;22(2):387 – 403.
[10] Rabinowitz M. Structure and function of the pulmonary vascular bed. Cardiol Clin 1989;7:227 – 38.
[11] Fox WW, Gewitz MH, Dinwiddie R, Drummond WH, Peckham GJ. Pulmonary hypertension in
the perinatal aspiration syndromes. Pediatrics 1977;59(2):205 – 11.
[12] Strang LB, MacLeish MH. Ventilatory failure and right-to-left shunt in newborn infants with
respiratory distress. Pediatrics 1961;28:17 – 27.
[13] Shankaran S, Farooki ZQ, Desai R. b-Hemolytic streptococcal infection appearing as persistent
fetal circulation. Am J Dis Child 1982;136(8):725 – 7.
[14] Crouse DT, Phillips J. Persistent pulmonary hypertension of the newborn. Perinatol Neonatol
1987;11:10 – 20.
[15] Spitzer AR, Davis J, Clarke WT, Bernbaum J, Fox WW. Pulmonary hypertension and persistent
fetal circulation in the newborn. Clin Perinatol 1988;15(2):389 – 413.
[16] Avery ME, Gatewood OB, Brumley G. Transient tachypnea of the newborn: possible delayed
resorption of fluid at birth. Am J Dis Child 1966;111(4):380 – 5.
[17] Oliver RE. Of labor and the lungs. Arch Dis Child 1981;56:559.
[18] Rigatto H. Control of breathing in fetal life and onset and control of breathing in the neonate.
In: Polin RA, Fox WW, editors. Fetal and neonatal physiology. 2nd edition. Philadelphia: WB
Saunders; 1998. p. 1118 – 29.
[19] Alexander G, Williams D. Shivering and non-shivering thermogenesis during summit metabo-
lism in young lambs. J Physiol 1968;198(2):251 – 76.
[20] Klein AH, Reviczky A, Padbury JF. Thyroid hormones augment catecholamine-stimulated
brown adipose tissue thermogenesis in the ovine fetus. Endocrinology 1984;114(4):1065 – 9.
[21] Padbury JF, Ogata ES. Glucose metabolism during the transition to postnatal life. In: Polin RA,
Fox WW, editors. Fetal and neonatal physiology. 2nd edition. Philadelphia: WB Saunders; 1998.
p. 592 – 6.
[22] Anwar M, Vannucci RC. Autoradiographic determination of regional cerebral blood flow during
hypoglycemia in newborn dogs. Pediatr Res 1988;24:41 – 5.
[23] Paton JB, Delannoy CW. Fasting plasma levels of glucose, acetoacetate, D-beta-hydroxy-
butyrate, glycerol, and lactate in the baboon infant: correlation with cerebral uptake of sub-
strates and oxygen. Pediatr Res 1977;11(4):298 – 302.
[24] Hawden HM, Ward Platt MP. Metabolic adaptation in small for gestational age infants. Arch Dis
Child 1993;68:262 – 8.
[25] Koh TH, Eyre JA, Aynsley-Green A. Neonatal hypoglycaemia: the controversy regarding def-
inition. Arch Dis Child 1988;63(11):1386 – 8.
[26] Srinivasan G, Pildes RS, Cattamanchi G, Voora S, Lilien LD. Plasma glucose values in normal
neonates: a new look. J Pediatr 1986;109(1):114 – 7.
[27] Heck LJ, Erenberg A. Serum glucose levels in term neonates during the first 48 hours of life.
J Pediatr 1987;110(1):119 – 22.
[28] Sacks DB. Carbohydrates. In: Burtis CA, Ashwood ET, editors. Tietz textbook of clinical
chemistry. Philadelphia: WB Saunders; 1996. p. 928 – 1001.
[29] Larsson-Conn U. Differences between capillary and venous blood glucose during oral glucose
tolerance tests. Scand J Clin Lab Invest 1976;36:805 – 8.
616 M.A. Friedman, A.R. Spitzer / Pediatr Clin N Am 51 (2004) 599–618

[30] Grazaitis DM, Sexson WR. Erroneously high Dextrostix values caused by isopropyl alcohol.
Pediatrics 1980;66:221 – 2.
[31] Kenepp NB, Kumar S, Shelley WC, Stanley CA, Gabbe SG, Gutsche BB. Fetal and neonatal
hazards of maternal hydration with 5% dextrose before caesarean section. Lancet 1982;1(8282):
1150 – 2.
[32] Procianoy RS, Pinheiro CE. Neonatal hyperinsulinism after short-term maternal beta sympatho-
mimetic therapy. J Pediatr 1982;101(4):612 – 4.
[33] Zucker P, Simon G. Prolonged symptomatic neonatal hypoglycemia associated with maternal
chlorpropamide therapy. Pediatrics 1968;42(5):824 – 5.
[34] Hawden HM, Ward Platt MP. Metabolic adaptation in small for gestational age infants. Arch Dis
Child 1993;68:262 – 8.
[35] Oski FA, Naiman JL. Normal blood values in the newborn period. In: Oski FA, Naiman JL,
editors. Hematologic problems in the newborn. 3rd edition. Philadelphia: WB Saunders; 1982.
p. 11.
[36] Yao AC, Lind J. Placental transfusion. Am J Dis Child 1974;127(1):128 – 41.
[37] Lane PA, Hathaway WE. Vitamin K in infancy. J Pediatr 1985;106(3):351 – 9.
[38] Manroe BL, Weinberg AG, Rosenfeld CR, Browne R. The neonatal blood count in health and
disease. I. Reference values for neutrophilic cells. J Pediatr 1979;95(1):89 – 98.
[39] Arant Jr BS. Postnatal development of renal function during the first year of life. Pediatr Nephrol
1987;1(3):308 – 13.
[40] Clark DA. Times of first void and first stool in 500 newborns. Pediatrics 1977;60(4):457 – 9.
[41] Lau C, Schanler RJ. Oral motor function in the neonate. Clin Perinatol 1996;23(2):161 – 78.
[42] Lucas A, Aynsley-Green A, Bloom SR. Gut hormones and the first meals. Clin Sci 1981;
60(4):349 – 53.
[43] Neville MC, Morton J, Umemura S. Lactogenesis: the transition from pregnancy to lactation.
Pediatr Clin North Am 2001;48(1):35 – 52.
[44] Powers N, Naylor A, Wester R. Hospital policies: crucial to breastfeeding success. Semin
Perinatol 1994;18:517.
[45] Annas GJ. Women and children first. N Engl J Med 1995;333(24):1647 – 51.
[46] Thilo EH, Townsend SF, Merenstein GB. The history of policy and practice related to the
perinatal hospital stay. Clin Perinatol 1998;25(2):257 – 70.
[47] Charles S, Prystowsky B. Early discharge, in the end: maternal abuse, child neglect, and phy-
sician harassment. Pediatrics 1995;96(4 Pt 1):746 – 7.
[48] Eidelman AI. Early discharge, early trouble. J Perinatol 1992;12(2):101 – 2.
[49] Lee KS, Perlman M, Ballantyne M, Elliott I, To T. Association between duration of neonatal
hospital stay and readmission rate. J Pediatr 1995;127(5):758 – 66.
[50] Maisels MJ, Newman TB. Jaundice in full-term and near-term babies who leave the hospital
within 36 hours: the pediatrician’s nemesis. Clin Perinatol 1998;25(2):295 – 302.
[51] Brown ER. Metabolic screening. Clin Perinatol 1998;25(2):371 – 88.
[52] McCabe ER, McCabe L, Mosher GA, Allen RJ, Berman JL. Newborn screening for phenylke-
tonuria: predictive validity as a function of age. Pediatrics 1983;72(3):390 – 8.
[53] Holtzman C, Slazyk WE, Cordero JF, Hannon WH. Descriptive epidemiology of missed cases of
phenylketonuria and congenital hypothyroidism. Pediatrics 1986;78(4):553 – 8.
[54] Davidson LT, Merritt KK, Weech AA. Hyperbilirubinemia in the newborn. Am J Dis Child
1941;61:958 – 80.
[55] Johnson L, Bhutani VK. Guidelines for management of the jaundiced term and near-term infant.
Clin Perinatol 1998;25(3):555 – 74.
[56] Maisels MJ, Newman TB. Kernicterus in otherwise healthy, breast-fed term newborns. Pediatrics
1995;96(4 Pt 1):730 – 3.
[57] Hansen TW. Kernicterus in a full-term infant: the need for increased vigilance. Pediatrics 1995;
95(5):798 – 9.
[58] Kramer LI. Advancement of dermal icterus in the jaundiced newborn. Am J Dis Child 1969;
118(3):454 – 8.
M.A. Friedman, A.R. Spitzer / Pediatr Clin N Am 51 (2004) 599–618 617

[59] 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(1):6 – 14.
[60] Duncan B, Ey J, Holberg CJ, Wright AL, Martinez FD, Taussig LM. Exclusive breast-feeding
for at least 4 months protects against otitis media. Pediatrics 1993;91(5):867 – 72.
[61] Popkin BM, Adair L, Akin JS, Black R, Briscoe J, Flieger W. Breast-feeding and diarrheal
morbidity. Pediatrics 1990;86(6):874 – 82.
[62] Saarinen UM, Kajosaari M. Breastfeeding as prophylaxis against atopic disease: prospective
follow-up study until 17 years old. Lancet 1995;346(8982):1065 – 9.
[63] Shu XO, Clemens J, Zheng W, Ying DM, Ji BT, Jin F. Infant breastfeeding and the risk of
childhood lymphoma and leukaemia. Int J Epidemiol 1995;24(1):27 – 32.
[64] Lawrence PB. Breast milk: best source of nutrition for term and preterm infants. Pediatr Clin
North Am 1994;41(5):925 – 41.
[65] Chua S, Arulkumaran S, Lim I, Selamat N, Ratnam SS. Influence of breastfeeding and nipple
stimulation on postpartum uterine activity. Br J Obstet Gynaecol 1994;101(9):804 – 5.
[66] Dewey KG, Heinig MJ, Nommsen LA. Maternal weight-loss patterns during prolonged lacta-
tion. Am J Clin Nutr 1993;58(2):162 – 6.
[67] Newcomb PA, Storer BE, Longnecker MP, Mittendorf R, Greenberg ER, Clapp RW, et al.
Lactation and a reduced risk of premenopausal breast cancer. N Engl J Med 1994;330(2):
81 – 7.
[68] Grimes DA, Economy KE. Primary prevention of gynecologic cancers. Am J Obstet Gynecol
1995;172(1 Pt 1):227 – 35.
[69] Verronen P. Breast feeding: reasons for giving up and transient lactational crises. Acta Paediatr
Scand 1982;71(3):447 – 50.
[70] Seidman DS, Stevenson DK, Ergaz Z, Gale R. Hospital readmission due to neonatal hyper-
bilirubinemia. Pediatrics 1995;96(4 Pt 1):727 – 9.
[71] Cooper WO, Atherton HD, Kahana M, Kotagal UR. Increased incidence of severe breast-
feeding malnutrition and hypernatremia in a metropolitan area. Pediatrics 1995;96(5 Pt 1):
957 – 60.
[72] World Health Organization. Protecting, promoting and supporting breastfeeding: the special role
of maternity services. A joint WHO/UNICEF statement. Geneva: WHO; 1989.
[73] Neifert MR. The optimization of breast-feeding in the perinatal period. Clin Perinatol 1998;
25(2):303 – 26.
[74] Kessel J, Ward RM. Congenital malformations presenting during the neonatal period. Clin
Perinatol 1998;25(2):351 – 69.
[75] Anonymous. Report of the New England regional infant cardiac program. Pediatrics 1980;
65(2 Pt 2):375 – 461.
[76] Scott DJ, Rigby ML, Miller GA, Shinebourne EA. The presentation of symptomatic heart
disease in infancy based on 10 years’ experience (1973 – 82). Implications for the provision of
services. Br Heart J 1984;52(3):248 – 57.
[77] Reich JD, Miller S, Brogdon B, Casatelli J, Gompf TC, Huhta JC, et al. The use of pulse
oximetry to detect congenital heart disease. J Pediatr 2003;142(3):268 – 72.
[78] Paidos Health Management Services, Inc. Treatment of sepsis in the full-term infant. In: Speak-
man A, editor. Neonatal practice benchmarks. Deerfield (IL): Paidos, Inc.; 2003. p. 7 – 8.
[79] Baker CJ, Edwards MS. Group B streptococcal infections: perinatal impact and prevention
methods. Ann N Y Acad Sci 1988;549:193 – 202.
[80] Yagupsky P, Menegus MA, Powell KR. The changing spectrum of group B streptococcal disease
in infants: an eleven-year experience in a tertiary care hospital. Pediatr Infect Dis J 1991;
10(11):801 – 8.
[81] Centers for Disease Control and Prevention. Prevention of perinatal group B streptococcal
disease: a public health perspective. MMWR Morb Mortal Wkly Rep 1996;45(RR7):1 – 24.
[82] Centers for Disease Control and Prevention. Prevention of perinatal group B streptococcal
disease: revised guidelines from CDC. MMWR Morb Mortal Wkly Rep 2002;51(RR11):1 – 22.
618 M.A. Friedman, A.R. Spitzer / Pediatr Clin N Am 51 (2004) 599–618

[83] Buchi KF. The drug-exposed infant in the well-baby nursery. Clin Perinatol 1998;25(2):335 – 50.
[84] American Academy of Pediatrics Committee on Fetus and Newborn. Standards and recom-
mendations for hospital care of newborn infants. Evanston (IL): American Academy of Pediat-
rics; 1948.
[85] American Academy of Pediatrics Committee on Fetus and Newborn. Standards and recommen-
dations for hospital care of newborn infants. 6th edition. Evanston (IL): American Academy of
Pediatrics; 1977.
[86] American Academy of Pediatrics and the American College of Obstetricians and Gynecologists.
Guidelines for perinatal bare. Evanston (IL): American Academy of Pediatrics/American College
of Obstetrics and Gynecology; 1983.
[87] American Academy of Pediatrics Committee on Fetus and Newborn. Hospital stay for healthy
term newborns. Pediatrics 1995;96(4):788 – 90.

You might also like