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Newborn with respiratory distress - Adam

February 5, 2016 2:55:09 PM EST

Knowledge

Risk Factors for Neonatal Respiratory Distress

Details of the delivery are always important to know when assessing a newborn. The following
perinatal information can provide important clues in determining the etiology of respiratory distress:

Maternal diabetes Prematurity Maternal group B strep infection C-section delivery Premature
rupture of membranes ≥ 18 hours (prolonged PROM) Meconium in the amniotic fluid
A risk factor for respiratory distress syndrome (RDS), among other difficulties

Predisposes to RDS caused by lung immaturity and lack of surfactant

Most infants born at 36 weeks' gestational age do not have RDS

A risk factor for neonatal sepsis (a cause of respiratory distress)

Predisposes to transient tachypnea of the newborn (TTN)

A risk factor for neonatal sepsis

A risk factor for meconium aspiration syndrome

The Apgar Score

The Apgar score describes the condition of the newborn infant immediately after birth and, when
properly applied, is a tool for standardized assessment.

It provides a mechanism to record fetal-to-neonatal transition.

The Apgar score is affected by gestational age, maternal medications, resuscitation, and
cardiorespiratory and neurologic conditions that may be present in the infant. Poor neurologic

O'Shea Dylan - doshea@uw.edu 1/19

outcome is better associated with documented asphyxia, and that is why it is important to obtain
arterial blood gases to look for metabolic acidosis. The Apgar score alone correlates poorly with
the future neurological outcome of the term infant.

Review criteria for assigning Apgar scores. (http://app1.med-

u.org/author/data/db/image/244870_400x300.jpeg)

Low Apgar scores at 1 and 5 minutes alone are not conclusive markers of an acute intrapartum
hypoxic event.

Health care professionals should be consistent in assigning Apgar scores during a resuscitation.

Classification of Birth Weight

A neonate's birth weight is a good indicator of the health of the intrauterine environment. Plotting
the weight against gestational age helps to identify infants with abnormal growth and allows the
anticipation of potential problems associated with each group.

Weight at birth is plotted against estimated gestational age and is used to classify infants as
"large," "appropriate," or "small" for gestational age.

Classification Definition and Etiology Potential Clinical Problems Large for gestational age (LGA)
Appropriate for gestational age (AGA) Small for gestational age (SGA)

Large infants often must

be delivered by c-
section, by forceps, or
vacuum extraction (all of
which have associated
complications)
Newborns with birth weight > 90th percentile. Although many Birth injuries are more
LGA infants are constitutionally large, the most important common, such as
pathologic etiology is maternal diabetes mellitus. fractured clavicle,
brachial plexus injury,
and facial nerve palsy
Hypoglycemia is
especially common in
LGA infants born to
diabetic mothers

Newborns with birth weights between the 10th and 90th

percentiles.

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Newborns with birth weights below either the 3rd or 10th
percentile (depending on the system used).

An infant may have low birth weight due to prematurity, but low
birth weight also results from many other causes. Depending on
the cutoff level used, up to 70% of SGA infants are small simply
due to constitutional factors determined by maternal ethnicity,
parity, weight or height. Temperature instability
(hypothermia)
An infant is diagnosed as being SGA at time of birth. Inadequate glycogen
stores (hypoglycemia)
Note that the terms SGA and intrauterine growth restricted Polycythemia and
(IUGR) are both used in the literature. While they are often used hyperviscosity
synonymously, they are not the same thing:

A growth-restricted fetus is one that has not reached its growth

potential at a given gestational age due to one or more causative
factors.

A fetus is noted to be IUGR during the pregnancy.

Transition to Extrauterine Life

Oxygenation changes dramatically at birth from a passive, placenta-provided source to an

active respiration-based process. In utero, oxygenated blood from the placenta is transported
to the fetus by the umbilical vein. A portion of this blood perfuses the liver. The remainder
bypasses the liver through the ductus venosus and enters the inferior vena cava. One-third of
this vena caval blood crosses the patent foramen ovale (PFO) to the left atrium and is
pumped to the coronary, cerebral and upper body circulations. The remaining two-thirds
combines with venous blood from the upper body in the right atrium, and is directed to the
right ventricle and out the pulmonary artery. In utero, vasoconstriction of the pulmonary
arterioles produces high pulmonary vascular resistance, allowing only 8-10% of the blood
from the right ventricle to flow through the pulmonary vasculature. The remainder, 90-92%, is
shunted through the patent ductus arteriosus (PDA) to the descending aorta.

At birth, successful transition to extrauterine life involves:

Removal of the low-resistance placental circulation by cutting the umbilical cord.

Initiation of air breathing by the newborn infant.
Reduction of the pulmonary arterial resistance.
Closure of the PFO and PDA.

First Breath

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At delivery, the infant's first breath results in the replacement of the lung fluid by air. This fluid is
thought to leave the lungs by a combination of being squeezed out during uterine contractions with
vaginal delivery, and absorption by the pulmonary lymphatics. Delayed absorption of pulmonary
fluid results in a condition known as Transient Tachypnea of the Newborn (TTN), also referred
to as persistent postnatal pulmonary edema.The first physical examination of the neonate provides
a good indication of the infant's successful transition to extrauterine life.

First Hour
In the first hour of life, as transition occurs, the respiratory and heart rates are often elevated:

Heart rate is often 160-180 per minute, and the respiratory rate is often 60-80 per minute.

Second Hour
In an infant with a successful transition, by the age of 2 hours:

Heart rate is usually 120-160 per minute, and the respiratory rate is usually 40-60 per minute.

Vital signs are most accurate if obtained when the infant is quiet and at rest. If the infant is crying,
the heart rate and the respiratory rate may be falsely elevated. (See the following for more
information about vital signs in the newborn: Thureen PJ, Deacon J, et al.: Assessment and Care
of the Well Newborn. WB Saunders, 1999: 188-192.)

Abnormal Transition
Clinical evidence of abnormal transition from to extrauterine life is seen in infants with TTN and
persistent pulmonary hypertension of the newborn (PPHN), also known as persistence of the
fetal circulation.

Signs of Respiratory Distress

The findings of tachypnea, retractions, and grunting are classic symptoms of respiratory distress
from any cause.

Intercostal and subcostal retractions reflect the increased work of breathing due to decreased
lung compliance, either due to primary lung pathology or edema.
Grunting occurs at the end of expiration, and is the audible sound of air being expelled
through a partially closed glottis as the infant attempts to increase transpulmonary pressures,
increase lung volumes, and improve gas exchange.

View a video of an infant in respiratory distress. The video demonstrates tachypnea, increased
respiratory effort, and subcostal retractions.

Hyperlink "View a video "

This Multimedia material is not included in this Summary, please open Case to review.

4/19
Conditions to Consider in the Cyanotic Newborn

Common

TTN
RDS

Uncommon
Respiratory
Pneumothorax
Diaphragmatic hernia
Choanal atresia
Pulmonary hypoplasia
Persistent pulmonary hypertension of the newborn (PPHN)

Common

Tetralogy of Fallot
Transposition of the great arteries (TGA): Defect in which t he aorta and
pulmonary arteries are transposed, resulting in respiratory distress and
severe cyanosis as the ductus arteriosus closes shortly after birth . One risk
factor for TGA is being born to a diabetic mother. TGA is often associated with
Cyanotic other congenital heart defects, such as a ventricular septal defect, so a
congenital murmur may be heard on physical examination.
heart
defects
Uncommon

Truncus arteriosus
Tricuspid atresia
Total anomalous pulmonary venous return
Pulmonary atresia

Hypoxic-ischemic encephalopathy
CNS Intraventricular hemorrhage
Sepsis/meningitis
Septic shock
Infectious
Meningitis
Respiratory depression secondary to maternal medications
Other Hypothermia
Polycythemia/hyperviscosity syndrome

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Fetal Effects of Maternal Hyperglycemia

High levels of maternal serum glucose during pregnancy result in hyperglycemia in the fetus. This
stimulates the fetal pancreatic beta cells and the development of hyperinsulinemia. (Maternal
insulin does not cross the placenta.)

Insulin is the primary anabolic hormone for fetal growth.

High levels in the third trimester result in increased growth of the insulin-sensitive organ
systems (heart, liver and muscle) and a general increase in fat synthesis and deposition.
This combination of increased body fat, muscle mass, and organomegaly produces a
macrosomic (LGA) infant.
Insulin-insensitive organs, such as the brain and kidneys, are not affected by the elevated
insulin levels, and have appropriate size for gestational age.

Control of diabetes during pregnancy is an important predictor of fetal outcome, especially

with regard to the risk of birth defects. The incidence of major malformations is directly related to
the first-trimester HbA1c level:

Infants born to women with HbA1c levels > 12% have at least a 12-fold increase in major
malformations.

Breastfeeding

Breast milk is the ideal nutrient for the newborn human. Breast milk:

Provides a lower renal solute load than formula

Has several anti-infective and anti-allergic properties
Fosters mother-infant bonding

Review the AAP's policy (http://pediatrics.aappublications.org/content/129/3/e827.full#content-block ) on the

benefits of breastfeeding and explore the AAP's breastfeeding initiatives web site
(https://www2.aap.org/breastfeeding/).

Feeding the Infant in Respiratory Distress

The recommendations for feeding infants with respiratory distress vary, depending on the
physician's experience or the policy of the neonatal unit.

When Does Tachypnea Preclude Oral Feeding?

There is no evidence from controlled studies that feeding a tachypneic infant by mouth is
contraindicated, although many physicians are reluctant to try this because they feel that oral

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feedings place the infant under greater stress. Many infants with respiratory rates of 60-80 per
minute tolerate oral feeds, but some may need nasogastric feeding or IV fluids if respiratory
distress worsens with feeding. Many infants with respiratory rates of > 80 per minute will have
difficulty with both oral and nasogastric feedings and will often require intravenous fluid support.

Breastfeeding
Separation of mother and infant poses a challenge for the successful establishment of
breastfeeding. This most often happens with the birth of a premature infant, or an infant requiring
special care. The infant's ability to breastfeed will be determined by letting his mother put him to
the breast as soon as possible.

If the infant cannot successfully breastfeed because of his tachypnea, it will be important that the
mother begin pumping her breasts as soon as possible after delivery. This will initiate milk
production and ensure an adequate supply when the baby is able to feed at the breast.

In the meantime, the infant would be fed expressed breast milk, supplemented with formula as
needed while breast milk volumes are low in the first 2-48 hours after birth.

Pumping breast milk is also psychologically helpful for mothers at a very stressful time: Breast milk
is the single thing that no one else can provide for their infants. The use of a nasogastric feeding
tube will avoid use of a bottle, which may facilitate the mother's wish to breastfeed. (After feeding
from a bottle, some babies may get frustrated when they breastfeed because the milk does not flow
as fast from the breast as from a bottle.)

Hypoglycemia in the Neonate

Glucose is the primary substrate for brain metabolism in the neonate, and even asymptomatic
hypoglycemia may have negative consequences for long-term neurodevelopment.

Definition
The precise definition of hypoglycemia in the neonate has been difficult to establish because
plasma glucose levels often do not correlate with symptoms and long-term outcome. A newborn
can be hypoglycemic yet be entirely asymptomatic. This is why it is important to screen not only
newborns exhibiting symptoms, but all newborns at risk for glucose instability-term infants who are
SGA or LGA, late pre-term, and infants of diabetic mothers-even if they are asymptomatic.

Glucose transport and stabilization

In utero, glucose crosses the placenta, maintaining the fetal blood glucose at approximately two-
thirds of maternal levels. At birth, separation from the placenta results in a decline in the infant's
glucose levels over the first 1-2 hours of life. Levels then increase and stabilize by 3-4 hours at
mean levels of 65-71 mg/dL.

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The infant of a diabetic mother has hyperinsulinemia, and the glucose level declines precipitously
at birth. Prompt intervention is required to raise glucose levels.

Indication for intervention

The target glucose screen value prior to routine feeds is > 45 mg/dL. The proposed threshold value
for administration of glucose (intravenous bolus or infusion) depends on the clinical situation:

If the infant is symptomatic from hypoglycemia and glucose is less than 40 mg/dL, IV glucose
should be administered.
If, during the first 4 hours of life, the infant shows no signs of hypoglycemia but the initial
screen and post-prandial glucose are less than 25 mg/dL, administration of IV glucose is
recommended.
Between 4 and 24 hours of life, the threshold for administration of IV glucose to an
asymptomatic infant increases to 35 mg/dL.

Evaluation of Gestational Age

The assessment of a neonate's gestational age and its relationship to birth weight are important in
identifying infants with abnormal fetal growth patterns.

Dubowitz Score: In 1970 the earliest system for evaluating gestational age was developed by Dr.
Lilly Dubowitz. This was a detailed scoring system based on the infant's external physical
characteristics and neurologic findings. The Dubowitz system requires that the infant be alert and
active, and In very immature or sick infants results were often skewed due to low neurologic
scores.

Ballard Score: In 1979 Dr. Jeanne Ballard, et al., developed a shortened version of the Dubowitz
exam. More recently this method has been modified to allow assessment in extremely premature
infants.

Gestational age assessment should be performed on every neonate within 12-24 hours of life.

Accuracy of results of each system is +/- 2 weeks.

Developmental Dysplasia of the Hip (DDH)

It is important to assess every newborn for DDH (previously known as congenital dislocation of the
hip).

Clinical features include:

Partial or complete dislocation

Instability of the femoral head.

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Risk factors include:

Breech position (30-50% of DDH cases occur in infants born in the breech position)
Gender (9:1 female predominance)
Family history

Screening recommendations

There are varied recommendations regarding screening for DDH:

American Academy of Pediatrics (AAP): 2000 American Academy of Orthopaedic Surgeons: 2014
(endorsed by AAP) Canadian Task Force on Preventive Health Care: 2001 US Preventive
Services Task Force (USPSTF): 2006

Serial clinical examinations of all infants' hips to the age of 12 months

Hip imaging for female infants born in the breech position
Optional hip imaging for boys born in the breech position
Optional hip imaging for girls with a positive family history

Limited recommendation for clinical examination of an infant's hips following a normal hip
examination on subsequent visits prior to 6 months of age
Moderate recommendation for an imaging study before 6 months of age in infants with one
or more of the following risk factors: breech presentation, family history, or history of clinical
instability

Serial clinical examinations of all infants' hips until they are walking independently
No radiographic screening

Insufficient evidence to recommend routine screening for DDH in infants as a means to

prevent adverse outcomes

Data from the Physician Insurers Association of America documents that medical malpractice
lawsuits related to DDH have decreased significantly over the years, presumably because of better
awareness of the condition with earlier and better diagnosis.

Pediatric care providers may need to make clinical decisions in the presence of differing
guidelines. Although practice variation exists, most pediatricians in the US follow the AAP
guidelines and routinely screen all infants by physical examination and by ultrasonography in the
circumstances indicated above.

View hip exam. (http://app1.med-u.org/author/data/db/video/244990.mov )

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Newborn Hospital Discharge Considerations

All of these factors are important in planning the discharge of newborns from the hospital.

Follow-up
It is important that the parents be prepared for the discharge, and that appropriate follow-up is
arranged in the first week after birth. Any infant discharged from the nursery before 48 hours of life
must be evaluated by a health care practitioner within 48 hours.

Feeding
The breastfed infant will typically feed on demand every 2-4 hours, feeding 10-15 minutes on each
side.

Jaundice
A total bilirubin should be measured prior to discharge. If a low level is identified, no further testing
may be needed. Parents should observe for development of jaundice over the next several days
and contact the physician if it does appear.

Vitamin D
The American Academy of Pediatrics (AAP) recommends that exclusively breastfed infants
receive a daily dose of 400 IU of vitamin D, because human milk does not provide adequate
intake. This supplementation should continue until the infant is weaned to either cow's milk or a
formula containing vitamin D. Standard formulas all contain at least 400 IU of vitamin D in a day's
supply.

Car seat
All infants must be transported in a car seat, following AAP guidelines
(http://www.healthychildren.org/English/safety-prevention/on-the-go/pages/Car-Safety-Seats-Information-for-
Families.aspx?nfstatus=401&nftoken=00000000-0000-0000-0000-
000000000000&nfstatusdescription=ERROR%3a+No+local+token).

Sleep position and co-sleeping

The Back to Sleep program has resulted in a significant decrease in the incidence of sudden infant
death syndrome (SIDS). Ensure that parents are aware of the guidelines. Co-bedding of an infant
with an adult increases the risk of death by suffocation should the adult accidentally roll onto the
infant. The AAP recommends that infants not bed share during sleep. Infants may be brought into
bed for nursing or comforting but should be returned to their own bassinet or crib when the parent
is ready to return to sleep. The infant should not be brought into bed when the parent is
excessively tired or using medications or substances that could impair his or her alertness. The
task force recommends that the infant's bassinet or crib be placed in the parent's bedroom, which
will allow for convenient breastfeeding and contact. Infants also should not bed share with other
children.

The AAP has established policy guidelines on hospital discharge, safe transportation of newborns,
breast feeding, sleeping position and SIDS, and vitamin D supplementation.
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Clinical Skills

Communicating with the Parent of an Ill Child

When discussing medical problems that are evolving, it is important to be clear about what you
know and what the next steps in the evaluation will be. It is difficult to balance the need to reassure
parents and help them understand the potentially serious causes of their child's symptoms.

Clinical Reasoning

Differential Diagnosis for Tachypnea in the Newborn

Diagnosis Comments Respiratory distress syndrome (RDS) Transient tachypnea of the newborn
(TTN) Pneumothorax Hypoglycemia Congestive heart failure (CHF) Neonatal sepsis Congenital
diaphragmatic hernia Severe coarctation of the aorta Meconium aspiration Maternal drug
exposure Hypothermia

Caused by a deficiency of lung surfactant and delayed lung maturation

Can occur as late as 37 weeks' gestation
Most common cause of respiratory distress in premature infants
Remember that there may be surfactant deficiency and delayed lung maturation in infants of
diabetic mothers

Result of delayed clearance of fluid from the lungs following birth

Much more common in infants born to diabetic mothers and in infants born by c-section
While generally considered a disorder of term infants, TTN does occur in premature infants

Caused by a collection of gas in the pleural space with resultant collapse of lung tissue
Common risk factors are mechanical ventilation or underlying lung disease (especially
meconium aspiration or severe infant respiratory distress syndrome).
While relatively uncommon, always an important consideration in an infant with respiratory
distress
More likely in a premature infant with RDS

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 May be seen in infants of diabetic mothers due to the chronic hyperinsulinemic state that
occurred during gestation
Can be more pronounced in premature infants
Tachypnea is a non-specific response to this metabolic derangement

In an infant, most often caused by a congenital heart defect

May present with early cardiac failure and tachypnea
Increased risk of heart defects in IDM infants, and therefore an increased risk of CHF

Can present initially with tachypnea and progress to more severe illness rapidly
Often due to infection with Group B Streptococcus (GBS), usually transmitted from the
mother during labor
Prolonged PROM is associated with an increased incidence of neonatal sepsis

Malformation resulting from a defect in the development of the diaphragm

Allows the passage of organs from the abdomen into the chest cavity and severely impairs
lung development
Most defects occur on the left side
Occurs in 1 out of every 2,200 to 5,000 live births
Most common type (accounting for > 95% of cases) is the Bochdalek hernia, which is
located posterolaterally
Absent breath sounds or presence of bowel sounds on one side of the chest are important
diagnostic clues

May cause respiratory distress if there is severe left ventricular outflow tract obstruction

Infants who aspirate meconium in utero or at the time of delivery often present with
symptoms of respiratory distress, including tachypnea

Maternal medication use may lead to tachypnea in the newborn

Low core temperature can lead to tachypnea

Premature newborns are more at risk to become hypothermic because of their small body
size

Studies

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Studies for the Evaluation of a Cyanotic Newborn

Arterial blood gases Blood and CSF cultures CBC with differential Chest radiograph
Echocardiogram Oxygen challenge test (hyperoxia test) Physical examination Pulse oximetry

These show the oxygenation, ventilation, and acid-base status of the infant.
Knowing the pCO2 is very helpful in understanding the cause of the cyanosis.

To identify infectious organism if sepsis is suspected

Useful to rule out neutropenia, leukopenia, abnormal immature-to-total-neutrophil ratio, and

thrombocytopenia as signs of sepsis.

Integral part of the initial assessment of the newborn with respiratory distress.
The size and the shape of the heart may yield some clues to the diagnosis.
The appearance of the lungs may suggest pneumonia, meconium aspiration, RDS,
pneumothorax, etc.
Normal inspiratory films should have eight or more intercostal spaces of lung fields on both
sides.

Gold standard in the diagnosis of congenital cardiac lesions and PPHN.

Indicated when there is persistent cyanosis and no indication of lung disease, or when
there are other signs suggesting a heart defect, such as a murmur, an abnormal ECG or a
chest x-ray showing an abnormal cardiac contour.

Valuable tool that can help differentiate between cardiac and pulmonary etiology in
cyanotic infants.
In brief, oxygen will increase the PaO2 of an infant whose cyanosis is caused by a
respiratory condition, but will not significantly increase the PaO2 if a cardiac lesion
causes cyanosis.

This test is described in some detail in the article by Sasidharan (see below).

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 Critical to identify heart murmurs and respiratory findings that might be the cause of the
cyanosis.
Remember, however, that some murmurs may not be present early in life because of the
elevated pulmonary vascular pressure.

Detects oxygen saturation in the blood.

Evaluation of Tachypnea in the Newborn

Laboratory and radiological evaluation of a tachypneic newborn should include the following:

CBC with differential Serum or plasma glucose level Blood culture CSF for culture Blood gas or
pulse oximetry monitoring Chest x-ray

Obtaining a CBC with differential is appropriate due to the possibility that respiratory
distress may be caused by sepsis.

This may be needed to confirm a low glucometer reading.

Tachypnea may be the only sign of early sepsis or pneumonia.

Performing a lumbar puncture is part of the evaluation for any newborn in whom sepsis or
meningitis is suspected
It is important to remember that the very young infant with sepsis and/or meningitis may
have no localizing signs and only subtle clinical symptoms, such as temperature instability,
lethargy, and poor feeding.

Blood gas should be considered in this case because of the tachypnea, which can be a
manifestation of respiratory distress.

Measurement of ABGs is used to assess oxygenation (PaO2), retention of carbon dioxide

(PaCO2), and acid-base states (pH and HCO3).
If the respiratory distress is mild, the infant pink in color, and the infant is not otherwise at
risk, blood gas determination is not essential.
Other risk factors for hypoxemia would include shock, severe sepsis, CNS depression, and
perinatal asphyxia.

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 Imaging the chest will assist in the evaluation of possible TTN, RDS, pneumonia, or
structrual abnormality that may be causing the tachypnea.

Comparison of Chest X-ray Findings

Transient tachypnea of the newborn (TTN) Respiratory distress syndrome (RDS) Diaphragmatic
hernia Neonatal pneumonia
This x-ray will show "wet" looking lungs, no consolidation, and no air bronchograms.
An infant with RDS would have radiographic findings that typically include a diffuse
reticulogranular appearance of the lung fields ("ground glass appearance") and air
bronchograms. X-ray of a newborn with RDS.
Most often a diaphragmatic hernia develops on the left side. A radiograph shows air-filled loops
of bowel in the left side of the chest, displacing the heart and mediastinum to the contralateral
side. X-ray of newborn with a diaphragmatic hernia.
X-ray findings of pneumonia may appear similar to those of an infant with TTN, but the clinical
findings would be much more concerning for sepsis.

Hyperlink "X-ray of a newborn with RDS. "

This Multimedia material is not included in this Summary, please open Case to review.

Hyperlink "X-ray of newborn with a diaphragmatic hernia. "

This Multimedia material is not included in this Summary, please open Case to review.

Management

Treatment of Hypoglycemia in the Neonate

Testing
The glucometer test is a screening test only, and must not be used to confirm hypoglycemia.
Glucose oxidase reagent strips are read by meter (glucometer) or by eye (Dextrostix, Chemstrip)
and measure whole blood glucose, which is 10-15% lower than plasma glucose levels. These
reagent strips are widely used as screening tools for hypoglycemia and may also be used for
ongoing monitoring of glucose levels.

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Any reagent-strip reading of whole blood glucose < 40 mg/dL must be confirmed by laboratory
analysis of serum or plasma glucose. Treatment should be started immediately, not delayed until
laboratory results are available.

Treatment
The choice of intervention depends on presence or absence of symptoms of hypoglycemia and
any additional problems such as tachypnea. Breastfeeding or bottle feeding of pumped breast milk
or formula depends on the ability of the infant to take feedings orally. Tachypnea may prevent
adequate intake of glucose via oral feeds. In this situation, placement of a nasogastric tube and
administration of either breast milk or formula would be appropriate, with resumption of breast or
bottle-feeding as soon as the respiratory rate allows.

If the baby is symptomatic from hypoglycemia, an intravenous infusion of dextrose should be

started immediately as it guarantees a stable source of glucose.

Most pediatricians would not give 5% glucose in water to a hypoglycemic infant, and if they did, the
infant would be fed with breast milk or formula as soon as possible after the glucose.

Glucose water does raise the serum glucose level, but only transiently.
Rebound hypoglycemia often develops 1-2 hours after feeding glucose water if the infant is
hyperinsulimemic (i.e., the infant of a diabetic mother).

Milk feeding (formula or breast) raises glucose levels, maintains stable levels, and avoids rebound
hypoglycemia.

Monitoring
Once feeds have been initiated, glucose levels should be closely monitored until levels are stable
(> 45 mg/dL). The frequency of monitoring will depend on the severity of the hypoglycemia and
may range from every 30 minutes to every 3 hours prior to feeds.

References

American Academy of Pediatrics and The American College of Obstetricians and Gynecologists.
Guidelines for Perinatal Care, 7th edition. Elk Grove Village, IL: AAP; 2012.

Escobar GJ, et al. Stratification of risk of early-onset sepsis in newborns > 34 weeks' gestation.
Pediatrics. 2014;133(1):30-36.

Polin RA and Committee on Fetus and Newborn. Management of neonates with suspected or
proven early-onset bacterial sepsis. Pediatrics. 2012;129(5):1006-1015.

Schuchat A, Zywicki SS, Dinsmore MJ, et al. Risk factors and opportunities for prevention of early-
onset neonatal sepsis: a multicenter case-control study. Pediatrics. 2000;10:21-24.

American Academy of Pediatrics Committee on Fetus and Newborn and the American College of
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American Academy of Pediatrics Committee on Fetus and Newborn and the American College of
Obstetricians and Gynecologists Committee on Obstetric Practice. The Apgar score. Pediatrics.
2006;117(4):1444-1447. (See the statement online
(http://pediatrics.aappublications.org/content/117/4/1444.full.pdf+html).)

American Academy of Pediatrics Committee on Fetus and Newborn and the American College of
Obstetricians and Gynecologists Committee on Obstetric Practice. The Apgar score. Pediatrics.
2015;136(4):819-822. (See the statement online (http://pediatrics.aappublications.org/content/136/4/819).)

Dupak DL, Trujillo AL. Ultrasound surveillance in pregnancy complicated by diabetes. Journal of
Reproductive Medicine. 2006;51:515-520.

Surkan PJ, Stephansson O, Dickman PW, et al. Previous preterm and small-for-gestational-age
births and the subsequent risk of stillbirth. New England Journal of Medicine. 2004;350:777-785.

Hermansen CL, Lorah KN. Respiratory Distress in the Newborn. American Family Physician.
2007;76:987-994.

Giannakos-Lennox, E. Congenital Heart Disease. In: Tschudy MM. Arcara KM. The Harriet Lane
Handbook, 19th edition. 2011: 183-185.

Kemper AR, Mahle WT, Martin GR, Cooley WC, Kumar P, Morrow WR, Kelm K, Pearson GD,
Glidewell J, Grosse SD, Howell RR. Strategies for implementing screening for critical congenital
heart disease. Pediatrics. 2011;128(5):e1259-1267.

Mahle WT, Martin GR, et al. Section on Cardiology and Cardiac Surgery Executive Committee.
Endorsement of Health and Human Services recommendation for pulse oximetry screening for
critical congenital heart disease. Pediatrics. 2012;129(1):190-192

Sasidharan P. An approach to diagnosis and management of cyanosis and tachypnea in term

infants. Pediatric Clinic North America. 2004;51:999-1021.

Studer MA, Smith AE, Lustik MB, and Carr MR. Newborn pulse oximetry screening to detect critical
congenital heart disease. J Pediatr. 2014;164:505-509

Reece EA, Homko C. Why do diabetic women deliver malformed infants? Clinical Obstetrics and
Gynecology. 2000;43(1):32-45.

Vogelhutt J. Breast Feeding. In Seidel HM, Rosenstein BJ, Pathak A. Primary Care of the Newborn
4th ed.; St. Louis MO: Mosby; 2006;25:372-382.

Adamkin DH and Committee on Fetus and Newborn. Clinical Report: Postnatal glucose
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Adamkin DH and Committee on Fetus and Newborn. Clinical Report: Postnatal glucose
homeostasis in late-preterm and term infants. Pediatrics. 2011;127(3):575-579

Pildes RS, Pyati SP. Hypoglycemia and hyperglycemia in tiny infants. Clinics in Perinatology.
1986;13:351-375.

Koh TH, Aynsley-Green A, Tarbit M, Eyre JA. Neural dysfunction during hypoglycemia. Arch Dis
Child. 1988;63:1353-1358.

Cornblath M. Metabolism and Endocrinology. In Seidel HM, Rosenstein BJ, Pathak A. Primary
Care of the Newborn (Fourth Edition); Mosby, 2006;23:354-357.

Cornblath M, Hawdon JM, Williams AF, et al. Controversies regarding definition of neonatal
hypoglycemia: suggested operational thresholds. Pediatrics. 2000;105:1141-1145.

Cornblath M, Ichord R. Hypoglycemia in the neonate. Semin in Perinatol. 2000;24(2):136-149.

Brady MT, Polin RA. Prevention and management of infants with suspected or proven neonatal
sepsis. Pediatrics 2013;132;166-168

Brouillette RT, Waxman DH. Evaluation of the newborn's blood gas status. Clinical
Chemistry 1997;43(1):215-221.

Camacho-Gonzalez A, Spearman PW, Stoll BJ. Neonatal infectious diseases: evaluation of

neonatal sepsis. Pediatr Clin North Am. 2013; 60(2); 367-389

Polin RA and the Committee on Fetus and Newborn. Management of neonates with suspected or
proven early-onset bacterial sepsis. Pediatrics, 2012;129(5); 1006-1015.

Dubowitz LMS et al. Clinical significance of gestational age in the newborn infant. Journal of
Pediatrics. 1970; 77: 1.

Ballard JL et al. A simplified score for assessment of fetal maturation of newly born infant. Journal
of Pediatrics. 1979; 95: 769.

Ballard JL et al. New Ballard Score, expanded to include extremely premature infants. Journal of
Pediatrics. 1991; 119 (3): 417.

American Academy of Pediatrics. Clinical Practice Guideline: Early detection of developmental

dysplasia of the hip. (http://pediatrics.aappublications.org/content/105/4/896.full.pdf+html) Pediatrics,
2000;105(4):896-905.

American Academy of Orthopedic Surgeons. Detection and non-operative management of

pediatric developmental dysplasia of the hip in infants up to six months of age: evidence-based

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clinical practice guideline. Pediatrics. 2015;136(4): e1141

Bickley LS. Bates Guide to Physical Examination and History Taking, 9th Ed. Philadelphia,
Pennsylvania. Lippincott Williams and Wilkins; 2007:727-728.

McAbee GN, Donn SM, Mendelson RA, et al. Medical diagnoses commonly associated with
pediatric malpractice lawsuits in the United States. Pediatrics. 2008;122:e1282

Patel H, the Canadian Task Force on Preventive Health Care. Preventive health care, 2001
update: screening and management of developmental dysplasia of the hip in newborns. CMAJ.
2001;164(12):1669-1677

U.S. Preventive Services Task Force. Screening for developmental dysplasia of the hip:
recommendation statement. Pediatrics. 2006;117:898-902.

Colvin JD, Collie-Akers V, Schunn C, and Moon RY. Sleep environment risks for younger and
older infants. Pediatrics. 2014;134(2):e407-412.

Hospital discharge: Committee on Fetus and Newborn. Hospital stay for healthy term newborns.
Pediatrics. 2004;113(5);1434-1436. http://pediatrics.aappublications.org/content/113/5/1434.full.pdf
Published May 4, 2004. Updated February 1, 2010.

Safe transportation: Committee on Injury and Poison Prevention. Safe transportation for newborns
at discharge. Pediatrics. 1999;104(4); 986-
987. http://pediatrics.aappublications.org/content/104/4/986.full.pdf+html

Breastfeeding: Section on Breastfeeding. Breastfeeding and the use of human milk. Pediatrics.
2005;115(2);496-506. http://pediatrics.aappublications.org/content/115/2/496.full.pdf+html
(http://pediatrics.aappublications.org/content/115/2/496.full.pdf+html)

Sleeping position and SIDS: Task Force on Sudden Infant Death Syndrome. The changing
concept of sudden infant death syndrome: diagnostic coding shifts, controversies regarding the
sleeping environment, and new variables to consider in reducing risk. Pediatrics.
2005;116(5);1245-1255 http://pediatrics.aappublications.org/content/116/5/1245.full.pdf+html

Vitamin D supplementation: Wagner CL, Greer FR, and the Section on Breastfeeding and
Committee on Nutrition. Prevention of rickets and vitamin D deficiency in infants, children, and
adolescents. Pediatrics. 2008;122(5);1142-1152.
http://pediatrics.aappublications.org/content/122/5/1142.full.pdf+html

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