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Late Preterm Infants 461

28 Late Preterm Infants

IntroductIon

Although often considered healthy, especially in comparison to their extremely premature counterparts, a growing body of evidence shows these infants are at substantial risk of neonatal and long-term morbidities, as well as mortality.

The decision to proceed with delivery, whether medically indicated or sec-ondary to preterm labor/premature rupture of membranes (PROM), requires balancing the consequences of continued pregnancy to both the mother and the baby.

I. Intensive careSome, but not all of late preterm (LPT) infants will require intensive care, while others may be cared for safely in the term nursery. Available term nursery resources, including expertise with LPT infants and nurs-ing availability, may dictate where the well-appearing LPT infant should be admitted.

A. Definition1. Infants born LPT are between 34 and 0/7 weeks’ to 36 and

6/7 weeks’ gestation.2. LPT infants are more likely to require assistance at delivery and

their deliveries should be attended by at least one person with expertise in newborn care and resuscitation.

3. Risk factors should be evaluated and assessment performed at delivery to allow proper admission of the infant to either the neonatal intensive care unit or the normal newborn nursery.

B. Incidence1. Premature infants account for more than 10% of deliveries; LPT

infants constitute the largest portion of prematurely delivered infants accounting for over 71% of all preterm births.

2. LPT infants frequently require intensive care unit (NICU) admission. Overall rates of NICU admission for LPT infants vary from 35% to 75% by center, with a smaller component of transfer from term nursery. Rates of NICU admission are inversely cor-related with gestational age: 34 weeks: 43% to 100%, 35 weeks: 22.5% to 43%, 36 weeks: 12.3% to 40.5%.

3. Many centers routinely admit all babies less than 35 weeks to a special care unit.

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462 MEdIcAL cArE oF tHE PrEtErM InFAnt

4. Growing national and international awareness of the conse-quences of LPT birth has finally led to a decrease in birth rates: following a steady increase in the number of infants born LPT since 1981, this number has now decreased each year since 2006. However, more than 339,000 LPT infants born in the United States in 2010 still create a substantial economic and health care burden.

C. Pathophysiology1. LPT infants are at risk for illness at birth due to both their

immaturity and a high incidence of complicated pregnancies in this group.

2. LPT infants are often the product of a medically complicated pregnancy and delivered by cesarean section, which further increases the risk to the neonate.

3. Immaturity causes delayed clearance of lung fluid, risk of respiratory distress syndrome, and increased risk of apnea.

4. LPT infants are also at increased risk for hypothermia, hypogly-cemia, and feeding difficulties due to their small size and imma-ture feeding skills.

5. There is also a higher risk on neonatal sepsis in pregnancies com-plicated by PROM and chorioamnionitis.

D. Risk factors1. Birth at each week earlier in gestation is a strong risk factor for

NICU admission.2. Maternal illness, including diabetes and preeclampsia, also

increases the risk for an LPT delivery and NICU admission. 3. Cesarean delivery in the absence of labor also increases the risk of

respiratory distress and requirement for NICU care. 4. Other pregnancy complications, including placental abruption,

bleeding, and PROM increase the risk for hypoxic events and infection, and thus both NICU admission and death.

5. Intrauterine growth restriction and infants born small for gesta-tional age (SGA, <10% tile) are also more likely to require NICU admission and have a higher risk of mortality.

E. Clinical presentation1. Signs and symptoms

To avoid NICU admission, the LPT infant must be well appearing in all areas.a. Any cardiorespiratory instability should be an indication for NICU

admission including hypoxia, tachypnea (respiratory rate >60), increased work of breathing, apnea, or heart rate instability.



b. Hypothermia and hypoglycemia that are unresponsive to simple interventions should also require ICU care (see below).

c. The infant must also demonstrate readiness to feed and an interest is feeding.

2. Clinical variability There is a wide variety of clinical presentations based on gesta-tional age, gender, pregnancy, and delivery factors. Each infant must be assessed individually.

F. Diagnosis1. Prenatal care allows for dating and best estimate of gestational

age, but evaluation of maturity should also be done at delivery. All suspected LPT infants should have a New Ballard Score Maturational Assessment of Gestational Age performed in order to accurately assess the level of maturity (Figure 28-1).

2. Patients may be younger or older than expected. 3. Evaluation should also be done for physiologic factors that

require ICU care.

G. ManagementAs shown in Figure 28-2, the composite incidence of respiratory distress, infection, hypoglycemia, feeding difficulties, and other neonatal morbidities is seven times higher in LPT infants com-pared to those born at term. Risk factors should be evaluated and a clinical assessment at delivery performed including assessment of gestational age, weight, respiratory distress, systemic illness, and readiness to feed to allow proper admission of the infant to either to neonatal intensive care unit or the normal nursery. Whether admitted to the NICU or term nursery, LPT infants need close observation. Because of the high risk of morbidities and NICU admission, some units choose to admit all infants born prior to 35 weeks’ gestation.

1. Respiratory distress syndromeRespiratory distress syndrome (RDS) is the pattern of hypoxia, poor gas exchange, and respiratory failure due to lung immatu-rity and insufficient production of pulmonary surfactant. a. RDS is significantly more common in LPT infants than those

born at term, occurring in 4% to 5% versus <0.1%. It is the most common cause of respiratory distress in LPT infants and the most common reason for NICU admission.

b. Incidence varies by gestational age and is highest at 34 weeks (10.6%), decreasing at 35 (6.0%) and 36 weeks (2.7%).



Incidence is also higher in early term (37 and 0/7 to 38 and 6/7) infants. Mechanical ventilation is required in 2% to 3% of LPT infants; this is primarily for RDS.

c. Pulmonary surfactant is composed of phospholipids and proteins produced by type II alveolar cells in the distal lungs and acts to reduce surface tension in the alveoli. This improves pulmonary compliance and decreases the pressure necessary to keep the alveoli open, preventing atelectasis. Surfactant production increases with advancing gesta-tional age with a surge at 35 weeks, but full production is not present until term.

NEUROMUSCULAR MATURITY

SIGNSCORE SIGN

SCORE

TOTAL NEUROMUSCULAR SCORE

MATURITY RATING

−10

TOTAL SCORE WEEKS

20

22

0 24

5 26

10 28

15 30

20 32

25 34

30 36

35 38

40 40

45 42

50 44

SIGNSCORE SIGN

SCORE−1 0 1 2 3 4 5

−1 0 1 2 3 4 5

Skin

Posture

Square

Window

Arm

Recoil

Popliteal

Angle

Scarf

Sign

Heel to

Ear

sticky, friable,

transparent

gelatinous, red,

translucentsmooth pink, visible veins

superficialpeeling and/or rash, few

veins

cracking, pale areas, rare veins

parchment, deep cracking,

no vessels

leathery,

cracked,

wrinkled

Lanugo none sparse abundant thinning bald areas mostly bald

Plantar

Surface

heel-toe40-50 mm: –1

<40 mm: –2>50 mm

no creasefaint red

marksanterior

transverse crease only

creases ant. 2/3

creases over entire sole

Breast imperceptable barely perceptable

�at areolano bud

stippled areola1-2 mm bud

raised areola full areola

5-10 mm bud

Eye/Earlids fusedloosely: –1tightly: –2

lids openpinna �at

stays folded

sl. curved pinna; so�; slow recoil

well-curved pinna; so� but

ready recoil

formed and firm

instant recoil

thick cartilageear sti�

Genitals

(Male)

scrotum �at, smooth

scrotum empty,

faint rugae

testes in upper canal,rare rugae

testes descending,few rugae

testes down,

good rugae

testes pendulous,deep rugae

Genitals

(Female)

clitorisprominent

and labia flat

prominentclitoris andsmall labia

minora

prominentclitoris andenlarging minora

majora andminora equally

prominent

majora large,minora small

majora cover clitoris and

minora

TOTAL PHYSICAL MATURITY SCORE

Gestation by Dates

weeksBirth date Hour

APGAR 1 min 5 min

ScoringGest. Age by Maturity Rating ________weeksTime of Exam Date_________

Hour______ Age at Exam

_________hoursSignature of Examiner

M.D. / R.N.

>90° 90°

180°

180°

140°–180° 110°–140° 90°–110° <90°

<90°

60° 45° 30° 0°

160° 140° 120° 100° 90°

−5

3-4 mm bud

ampm

ampm

Figure 28-1 The new Ballard score. (Reproduced with permission from Ballard JL, Khoury JC, Wedig K, et al: New Ballard Score, expanded to include extremely premature infants. J Pediatrics. Sep 1991;119(3):417-423. Copyright Ballard Score.)



d. Prematurity is the most important risk factor, but absence of spontaneous labor and delivery by cesarean section also increase risk.

e. RDS is characterized by tachypnea with evidence of increased work of breathing (nasal flaring, retractions, grunting), and hypoxia. • Respiratory examination often reveals poor air entry. • Blood gas analysis may reveal hypoxia (PaO2 <80) and

hypercarbia (PaCO2 >50). • Typical chest x-ray (CXR) findings include opacification

(“ground-glass” appearance), air bronchograms, and atelec-tasis; the heart borders may be obscured.

f. There is large variability in clinical appearance with some infants having mild disease and other in fulminant respi-ratory failure; this does not always correlate with CXR appearance. There is often overlap with other neonatal causes of respiratory distress, including transient tachypnea of the newborn and pneumonia.

g. RDS is a clinical diagnosis, made in infants that fit the clin-ical picture as described above and respond to therapies, including exogenous surfactant.

34

35

36

37

38

39

40

41

34-36

37-41

0

3.0

22.2

2.6

3.3

5.9

12.1

25.6

51.7

2.5

2.8

10 20 30Morbidity risk, percentage

Ges

tatio

nal a

ge, w

eeks

40 50 60

Figure 28-2 Composite risk of neonatal morbidities varies inversely with gestational age. (Adapted with permission from Shapiro-Mendoza CK, Tomashek KM, Kotelchuck M, et al. Effect of late-preterm birth and maternal medical conditions on newborn morbidity risk. Pediatrics. Feb 2008;121(2):e223-232.)



h. Management includes• Respiratory support should be given as needed to treat

hypoxia, hypercarbia, and work of breathing. Oxygen administration alone is often insufficient and can be detri-mental: Affected infants usually require positive end expi-ratory pressure (PEEP) in the form of continuous positive airway pressure (CPAP) or intubation.

• Intubated infants should receive surfactant. • Further details of respiratory care are described in Chapter 7.• Prenatal administration of betamethasone, which decreases

the risk of RDS in more preterm infants, has not been shown to be helpful in LPTs.

i. Prognosis• Infants that require only CPAP or respond well to a single

dose of surfactant often recover and have a low incidence of permanent sequelae. Infants intubated more than 6 hours are more likely to have prolonged courses and have a higher risk of mortality.

• Despite their relatively large size, LPT infants can have severe RDS, resulting in prolonged hospital stays, pulmo-nary hypertension, need for extracorporeal membrane oxygenation (ECMO), and even death.

• Chronic lung disease, or bronchopulmonary dysplasia, is diagnosed in ~3% of LPT infants.

• Mortality from severe RDS is around 1%; this is responsible for a significant component of the mortality in LPT infants. However the large majority of infants recover well, without permanent sequelae.

2. Transient tachypnea of the newbornTransient tachypnea of the newborn (TTN) is characterized by significant tachypnea with mild increase in work of breathing that results from delayed resorption of fetal lung fluid.a. TTN is generally considered the second most common cause

of respiratory distress in the LPT infant, occurring in 3% to 4% of the population, though in some studies it is more common than RDS.

b. Once again, incidence is increased at lower gestational ages: The Consortium on Safe Labor found the incidence of TTN was high-est at 34 weeks (64/1000 births) and 35 weeks (46/1000 births) and decreased with advancing gestational age until 39 weeks.



c. The primary mechanism causing TTN is delayed resorp-tion of fetal lung fluid, a complex process that is now understood to begin several days before spontaneous delivery. Hormonal changes that accompany labor and the addition of exposure to oxygen and mechanical stretch at delivery cause the lung epithelium to become a highly effective absorptive surface. The sodium selective epithe-lial channel, ENaC, plays an essential role via active sodium transport. ENaC production is developmentally regulated with lower levels in preterm infants, especially those with evidence of respiratory distress and TTN.

d. In addition to prematurity, maternal and infant factors can increase the risks of TTN. • Maternal diabetes.• Maternal asthma.• Cesarean delivery, especially in the absence of labor. This

effect is exaggerated in preterm infants. • Macrosomia.• Polyhydramnios.• Male gender.

e. Infants present with marked tachypnea beginning in the first 4 hours of life (80 to 140 breaths/min), mild cyanosis, mild work of breathing, no evidence of infection, classic CXR findings (see below), and resolution by 2 to 5 days.

f. There is wide variability with many infants having mild tachypnea that requires only observation and others with more significant tachypnea necessitating nutritional support and supplementary oxygen. A very small portion of neonates with TTN will have fulminant respiratory failure that requires mechanical ventilation and substantial support.

g. History, clinical appearance, and CXR findings are used in the diagnosis of TTN. Characteristic CXR findings consis-tent with TTN include hyperinflation with flattened dia-phragms, signs of vascular congestion including increased perihilar markings, fluid in the interlobar fissures, and mild streaky opacity that is uniform across lung fields. There is no specific testing that confirms the diagnosis of TTN.

h. The mainstay of treatment for TTN is supportive care, as there are no specific targeted therapies that are standard of care. Infants whose primary symptom is tachypnea, without hypoxia or signs of increased work of breathing such as



grunting or retractions, may be observed until symptom reso-lution without specific respiratory treatment.

i. Tachypnea that is accompanied by additional signs of respiratory distress, hypoxia, persists longer than 6 hours, or is accompanied by other systemic symptoms merits an evaluation and presump-tive treatment for sepsis as well as the appropriate respiratory support. Supplemental oxygen should be provided to keep satu-rations >95% with additional support as needed.

j. The prognosis for TTN is generally excellent, with full recovery expected in two-thirds to three-quarters of infants by 72 hours. Rapid resolution of symptoms is seen in majority of the infants. However, secondary complica-tions including prolonged tachypnea, respiratory failure, pulmonary hypertension, acidosis, and air leak syndrome can occur; this is estimated in less than 10% of infants with TTN. Long-term morbidities and mortality are rare and mostly occur in infants with severe illness and secondary complications.

3. Hypoglycemiaa. Generally defined as a blood sugar <40 mg/dL in the first

4 hours and <47 mg/dL thereafter is considered hypoglycemia. However, here is no firm consensus definition as healthy infants may have blood sugars <40 mg/dL in the early hours of life that resolve spontaneously. Symptomatic or persistent hypoglycemia that does not respond to feeding is of much larger concern.

b. The incidence is estimated at 6% to 15% in LPT infants and varies with gestational age, size, risk factors, and definition of hypoglycemia, but may be even higher if close screening is done.

c. At birth the infant is separated from a constant energy sup-ply and must transition to enable glucose homeostasis. • LPT infants have immature liver mechanisms for

gluconeogenesis and decreased energy stores. • Infants born to diabetic mothers (IDM) frequently have bet-

ter stores but may have excessive insulin production result-ing in hypoglycemia.

• Poor oral feeding skills are common in LPT infants and con-tribute to the problem.

d. Large for gestational age (LGA) and SGA infants are at increased risk for hypoglycemia. IDM infants are at high risk and may have prolonged hypoglycemia. Respiratory distress and systemic ill-ness both increase the risk for delayed feeding and hypoglycemia.



e. Infants may initially present with fussiness, irritability, jit-teriness or tremors, and poor feeding. More severe symp-toms include lethargy, seizures, poor tone, abnormal cry, and eventually apnea and coma.

f. There is a substantial variability in level, which results in symptoms, with some infants asymptomatic even at glucose <30 mg/dL.

g. Bedside glucose test strips may be used for screening, but are unreliable at low and high glucose levels. STAT serum glucose level should be evaluated in the laboratory for symptomatic infants or those with low screens.

h. Medical management of LPT infants and those with risk factors should be screened routinely for hypoglycemia. • Three normal levels prior to feeds are sufficient in well infants

with adequate oral intake, though those with risk factors require more prolonged screening (48 to 72 hours).

• Asymptomatic infants can be initially fed by mouth or gavage fed, though intravenous (IV) glucose may be required.

• Symptomatic infants should be treated with IV dextrose immediately with the level rechecked after treatment.

• Treatment is discussed in more detail in Chapter 20. The Committee on Fetus and Newborn has published general guidelines for management.

i. Hypoglycemia that is easily treatable with oral, orogastric feeds or small amounts of IV dextrose usually resolves quickly with-out permanent sequelae. Brief, transient, and asymptomatic hypoglycemia has a good prognosis, regardless of glucose level. Infants of diabetic mothers often have longer courses and require IV glucose but will eventually self-resolve. Pro-longed, repeated, and significant (<40 mg/dL) hypoglycemia requires more of a workup and is associated with neuronal cell death with serious neurodevelopmental sequelae.

4. Thermoregulation and hypothermiaa. Normothermia is conventionally defined as a temperature

from 36.5°C to 37.4°C. Lower temperatures, especially under 36.0°F, can lead to cold stress and compromise infant well-being.

b. Up to 30% of infants in term nursery may have a tempera-ture <36.5°C. Incidence of lower temperatures (<36.0°C) is up to 40% in LPT infants treated in term nurseries. Risk of hypothermia in the NICU, where infants are often in ser-voregulated beds, is lower, around 2%.



c. Delivery removes the maternal heat source and requires the neo-nate to make a rapid adjustment to maintain his own tempera-ture. The largest part of heat losses are evaporative and radiation losses to the external world. Heat is normally generated through oxidation of brown adipose tissue. Preterm infants are deficient in adipose tissue and have thin, unkeratinized skin, leading to decreased heat production and increased loss.

d. Lower gestational age and size, low birthweight (<2500 g), and SGA infants are at increased risk. Maternal diabetes is protective.

e. Hypothermia/cold stress can present with shivering, increased respiratory distress, poor perfusion, hypoglycemia, metabolic acidosis, and apnea. It can be difficult to differentiate from sepsis.

f. Depending on size and degree of prematurity, some LPT infants will have adequate thermoregulation.

g. Central temperature should be taken for accurate diagno-sis, usually via the axilla or rectally. LPT infants should be monitored rather than waiting for the onset of symptoms.

h. For managing the LPT infant at risk for hypothermia, tem-perature should be monitored every 3 to 4 hours until the infant has demonstrated good thermoregulation while lightly dressed with one thin blanket. • Infants being cared for in the term nursery should also be

monitored for at least 24 hours. • Persistent hypothermia may require NICU admission and

evaluation for sepsis. • Effective drying at delivery and avoiding early baths

(<4 hours) may help prevent hypothermia. • Small infants (<2000 g) may require an isolette to maintain

temperature and avoid radiant loss.i. Though easily treatable, hypothermia can worsen respiratory

illness or hypoglycemia and require additional care. Hypo-thermia is associated with increased mortality in extremely premature infants but this association has not been shown for LPTs.

5. Sepsis/pneumoniaa. Bacterial or viral infection can occur in the neonate prior to,

during, or after delivery. LPT infants are at increased risk of infection both in the peripartum and early neonatal period.

b. The nonspecific nature of the symptoms of sepsis means a larger portion of LPT infants are treated with antibiotics



(14.6% to 37.1%), though less than 2% will have culture proven sepsis. Suspected or diagnosed infection is also a common reason for readmission of the LPT infant.

c. Perinatal infection and chorioamnionitis are implicated in preterm birth and may be the reason an infant is delivered prematurely. In addition, an immature immune system and decreased transfer of maternal antibodies in the LPT infant increase the risks of infection and disease severity in the first several weeks of life.

d. Known risk factors for infection include maternal fever, chorioamnionitis, malodorous amniotic fluid, prolonged rupture of membranes, and fetal tachycardia. However, a large number of infants diagnosed with sepsis have no doc-umented risk factors.

e. Signs of infection include temperature instability, hypoglycemia, poor feeding, tachypnea, and apnea in the early stages, and may not be distinguishable from consequences of prematurity itself. Specific symptoms of infection are rare, which necessitates a low threshold for evaluation and treatment.

f. There is wide variability in symptomatology with some infants having mild symptoms and others presenting severely ill with cardiovascular and respiratory collapse.

g. Infants with the above signs and symptoms should have eval-uation for sepsis with a blood culture and CBC. Inflammatory markers, such as C-reactive protein (CRP) and erythrocyte sedi-mentation rate (ESR) are nonspecific but trending values can be useful in infants with a prolonged course. Additional evaluation, including lumbar puncture, is done on a case-by-case basis.

h. Supportive care and antibiotic therapy are mainstays of treatment. Ampicillin, which covers group B Streptococcus and Listeria, is usually appropriate in combination with a gram-negative agent, such as gentamycin. Local resistance patterns and any antibiotic treatment of the mother during pregnancy should be taken into account.

i. Early treatment of suspected sepsis is key as there is signifi-cant morbidity and mortality if the neonate is severely ill when treatment begins. Infants that are diagnosed quickly without significant systemic illness do well and often have a quick recovery. Long-term sequelae are dependent on degree of illness and compounding factors, such as men-ingitis. Full recovery is expected in infants with minimal symptoms. Infants presenting in shock with respiratory



and cardiovascular failure or coagulopathy have substantial morbidity and mortality.

H. Early developmental/therapeutic interventions 1. Feeding therapy

a. Use of a speech or occupational therapist skilled at infant feeding may be helpful; however, slow oral feeding is likely just a sign of immaturity in the LPT infant and will resolve with or without therapy.

b. A lactation specialist is useful to support the mother and her breast-feeding infant.

2. Physical therapyAn LPT infant with a prolonged NICU stay may benefit from a PT consult to evaluate positioning, state regulation, and early gross motor skills, as well as parent education on the expected patterns of development in preterm infants.

I. Prognosis1. Early predictors

a. Older, larger infants are more like to remain in term nursery and can be discharged after 48 hours with close follow-up.

b. Average length of stay (LOS) is approximately 6 days, two to three times that for term infants.

c. Infants with multiple morbidities will require more prolonged care.

2. Outcomes a. Rates of serious long-term morbidities and mortality are low

but significantly higher than for term infants. b. Neonatal mortality rates increase with each week earlier

in gestation (36 weeks 2.8/1000, 35 weeks 4.8/1000, and 34 weeks 7.1/1000).

c. Infants with congenital anomalies are often delivered in the LPT period and have worse outcomes.

d. Singleton LPT infants delivered after spontaneous labor and an uncomplicated pregnancy are at lowest risk and have mortality rates approaching those of term infants (<0.5/1000 live births).

II. Convalescent careFor the majority of LPT infants, intensive care issues are resolved in a matter of days, but feeding issues, lack of weight gain, and jaun-dice may require prolonged hospitalization. LPT infants have much



higher rates of rehospitalization than term infants, so focus should include proper preparation for discharge.

A. Feeding and dehydration1. Definition: Whether the infant is fed from the breast or bottle,

adequate oral intake by discharge is key to preventing dehydra-tion and jaundice and allowing proper weight gain.

2. Incidence: Poor feeding is common in LPT infants, with an increased frequency at earlier gestational ages (34 weeks 60.6%, 35 weeks 50%, 36 weeks 29.1%). a. It is the most common reason for prolonged hospitalization

in LPT infants.b. It is also the second most common reason for readmission

(15% to 20%). c. Exclusively breast-fed babies are at the highest risk

for rehospitalization.3. Pathophysiology: The coordination of the “suck, swallow,

breathe” functions is one of the most complicated tasks an infant has to perform. This system is often immature in LPT infants, placing them at risk for dehydration, poor nutrition, and aspiration.

4. Risk factors: Younger infants are at greater risk, as are SGA, LGA, and IDM infants. Infants born to first-time mothers and exclu-sively breast-fed infants are also at increased risk.

5. Clinical presentationa. Signs and symptoms: Poor oromotor skills may be evident

during feeding if the infant demonstrates poor latch, weak suck, coughing, choking, or sputtering. The infant may also demonstrate signs of dehydration, including poor urine out-put and excessive weight loss.

b. Clinical variability: Even an infant that appears to have good oromotor skills may not be taking in adequate fluid and calories.

6. Diagnosis: Feeding dysfunction and immature oromotor skills are often observable with close attention both by staff (nurses, lactation consultants, speech and feeding therapists) and fami-lies. Weights should be followed closely for the first week of life, even if the infant has been discharged. Whereas loss of >10% of body weight is excessive in term infants, loss of >7% in the LPT infant is concerning. Clinical signs of dehydration may also be evident.



7. Managementa. Close attention must be paid to feeding skills in all LPT infants. b. Exclusively breast-fed infants require specific observation

of latch skills, milk transfer, and weight loss. The Academy of Breastfeeding Medicine has a specific protocol for LPT infants (see also Chapter 12).

c. LPT infants without maturity of the oropharyngeal sys-tem will require supplementation of intake by nasogastric or orogastric tube. Weight loss greater than 7% should be followed closely; greater than 10% will often require evalu-ation for dehydration and supplementation.

d. Infants who have been discharged may require readmission. Intravenous fluids may be required, but special attention to feeding skills and the assistance of skilled personnel may avoid this.

e. Goal intake by a week of life is 150 to 170 mL/kg/d, as needed to achieve proper ex utero growth (goal 30 g/d).

8. Ongoing developmental/therapeutic interventions: Skilled nurses, lactation consultants, and feeding therapists knowledgeable in the care of preterm infants should be involved during prolonged hos-pital stays or readmissions. a. Cue-based feeding may help shorten hospital stay. b. Infants with persistent feeding dysfunction should be

referred for outpatient therapy.9. Prognosis

a. Early predictors: More mature infants and those without respiratory or infectious complications of prematurity are more likely to have adequate oromotor skills. Infants admitted to the NICU are more likely to have feeding difficulties and more likely to require readmission.

b. Outcomes: Prognosis is generally excellent for otherwise healthy infants, as oromotor skills improve with advancing age and maturity. By 1 year of age, the majority of parents do not report difficulty with feeding.

B. Hyperbilirubinemia1. Definition: High levels of bilirubin in the blood lead to the clini-

cal appearance of jaundice; when severe, it can result in bilirubin- induced neurologic dysfunction and kernicterus. Age- and risk factor–specific curves available from the AAP define normal, safe levels of bilirubin, and those requiring treatment. (see Chapter 19).



2. Incidence: Hyperbilirubinemia requiring phototherapy occurs in 20% to 25% of LPT infants, 2.4 times the rate in term infants. It is also the most common reason for early (<14 days) hospital readmission.

3. Pathophysiology: Preterm infants have immaturity of multi-ple liver enzymes including UDT glucuronyl transferase, which enable the conjugation and excretion of bilirubin. Delayed enteral feeding, poor feeding, and dehydration all result in decreased hepatic excretion of bilirubin and increased resorption from the gastrointestinal tract.

4. Risk factors: Immaturity, poor feeding, and exclusive breast-feeding are all specific risk factors for extreme hyperbiliru-binemia and kernicterus in LPT infants, in addition to hemolytic disease and other risk factors noted in Chapter 19.

5. Clinical presentationa. Signs and symptoms: Visible jaundice may present with dis-

coloration of the skin and eyes. Poor feeding is also common and stool and urine output may be decreased and discolored. Neurologic symptoms such as lethargy, apnea, seizures, and opisthotonic posturing are an emergency.

b. Clinical variability: Visible detection of jaundice may be difficult, especially in dark skinned infants. Kernicterus may also present with fever.

6. Diagnosis: In addition to prematurity, blood group incompatibil-ity, and poor feeding are risk factors, and these infants should be evaluated prior to the onset of visible jaundice. Transcutaneous bilirubin evaluation may be used for screening but a serum value is the gold standard. Age- and risk factor–specific curves should be used along with clinical course to evaluate need for therapy and risk of sequelae.

7. Management: As described in Chapter 19, phototherapy is first line with fluid supplementation as necessary to correct dehy-dration. Attempts should be made to continue enteral feeds and support breast-feeding unless additional therapies are required. IVIG and exchange transfusion are used in cases of significant bilirubin elevation unresponsive to maximal phototherapy.

8. Early therapeutic interventions: Close observation in the hos-pital and frequent outpatient visits until bilirubin has begun to decline will prevent cases of severe jaundice and kernicterus. Most described cases of kernicterus occurred in LPT infants who were discharged early and not followed up until 2 weeks of life.



9. Prognosisa. Early predictors: Infants closely followed without neurologic

symptoms have an excellent prognosis. A bilirubin >25 mg/dL or any neurologic symptoms are risk factors for sequelae.

b. Outcomes: Hyperbilirubinemia requiring phototherapy often results in a several day hospital stay but infants are expected to recover fully. Those with severe jaundice or requiring exchange transfusions may have long-term sequelae including hearing loss, seizures, and kernicterus. LPT infants are more likely than term infants to have neurologic sequelae from severe hyperbilirubinemia and are overrepresented in documented cases of kernicterus.

C. DischargeLPT infants are at high risk for rehospitalization, higher than that for either term or even very preterm infants. Special attention should be paid to discharge planning for these infants, whether they are cared for in the NICU or term nursery. General guidelines for safe dis-charge of the LPT infant are listed in Table 28-1. LPT infants are not candidates for early (24 hours) discharge.1. Teaching

a. Parents should understand that they are taking home a preterm infant, who is at greater risk for rehospitalization. Estimated rates of hospital readmission are 4% to 6% for LPT

Infant is more than 48 hours old

Satisfactory evaluation of parenting skills

Stable temperature in light clothing

Respiratory stability and apnea free

24 hours of successful feeding

Acceptable weight loss (<7%) or sustained weight gain, depending on age of infant

Normal stooling and voiding patterns established

Risk assessment and evaluation for jaundice

Immunization (hepatitis B), metabolic screening, and hearing evaluation performed

Passed car seat safety test (if appropriate)

Follow-up visit scheduled in 24 to 48 hours

Table 28-1. Criteria for safe discharge of the late preterm infant

Data from Whyte RK. Neonatal management and safe discharge of late and moderate preterm infants. Semin Fetal Neonatal Med. Jun 2012;17(3):153-158; Ramachandrappa A, Jain L. Health issues of the late preterm infant. Pediatr Clin North Am. Jun 2009;56(3):565-577.



infants, twice that of term infants: they are also overrepresented in newborn ER visits. If the infant is not waking up to feed, feeding poorly, or is acting differently, then they must bring the infant in to see their pediatrician.

b. Breast-feeding moms should meet with a lactation specialist prior to discharge, in order to observe the infant’s feeding abilities and together they can design a specific discharge feeding plan that may include supplemental bottle feeds with either expressed breast milk or infant formula.

c. If the facilities are available, consider having the parent(s) room-in with their baby prior to discharge.

2. Monitoringa. Early readmission (<14 days) of the LPT infant is usually

related to relative immaturity, the most common reasons being hyperbilirubinemia and poor feeding. LPT infants should follow-up with their primary care providers soon after hospital discharge—no more than 72 hours.

b. Parents who are young or first-time breast-feeding moms should have close follow-up with their pediatrician and they should have identified community resources that can assist with the transition home, prior to hospital discharge.

c. In addition to jaundice and dehydration, weight gain needs to be followed closely in LPT infants, especially if breast-feeding at discharge.

3. Safetya. Ways to minimize infectious risks should be discussed prior to

discharge, including eligibility for RSV prophylaxis.b. Smoking cessation should be discussed, when appropriate.c. All LPT infants should undergo a car seat safety evaluation

for at least 90 minutes to assess for cardiorespiratory insta-bility. If the infant is not yet 5 lb at the time of discharge, an infant car seat that has been safety tested down to 4 lb should be strongly recommended.

d. All caretakers should be taught infant CPR. III. Follow-up care

Increased health care costs and need for subsequent hospital admissions and health services persist for LPT infants through the first years of life. Recent evidence shows increased need for early intervention and special education services well into childhood.



A. Growth outcomes and monitoring1. Definition: Poor growth in childhood is diagnosed after a failure

to follow normal growth curves or crossing into a lower growth percentile. Preterm infants are also expected to achieve “catch-up growth,” showing growth compatible with full-term children by 2 years of age.

2. Incidence: 4.9% of LPT infants are underweight at 6 months, compared to 0.9% of term infants. Differences persisted at 12 months and were also seen in early term infants. LPT infants of normal weight at birth were also more likely to have lost per-centiles and be underweight. Limited data also show lower height attainment even up to 5 years of age.

3. Pathophysiology: Feeding difficulties often persist into the first year affecting both normal growth and catch-up growth. Increased read-mission and an increased frequency of chronic illness may also play a role. Infants born prematurely due to congenital anomalies may never achieve normal growth velocity.

4. Risk factors: Earlier gestation, SGA infants, lower socioeconomic status, gastroesophageal reflux disease.

5. Clinical presentation:a. Signs and symptoms: The failing to thrive child is usually well

appearing except for poor weight gain. Parents may give a history of poor appetite, feeding difficulty or food refusal, or reflux symptoms.

b. Clinical variability: Severe cases may present with failure to gain weight, even weight loss, and a severely malnourished infant, but this is usually due to more than prematurity alone.

6. Diagnosis: Special attention should be paid to weight gain and growth curves for formerly LPT infants in infancy and childhood; this may require additional pediatrician visits. Parental concerns should also be addressed. Standard CDC growth curves, plot-ted according to adjusted age, should be used.

7. Management: Close follow-up can allow early treatment includ-ing increased calorie provision and referral to feeding therapy if necessary. Severe failure to thrive or an ill-appearing infant should receive evaluation for other causes of poor weight gain including chronic illness and child neglect. In rare cases, nasoga-stric feeds and hospital admission are required.

8. Early developmental/therapeutic interventions: Infants with poor weight gain are at risk for long-term developmental sequelae and referral to early intervention should be considered. Parents of



LPT infants should be advised to pay special attention to rates of growth. Infants or children with poor growth should be followed closely and referred for specialty care (nutrition, gastroenterol-ogy) if growth does not improve.

9. Prognosisa. Early predictors: Infants born SGA are much more likely

to remain so; they may be perfectly healthy but should still demonstrate steady weight gain. LPT infants with complicated hospital courses and chronic illness are more likely to have growth failure.

b. Outcomes: Poor growth and feeding difficulties will often improve over the first several years of life, but there is lim-ited evidence of persistent differences later in childhood. Postnatal growth failure, especially if severe, is a risk factor for poor neurodevelopmental outcomes.

B. Respiratory infections and respiratory syncytial virus1. Definition: Respiratory infection can be defined as upper

respiratory tract (URT) or lower respiratory tract (LRT) disease due to an infectious agent causing poor feeding, increased breath-ing difficulty, and potentially hypoxia and respiratory failure. a. Respiratory syncytial virus (RSV) is a common cause of symp-

tomatic respiratory infection in preterm infants, including those born LPT.

b. It can spread to the LRT, causing bronchiolitis and pneumonia.2. Incidence: LPT infants are at higher risk of hospitalization for

RSV infection and of increased disease severity. a. RSV rehospitalization rates of 2.3% are seen in LPT infants;

this is highest in the first 3 months of life. b. There may also be an increased risk of childhood asthma in

LPT infants, though this is not seen in all follow-up studies. 3. Pathophysiology: Any preterm birth will interfere with normal

lung growth and development, causing decreased lung function, which may be clinically silent until illness occurs, but this is detectable with spirometry. a. The smaller diameter of airways in LPT infants hinders gas

exchange, especially when there is increased mucous produc-tion and plugging due to infection.

b. Transfer of maternal antibodies occurs late in gestation and may be deficient in LPT infants, leading to increased sus-ceptibility to infection.



4. Risk factors: Earlier gestation, shortened duration of breast-feeding, day care attendance, season of birth (young age in RSV season), preschool age siblings, multiple gestation, and smoking in the home are known risk factors.

5. Clinical presentation:a. Signs and symptoms: The infant may present initially with

increased nasal discharge and poor feeding. This may progress to cough, tachypnea, increased use of accessory respiratory muscles, and signs of pneumonia including cyanosis. Apnea and progressive respiratory failure may occur.

b. Clinical variability: There is large variety in presentations, with some infants experiencing only mild nasal congestion and others fulminant respiratory failure.

6. Diagnosis: Clinical symptoms compatible with RSV or other respiratory infections in young infants should lead to disease- specific testing including rapid testing (DNA or Antigen testing) and viral culture.

7. Managementa. Mild URT symptoms can be managed on an outpatient basis

with frequent nasal suctioning and attention to hydration, changing respiratory symptoms, and close follow-up.

b. When hospitalization is required, the mainstay of treatment is supportive care including hydration, airway clearance, supplemental oxygenation, and if necessary, ventilation.

c. There are no disease-specific therapies for RSV. RSV immune globulin (RespiGam) is rarely used in this population.

d. LPT infants with risk factors should be given prophylaxis for RSV with Palivizumab following local guidelines, as this has been shown to decrease the risk of hospitalization (see Table 7-1).

8. Early developmental/therapeutic interventions: Parents should be advised about the increased susceptibility to respiratory infec-tion and severe disease, including need for hospital admission, and should limit sick contacts (including therapy visits).

9. Prognosisa. Early predictors: Young age is a risk factor for hospitalization

and increased disease severity. Infants requiring intensive care unit admission or intubation have longer hospital stays and increased morbidities.

b. Outcomes: LPT infants are more likely to have prolonged hos-pital stays (up to 14 days) and experience recurrent wheezing in the year after RSV infection. The risk of RSV bronchiolitis



mortality is low even for low birthweight infants 1500 to 2499 g (6.4/100,000) but higher than for larger, more mature infants.

C. Neurodevelopmental outcomes1. Definition: Severe abnormalities in development are rare in LPT

infants and often related to congenital anomalies. However, there is increasing evidence of subtle abnormalities in cognition and be-havior in these infants that may not be apparent until school age.

2. Incidence: Rates of cerebral palsy (CP) and severe developmental delay are low (7.3/1000 and 12.2/1000 live births) but significantly higher than for term infants. a. Approximately 1/3 of LPT infants have need for early inter-

vention services at 3 years and this continues as increased need of special education services (28.9% to 34.5%) at school.

b. Rates of delay are linear and decrease with advancing gesta-tional age until 39 weeks.

c. Lower IQ scores are also seen in some studies, though a portion of this may be due to poor socioeconomic status, which is also more common in preterm infants.

d. Behavior problems are reported in 20% of former LPT infants, double that for term infants.

3. Pathophysiology: Neurodevelopmental sequelae are the result of the interaction of complicated pregnancies (a higher rate of congenital anomalies, maternal illness, IUGR, emergency delivery, and low Apgars) and developmental immaturity of the premature brain.a. The brain of an LPT infant is substantially smaller and less

complex than that of a term infant, with only 60% of the weight of the term brain at 36 weeks.

b. The effect of preterm birth on subsequent brain develop-ment is variable with a negative effect of systemic illness, but even well LPT infants (defined as hospital stay <72 hours) have increased need for special education services.

4. Risk factors: Risk increases with declining gestational age and increased pregnancy and delivery complications. Infants born to mothers with low education level or socioeconomic status are at higher risk.

5. Clinical presentation:a. Signs and symptoms: Infants may present with a history of a

complicated neonatal course such as resuscitation at delivery, infection, or intraventricular hemorrhage, which makes an increased risk for neurodevelopmental sequelae clear.



b. Clinical variability: Infants may also have no risk factors except prematurity. Attention should be paid to these infants throughout childhood as problems may not be apparent early.

6. Diagnosis: Infants with a complicated course or evidence of delay should be sent for more extensive developmental testing to eluci-date specific areas and allow a treatment plan. Educational testing is appropriate for school age children.

7. Managementa. Specific developmental follow-up is necessary, wherever it can

practically occur. b. Therapy services should be targeted at specific areas of con-

cern as deemed appropriate for the child. c. Ensuring good growth and care for other chronic health

issues will also optimize outcomes.8. Early developmental/therapeutic interventions: LPT infants are

often not routinely included in neonatal follow-up programs due to their sheer number, which would overwhelm such pro-grams. However, infants at higher risk due to illness or other factors should be included. a. Close attention should be paid to all formerly preterm infants,

though this may fall on the parents, pediatrician, and school system.

b. Appropriate use of early intervention and special education services should be utilized.

9. Prognosisa. Early predictors: Early signs of developmental delay and

behavior problems (<3 years) often persist at school age. b. Outcomes

• Overall outcomes are good, with a majority of LPT infants having normal IQ and school performance despite the increased risks.

• Severe delay is rare and likely not related to prematurity alone. • Nevertheless the large number of these infants results in

a substantial burden on early intervention and special education services.

D. Referrals1. High-risk infant follow-up clinic

LPT infants at greatest risk (h/o IVH, significant lung disease, ongoing feeding difficulties, IUGR) should have scheduled



follow-up with their local high-risk clinic for further monitoring and management of associated medical and development needs.

2. Early intervention servicesTherapy services as needed for developmental delays and feeding concerns beyond that which should be expected for the infant’s gestational age (use adjusted age to determine appropriate devel-opmental level for at least the first year in LPTs).

SELECTED REFERENCES1. Shapiro-Mendoza CK, Lackritz EM. Epidemiology of late and moderate preterm birth.

Semin Fetal Neonatal Med. June 2012;17(3):120-125.2. Shapiro-Mendoza CK, Tomashek KM, Kotelchuck M, et al. Effect of late-preterm birth

and maternal medical conditions on newborn morbidity risk. Pediatrics. February 2008;121(2):e223-e232.

3. Ramachandrappa A, Jain L. Health issues of the late preterm infant. Pediatr Clin North Am. June 2009;56(3):565-577, Table of Contents.

4. McCormick MC, Escobar GJ, Zheng Z, Richardson DK. Place of birth and variations in man-agement of late preterm (“near-term”) infants. Semin Perinatol. February 2006;30(1):44-47.

5. Gouyon JB, Iacobelli S, Ferdynus C, Bonsante F. Neonatal problems of late and moderate pre-term infants. Semin Fetal Neonatal Med. June 2012;17(3):146-152.

6. Medoff Cooper B, Holditch-Davis D, Verklan MT, et al. Newborn clinical outcomes of the AWHONN late preterm infant research-based practice project. J Obstet Gynecol Neonatal Nurs. 2012;41(6):774-785.

7. de Araujo BF, Zatti H, Madi JM, Coelho MB, Olmi FB, Canabarro CT. Analysis of neonatal morbidity and mortality in late-preterm newborn infants. J Pediatr (Rio J). May 2012;88(3):259-266.

8. Reddy UM, Ko CW, Raju TN, Willinger M. Delivery indications at late-preterm gestations and infant mortality rates in the United States. Pediatrics. July 2009;124(1):234-240.

9. Pulver LS, Guest-Warnick G, Stoddard GJ, Byington CL, Young PC. Weight for gestational age affects the mortality of late preterm infants. Pediatrics. June 2009;123(6):e1072-e1077.

10. Whyte RK. Neonatal management and safe discharge of late and moderate preterm infants. Semin Fetal Neonatal Med. June 2012;17(3):153-158.

11. Khashu M, Narayanan M, Bhargava S, Osiovich H. Perinatal outcomes associated with pre-term birth at 33 to 36 weeks’ gestation: a population-based cohort study. Pediatrics. January 2009;123(1):109-113.

12. Teune MJ, Bakhuizen S, Gyamfi Bannerman C, et al. A systematic review of severe morbidity in infants born late preterm. Am J Obstet Gynecol. October 2011;205(4):374 e371-e379.

13. Raju TN. Developmental physiology of late and moderate prematurity. Semin Fetal Neonatal Med. June 2012;17(3):126-131.

14. Hibbard JU, Wilkins I, Sun L, et al. Respiratory morbidity in late preterm births. JAMA. July 2010;304(4):419-425.

15. Jain S, Cheng J. Emergency department visits and rehospitalizations in late preterm infants. Clin Perinatol. December 2006;33(4):935-945; abstract xi.

16. Academy of Breastfeeding Medicine. ABM clinical protocol #10: breastfeeding the late pre-term infant (34(0/7) to 36(6/7) weeks gestation) (first revision June 2011). Breastfeed Med. June 2011;6(3):151-156.

17. DeMauro SB, Patel PR, Medoff-Cooper B, Posencheg M, Abbasi S. Postdischarge feeding patterns in early- and late-preterm infants. Clin Pediatr (Phila). October 2011;50(10):957-962.



18. American Academy of Pediatrics Subcommittee on Hyperbilirubinemia. Management of hyperbilirubinemia in the newborn infant 35 or more weeks of gestation. Pediatrics. July 2004;114(1):297-316.

19. Harijan P, Boyle EM. Health outcomes in infancy and childhood of moderate and late pre-term infants. Semin Fetal Neonatal Med. June 2012;17(3):159-162.

20. Santos IS, Matijasevich A, Domingues MR, Barros AJ, Victora CG, Barros FC. Late preterm birth is a risk factor for growth faltering in early childhood: a cohort study. BMC Pediatr. 2009;9:71.

21. Berard A, Le Tiec M, De Vera MA. Study of the costs and morbidities of late-preterm birth. Arch Dis Child Fetal Neonatal Ed. September 2012;97(5):F329-334.

22. Abe K, Shapiro-Mendoza CK, Hall LR, Satten GA. Late preterm birth and risk of developing asthma. J Pediatr. July 2010;157(1):74-78.

23. Petrini JR, Dias T, McCormick MC, Massolo ML, Green NS, Escobar GJ. Increased risk of adverse neurological development for late preterm infants. J Pediatr. February 2009;154(2):169-176.

24. Chyi LJ, Lee HC, Hintz SR, Gould JB, Sutcliffe TL. School outcomes of late preterm infants: special needs and challenges for infants born at 32 to 36 weeks gestation. J Pediatr. July 2008;153(1):25-31.

25. Morse SB, Zheng H, Tang Y, Roth J. Early school-age outcomes of late preterm infants. Pediatrics. April 2009;123(4):e622-e629.

26. Ballard JL, Khoury JC, Wedig K, et al. New Ballard Score, expanded to include extremely pre-mature infants. J Pediatrics. 1991;119:417-423. Copyright Ballard Score. http://ballardscore.com/Pages/ScoreSheet.aspx. Accessed June 17, 2014.

29 Surgical care of the nIcu Graduate

I. Congenital diaphragmatic herniaFor children born with a congenital diaphragmatic hernia (CDH), modal-ities such as nitric oxide (NO), high-frequency oxygenation (HFO), and extracorporeal membrane oxygenation (ECMO) have improved survival, resulting in a growing recognition of many long-term CDH-associated complications. Given the complexity of these children, comprehensive long-term multidisciplinary care is essential. Chapter 31 discusses the complex medical and developmental care of infants with a CDH. Below, surgical considerations of the CDH survivor are discussed.

A. Gastroesophageal reflux1. Gastroesophageal reflux disease (GERD) has a well-recognized

association with CDH. 2. Proposed mechanisms for GERD in babies with CDH include

elevated intra-abdominal pressure from positioning the hernia


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