Nutrition for

Premature Infants &

Pediatric Dysphagia
Contents
• Etiology, physiologic development and problems for SGA & LGA births

• Nutrition assessment, potential problems – risk factors for nutritional

deficiencies, long term outcome

• Nutrition support - feeding methods, milk & formula selection – indications

& concerns, discharge care

• Pediatric dysphagia – concerns and management

Definitions
• SGA is based on physical evaluation at birth- weight is <10th percentile, the
infant is SGA.

• IUGR is a prenatal diagnosis to describe a fetus who fails to reach in utero

growth potential, often diagnosed by the obstetrician. Therefore, not all
infants with IUGR are SGA, and similarly, not all infants who are SGA have
IUGR.

• IUGR may be a normal fetal response to nutritional or oxygen deprivation;

therefore the issue is not the IUGR but rather the ongoing risk of fetal
malnutrition or hypoxia.
• IUGR is often classified as reduced growth that is symmetric (head
circumference, length, and weight equally affected) or asymmetric (with
relative sparing of head growth).
Types of IUGR
•An earlier onset in the first
first trimester of
trimester

pregnancy
Symmetric •Is associated with diseases that seriously affect
fetal cell number, such as conditions with
IUGR chromosomal, genetic, malformation,
teratogenic, infectious, or severe maternal
hypertensive etiologies.

•Late onset in the 2nd half of pregnancy

•Is associated with poor maternal nutrition or
Assymmetric with late onset or exacerbation of maternal
vascular disease (preeclampsia, chronic
IUGR hypertension).
Physiological
Development of
LBW/SGA
Thermal regulation
• Thermal control is dependent on gestational and postnatal age, birth weight,
and the clinical conditions of the newborn.

• Newborns can lose heat through evaporation (skin and respiratory tract),
convection (loss to colder environment), conduction, radiation, or
combinations thereof.

• The large skin surface area-to-body mass ratio in newborns presents a large
area for heat loss. The head may account for as much as 20% of the infant’s
total surface area.

• With greater prematurity, the skin becomes thinner, with fewer tight
junctions and a thinner layer of subcutaneous fat.

• The infant responds with non-shivering thermogenesis, a process that

involves brown fat metabolism and significant oxygen consumption (up to
25% of total oxygen consumption).
Glucose regulation
• The fetus exists in an anabolic state, with high endogenous concentrations of
insulin and fetal glycogen, promoting glycogenesis and lipogenesis.

• After birth, there is an increase in the concentration of glucagon, plasma

catecholamines, and cortisol, and a decrease in insulin concentration,
thereby promoting glycogenolysis, gluconeogenesis, and lipolysis in order to
provide energy to the newborn.

• During the transition to extrauterine life, the BG in healthy newborns

lowers in the first hours of life, with BG approximating 55–60 mg/dL.

• It is important to differentiate this normal transient physiological response

from disorders that result in persistent or recurrent hypoglycemia, which
can lead to neurological sequelae.
• Hypoglycemia – 15% at term.
Hypoglycemia
• Pre term at higher risk - due to inadequate storage of glycogen, proteins,
and fats, which occurs during the third trimester of pregnancy

• Lipolysis - neonatal metabolic demands when glycogen is depleted, either by

producing glycerol or ketone bodies. However, lipolysis and ketogenesis are
limited in premature infants due to the loss of fat in adipose tissue
Hyperglycemia
• Hyperglycemia is prevalent VLBW, especially during the first week of life,
with the highest numbers seen in infants who are also growth-restricted or
who receive intravenous glucose.

• ≥80% VLBW - may be affected by hyperglycemia.

• Its etiology involves an inability to inhibit gluconeogenesis, relative insulin

resistance (possibly related to elevated growth hormone, cortisol, and
catecholamine concentrations), defective proinsulin processing, and delayed
secretion.

• Untreated hyperglycemia can lead to significant complications, including

hyperosmolality, osmotic diuresis, dehydration, and possible intracranial
bleeding and additive effects on ischemic brain injury
Respiratory function
• During intrauterine development - airways are completely formed at around
16 weeks of gestation.

• Between weeks 16 and 24, these conductive structures increase in caliber;

between weeks 24 and 36 – the pre-acinar airways grow, the bronchioles
develop, and the acini are formed.

• At around 28 weeks of gestation, the alveoli begin to develop.

• The pulmonary surfactant begins to be produced around 34 weeks of

gestation. This surfactant reduces the surface tension in the alveoli,
allowing them to remain inflated.

• Pulmonary surfactant deficiency or dysfunction can lead to respiratory

distress syndrome (RDS), a common disorder in premature infants
• Apnea of prematurity is experienced by 85% of babies born before 34 weeks
of gestation

• The risk of developing it rises substantially with every additional week of

gestation missed.

• Defined as cessation in breathing with a >15–20 sec duration

• It is believed to result from immaturity of the central respiratory control

mechanisms (e.g., reduced sensitivity to CO2 and hypoxia) and from an
exaggerated protective response to laryngeal stimulation (to acid),
ultimately leading to the interruption of inspiratory activation of the
respiratory muscles and closure of the upper airways
Immune function
• The fetal immune system develops in a sterile and protected environment,
therefore requiring antigenic exposure.

• Immune competence develops during the first three months postpartum.

• The complement system is the most important component of innate

immunity, and it is likely to contribute to the performance of the adaptive
immune system.

• In healthy, at-term newborns, the complement system is already

underdeveloped; this is aggravated in premature infants.
• Premature neonates are the most vulnerable to intracellular pathogens that
cause infections in the uterus (intrapartum and postpartum).
• Regulatory T cell functionality is temporarily reduced in premature infants,
which can lead to dysregulation or overactivation of the immune response
Hepatic function
• In intrauterine life, the fetus depends on the mother’s liver function while
its own liver develops.

• Preterm infants, however, are susceptible to the consequences of immature

liver function, which can include hypoglycemia, hyperbilirubinemia,
cholestasis, bleeding, and impaired drug metabolism
Renal function
• Premature infants may have reduced or abnormal nephrogenesis after birth,
and may not reach the same number of nephrons as their full-term peers.

• Due to the limitation of renal blood flow and glomerular filtration rate,
newborns – and especially premature infants – have a limited ability to
handle fluid overload
Body Composition & Physiological
Wt Loss
• 80% of wt is gained between 24 – 28 weeks is water.

• Body water decreases to 60% between 36 – 40 wks

• Wt gained at-term is fat (8 to 20%).

• Decrease in EC water is compensated by increase in IC – physiological wt

loss after birth
• More in preterm 5 -15%

• Normal – 3-5%
Fluid loss
Fluid loss > 1500 g BW < 1500 g BW
Postnatal physiological 5 – 10 ml/kg/d 20 ml/kg/d
loss (3 – 4 days)
Insensible water loss 20 ml/kg/d 40 – 60 ml/kg/d
Urine output (first 3 50 – 70 ml/kg/d
days)
Urine output (thereafter) 70 – 100 ml/kg/d
Stool losses (after first 3 10 ml/kg/d
days)
Growth of SGA infants
• Slow neonatal weight gain is common in preterm born children of all
birthweights, and is more pronounced the lower the gestational age and
comorbidity

• SGA experiences a period of accelerated linear growth during the first 12

months of life that results in a stature above −2 SD in up to 90%. Most of the
catch-up growth occurs during the first year and is near completion by 2 yr
of age

• Those born very prematurely and with more severe degrees of growth
retardation, especially reduced birth length, are less likely to reach a stature
within the normal range, whereas those with taller parents are more likely
to reach a normal adult height

• The preterm SGA infant can take four or more years to achieve a height in
the normal range
 SGA: Early growth and BMI @ 3
years
• Children born SGA and moderate to late
preterm were shorter and lighter and
had a lower BMI than children born AGA
and term throughout the whole follow-up
period of 5 years.
• There was a pattern of larger differences
with decreasing gestational age at birth.
• At age 5 years, fewer children born SGA
and moderate preterm had a normal BMI
compared with those born AGA and late
term.
• Rapid weight gain in infancy is
associated with increased incidence of
obesity in later life
• Breast feeding in infancy may protect
against the long-term risk of developing
obesity
Neurological and intellectual
consequences
• In large observational studies, cognitive impairment is independently
associated with LBW, short birth length, and small HC for gestational age.
The effect is moderate but significant.

• Those without catch-up in height and/or HC have the worst outcome.

• Being born SGA is associated in particular with lower cognitive ability in

mathematics and reading comprehension and with more emotional, conduct,
and ADHD.

• Long-term exclusive breastfeeding (24 wk or more) may prevent some of the

intellectual impairment
Puberty and adrenarche
• Most children born SGA have pubertal timing within normal limits.

• However, some studies in boys and girls born SGA indicate that pubertal
growth is modestly decreased, whereas in girls, menarche occurs 5–10
months earlier than normal.

• In those who do have early puberty, there is typically a rapid progression

through puberty leading to loss of adult height.

• SGA girls who display rapid weight gain during early childhood are more
likely to have premature adrenarche.
• The variations in pubertal timing and progression recognized in the SGA
child are likely to be related to many factors, including ethnicity, background
population trends, nutrition, and other unknown influences.
Ovarian function
• Some adolescents who were born SGA may have reduced ovulation rates,
increased secretion of adrenal and ovarian androgens, excess abdominal fat
(even in the absence of obesity), and hyperinsulinemia.

• This variation in the frequency of polycystic ovary syndrome in women born

SGA may be due to ethnic and geographic background and variation in the
definition of the syndrome.

https://academic.oup.com/jcem/article/92/3/804/2596891
Nutritional
Assessment
Nutritional Support
Feeding methods, milk & formula selection – indications & concerns,
discharge care
Early Aggressive Nutrition
• Better nutrition in the early postnatal phases in preterm --- higher verbal
IQ scores and improved cognitive function in the long term.

• Higher protein and energy intake during the first week after birth in
extremely LBW infants ---- higher mental development index scores and
lower risk of growth retardation at 18 months after birth.

• Early and higher protein and energy intake have also been correlated with
faster head growth and an increase in head circumference in preterm
infants; increase in head circumference has been positively correlated with
improved cognitive outcomes.
• Therefore, the administration of early aggressive nutritional enteral and
parenteral support may help improve growth and developmental outcomes
in preterm newborn LBW infants
EN v PN
• Enteral feeding is preferred to parenteral feeding, as the latter may be
associated with catheter-related complications, infections, and sepsis, among
others.

• Complications associated with EN – NEC

• There has been no increase in the risk of NEC with fast or early enteral
feeding of expressed breast milk (EBM) or formula milk as compared to slow
or delayed introduction of enteral feeding in LBW infants
• Systematic reviews have reported that delaying enteral feeding does not
lead to a reduction in the risk of NEC.

• On the contrary, this approach may prolong the time to achieve full enteral
feeding.

• Furthermore, early versus late (<48 versus >72 h after birth) initiation of
enteral feeding has been found to be associated with a significantly lesser
time to gain birth weight, and shorter duration of parenteral nutrition and
hospital stay, without any increase in the complication rate.

• A reduced incidence of osteopenia of prematurity and jaundice has also been

noted with early versus late enteral feeding in very LBW infants.
Trophic feeds
• Trophic feeds are defined as minimal volumes of milk feeds (10–15
mL/kg/day).

• Start trophic feeds preferably within 24 h of life.

• Exercise caution in extremely preterm, extremely low birth weight (ELBW),

or growth-restricted infants.

• If, by 24–48 h, no maternal or donor milk is available, consider formula

milk.

• There is not enough evidence to recommend the maximum duration of

trophic feeding before starting nutritional feeds.
Day of Starting, Volume, Frequency,
Increase
• In babies weighing <1 kg at birth, start nutritional feeds at 15–20
mL/kg/day and increase by 15–20 mL/kg/day.

• If the feeds are tolerated for around 2–3 days, consider increasing faster.

• For babies weighing ≥1 kg at birth, start nutritional feeds at 30 mL/kg/day

and increase by 30 mL/kg/day.

• Fast increment did not increase the risk of NEC and mortality.

• The trials individually reported that the fast daily increment group regained
birth weight and reached full feeds faster
Type of feed
• The first choice is own mother’s expressed breast milk or colostrum. This
should preferably be fresh; if not, provide previously frozen milk in the same
sequence in which it was expressed.

• Second choice: donor human milk.

• Third choice: preterm formula.

• Neonates who receive an exclusively human milk-based diet (mother’s milk

or donor human milk with human milk-based fortifier) have significantly
lower rates of NEC compared to those who receive preterm formula or
human milk with a bovine milk-based fortifier
Human Milk Fortification
• HMF is recommended for preterm infants with birth weight less than 2000 g when
feeding volume reaches 50~100 ml/kg/d (E).

• The infants are recommended to use half-fortified breast-milk initially, and then switch
to full-fortified milk based on the enhancement of feeding tolerance.

• The preterm infants who still have growth retardation at discharge should continue to
use fortified breastmilk until at least 40 weeks corrected gestational age, or continue to
use fortified breast-milk until 52 weeks corrected gestational age based on the growth
status
Formula Milk
Feeding Methods
• i) Bolus: Suitable for mature, gastrointestinal tolerant,
orogastric/nasogastric fed neonates, but not suitable for those with GER and
delayed gastric emptying. Bolus rate should be limited.

• ii) Intermittent: Suitable for the infants with GER, delayed gastric emptying
and high risk of inhalation. Each infusion should be lasted from 30 minutes
to 2 hours (infusion pump is recommended). Intermittent infusion should be
administrated at 1~4 hours interval according to gastrointestinal tolerance.

• iii) Continuous: Suitable for infants intolerant to bolus or intermittent

infusion. The infusion should be administrated continuously during 20~24
hours and controlled by syringes. The formula in the syringes should be
changed every 3 hours.
Route of feeding
• (1) Oral feeding: Suitable for newborns who have normal suckling, swallowing and
breathing functions normal suckling, swallowing and breathing functions and
gestational age ≥ 32~34 weeks.

• (2) Tube feeding:

• 1) Indications: i) Preterm infants with gestational age <32~34 weeks;

• ii) Those who have dysfunction of sucking and swallowing, or cannot be fed orally;

• iii) Those who cannot be fed orally due to illness or medical condition;

• iv) As a supplement of inadequate oral nutrition intake.

Recommended EN for Preterm
Infants
Fluid requirements

Requirements < 1500 g BW > 1500 g BW

First day 80 ml/kg/d 60 ml/kg/d
Increment 10 -15 ml/kg/d 15 – 20 ml/kg/d
Maximum by the end of 160 ml/kg/d 160 ml/kg/d
first week
Parenteral Nutrition (NICE, 2020)
Challenges in PN for Pre-term
• After preterm birth, survival, growth, and development are dependent on
the nutritional supply of amino acids, fat, and carbohydrates.

• In utero, the fetal amino acid uptake exceeds the amount that is necessary
for net protein accretion, which indicates that the human fetus oxidizes
amino acids to generate energy.

• Fear of providing excess amino acids to preterm infants therefore is not

justified. Therefore, many very-low-birth-weight infants received only
glucose or small amounts of amino acids during the first few days of life,
resulting in large protein and energy deficits subsequently accompanied by
weight loss.

• Retrospective data indicate that initial suboptimal management might have

detrimental implications for future neurocognitive development
• Several studies have demonstrated that the administration of 1.0–2.5 g
amino acids/(kg body weight/d), starting within a few hours of birth, can
reverse a negative nitrogen balance into a positive balance, thus leading to
anabolism.

• More recent studies demonstrated that the nitrogen balance can be

improved further by administration of amino acids up to 3.6 g/(kg d) (12–14)
when provided with additional energy.

• Despite this knowledge, many hospital units do not comply with the existing
guidelines, which advise providing preterm infants with both amino acids
and lipids from birth onward.

• Appropriate administration of nutrients in the first few days to weeks of life

will reduce the growth restriction that is frequently observed.
• The goal of early appropriate amino acid and fat administration is to
promote anabolism and a normal cellular development. This is not always
reflected by weight gain, which is affected by other factors, i.e., fluid status.

• The composition of the lipid emulsion might affect infection rate or

associated liver disease, whereas the quality of the amino acid solution can
be further improved.
Pediatric Dysphagia
• Dysphagia is defined as any disruption to the swallow sequence that results
in a compromise in the safety, efficiency, or adequacy of nutritional intake.

• It is important to note that dysphagia is a skill-based disorder distinct from

behavioral feeding problems that may arise in children who have sufficient
skills for normal eating and drinking.
Normal Swallowing
• (1) oral phase (i.e. suckling or mastication, and the transportation of the
bolus towards the pharynx);

• (2) triggering of the swallowing reflex;

• (3) pharyngeal phase (i.e. transportation of the bolus through the pharynx)

• (4) esophageal phase (i.e. transportation of the bolus through the esophagus
to the stomach).
Swallowing – Neonates, Infants,
Children
• In neonates and young infants, all four components of swallowing are
reflexive and involuntary.

• Later in infancy, the oral phase comes under voluntary control, which is
essential to allow children to begin to masticate solid food.

• Safe and effective mastication (i.e. biting and chewing) relies on appropriate
sensory registration of the food source and a coordinated motor response
Consequences of Pediatric Dysphagia
Management
• Therapeutic interventions for children with oral-phase
swallowing problems are aimed at improving the sensory and
motor skills needed for drinking and eating.
• For children with swallowing problems affecting the pharyngeal
phase, therapy generally involves modifying the child’s
swallowing strategy or modifying the food bolus.
• The return to a normal diet in children with dysphagia requires a
gradual, multidisciplinary approach that enables systematic
neuromuscular training of the relevant phase of swallowing.