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Departments of Pediatrics and Nutritional Sciences, University of Wisconsin, Madison, WI 53715
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ABSTRACT |
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 TOP ABSTRACT INTRODUCTIONREFERENCES |
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KEY WORDS: • premature infants • history • feeding
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INTRODUCTION |
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TOPABSTRACTINTRODUCTIONREFERENCES |
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).
At the beginning of the 20th century, the care of the premature infant
was in its infancy. Breast milk was the feeding of choice and the
common practice was to begin the feeding of premature infants very soon
after birth. This was largely a result of the work and teachings of
Stephane Tarnier (1828–1897) and his even better known student Pierre
Budin (1846–1907) at L’Hôpital Maternité in Paris.
Although obstetricians by training, they were the first clinicians to
champion the care of the premature infant, or "weakling," as they
were known at the time. Key points of their care, which have come down
to us through the published lectures of Budin were as follows: warming,
protection from infection and nutrition (Budin 1907
). In
addition to advocating the use of breast milk, it was Tarnier who
popularized the technique of gavage feedings in premature infants who
were too weak to receive breast milk from a syringe, spoon or the
breast (Berthod 1887
).
Surprisingly enough, the basic energy requirements for infants were
determined more or less during the late 19th century because it was
relatively easy to place infants in the "closed systems" (bell
jars) used to measure oxygen consumption and carbon dioxide production
during this period (Nichols 1993
). After Heubner
determined the energy content of human milk in 1897, the energy
quotient for premature infants was reported by a number of
investigators between the years 1907 and 1920. The range was 95–160
kcal/(kg · d) (Nichols 1993
). It was the practice to
provide these infants with high energy intakes of 150–200
kcal/(kg · d) because it was the common belief that a high energy
intake was not only required but that more rapid weight gain was
beneficial. Gordon and Levine restudied the energy issue in the 1930s
using a combination of closed (2 infants) and open circuit (9 infants)
calorimetry. These premature infants ranged in birth weight from 1130
to 2220 g and were studied between 10 and 44 d after birth.
The daily energy requirement was determined to be 120 kcal/(kg · d)
[68 kcal(kg · d) for catabolism, 18 kcal/(kg · d) lost in
feces and 34 kcal/(kg · d) stored as energy]. Average weight gain
was 16 g/(kg · d) (Gordon et al. 1940
). These energy
requirements for growing premature infants have withstood the test of
time.
It was in 1913 that Julius H. Hess (1876–1955) began the first
continuously operated center for premature infants in the United States
at Michael Reese Hospital in Chicago. Dr Hess, who had spent several
years in Europe visiting centers caring for premature infants, also
published the first book ever written dealing with the subject of the
premature infant, [Hess (1922)
]. Hess also advocated
that human milk was the choice of feeding for the premature infant and
that artificial milk preparations were a poor substitute, which
resulted in an increased mortality rate. He advocated beginning
feedings of breast milk in the second 12 h of life with the milk
supplied by a wet nurse. During the first 3 wk of life, breast milk
intake was progressively increased from 140 to 200 mL/(kg · d). His
textbook had elaborate guidelines for "Hygiene of the Wet Nurse"
and breast feeding the premature infant. He also favored gavage feeding
with gravimetric flow for infants unable to nurse at the breast
(Fig. 1
). Even for breast-fed infants, he advocated water or a 1% lactose
solution up to one sixth of the infant’s body weight, to be
administered daily to "compensate for the loss of body fluids through
the kidneys, bowels, lungs and skin." If "artificial feeding" had
to be used of necessity, he recommended a buttermilk and skim milk
mixture with the addition of sugar (low fat, high carbohydrate) or
boiled milk with the addition of water and sugar. Artificially fed
infants were to be fed orange juice by wk 3 (2–4 mL/d) to counteract
the effects of boiling. Small amounts of cod-liver oil were
introduced at 4 wk and increased to 2 mL/d by 8 wk. He also recommended
daily supplements of iron by wk 4. Solid foods were not instituted
until mo 5, beginning with well-cooked cereal (Hess
l922
).
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). This practice, to delay feedings for up to
as long as 4 d in the smallest, sickest premature infants,
originated in the United States. Budin’s earlier advice was ignored:
"The path of pleasure for adults is drinking. May it not be the same
for weaklings?" (Budin 1907
). Hess wrote in his 1941
textbook: "It has been our experience that too early feeding may
often be the cause of aspiration pneumonia and is, therefore, to be
avoided .... Small premature babies (those weighing under 1200 g) were not fed for 24–48 h .... During this time the premature
baby receives physiologic salt solution, subcutaneously in the thighs,
one to three times daily." He also recommended that infants <1000 g
should not receive food by mouth for 24–48 h. This trend of delaying
early feedings persisted as mainstream neonatal practice for 25 y.
Not only was it thought that delayed feedings prevented aspiration
pneumonia but also there was a growing belief that many premature
infants were retaining an excessive amount of extracellular fluid so
that early feeding was stressful to the infant’s kidneys
(Hansen and Smith 1953
). There were reports of severe
weight loss (>20% of birth weight), hemoconcentration,
hyperosmolality and hyperbilirubinemia in these infants during this
period; because these were quickly reversed, however, when feedings
were begun, clinicians obviously believed that premature infants could
tolerate these initial periods of starvation without long-term
adverse affects (Davies 1978
, Hansen and Smith 1953
). The 1958 version of Hess’s textbook had the following
to say about initiating early feedings in the premature infant: "The
average premature infant does better if it is not fed for at least
12 h after birth, and babies weighing <1200 g at birth are not
fed for 36 to 72 h. All feedings are withheld for at least 48 h in any baby having marked generalized edema or respiratory
embarrassment" (Lundeen and Kunstadter 1958
). To be
sure there were a few "voices in the wilderness during this
period," and in 1955 it was reported that there was a 28% lower
mortality rate in premature infants who were fed between 12 and 24 h of life compared with a 41% rate when feedings were delayed until
36 h of life (Gleiss 1955
).
Another major change in the 1940s resulted from the work of
Gordon and co-workers (1947)
. These investigators
reported that premature infants fed a diluted "half-skimmed cow’s
milk formula" gained weight more rapidly than those fed breast milk.
In this study, 122 premature infants (birth weight 1022–1996 g) were
fed three different diets supplying 120 kcal/(kg · d). The three
diets were human milk, evaporated cow’s milk formula and partially
skimmed cow’s milk formula. The milk used in the two
last-mentioned diets was diluted with water and Dextri-Maltose
was added. For the 16 infants fed human milk, the average weight gain
was 12.5 g/(kg · d), compared with 14.1 g/(kg · d) for the 39
infants fed evaporated milk and 15.7 g/(kg · d) for the 67 infants
fed half-skimmed milk (Fig. 2
). The differences between these three groups were significant.
Differences were even more striking for the 49 infants with birth
weights between 1000 and 1600 g. The implications were that it was
the increased protein in the cow’s milk–based feedings that promoted
the increased weight gain in these infants, and this study led to the
widespread use of such feedings in the premature infant. Furthermore,
in 1943, Benjamin et al. (1943)
compared premature
infants fed human milk with infants fed a mixture of skimmed-milk
and olive oil, and demonstrated that human milk, even in the presence
of added vitamin D, was not the food of choice for the formation of the
skeleton of premature infants unless supplemented with calcium and
phosphorus. No wonder the 1958 revision of Hess’s textbook toned down
the promotion of breast milk for premature infants and included an
expanded section on "artificial feeding" (Lundeen and Kunstadter 1958
).
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). It was also pointed out that
infants fed early did not have an increased incidence of aspiration
pneumonia and that much of the edema reported in these infants
previously could be attributed to tissue catabolism from starvation
(Davies 1978
).
Second, it was demonstrated that some of the weight gain attributed to
artificial formulas for premature infants was secondary to the
increased electrolyte intake and water retention with such formulas.
Kagan et al. (1972)
noted that both total body water and
extracellular fluid volume of infants fed high protein, high solute
load intakes were greater than those observed in patients receiving low
solute formulas and human milk. The increase in dry weight (total
weight gain minus increase in total body water) was similar with
protein intakes ranging from 2 to 6 g/(kg · d). However,
Babson and Bramhall (1969)
reported no increase in dry
weight gain when only minerals were added to a formula providing
1.5 g protein/100 mL. Their study also found that higher protein
intakes from formula containing 3.5 g protein/100 mL did not lead
to greater weight gains unless accompanied by higher solute intakes,
although the increase in protein intake (regardless of solute load) did
result in greater increase in length. They suggested that changes in
length were a better indicator of nutritional adequacy of high
protein/high solute load formulas.
Finally, in the 1970s, Raiha and colleagues (1976)
pointed out that protein quality, not quantity, played an important
role in the feeding of the premature infant. In these studies, infants
were randomly assigned to pooled (banked) human milk (protein content
1.0 g/dL) or one of four isocaloric cow’s milk–based formulas
differing in protein quantity (1.5 vs. 3.0 g/dL) and quality (ratio of
whey proteins to casein of 60:40 or 18:82). Although the weight gain
was highest in the infants receiving the high protein formula [protein
intake of 4.5 g/(kg · d)], some of these infants developed
azotemia, hyperammonemia and metabolic acidosis. The intrauterine rate
of weight gain was not achieved in any group. This study suggested that
human milk was as adequate for low-birth-weight
(LBW)2infants as currently available formulas. Another study from the early
1980s clearly established that LBW infants fed their own mother’s milk
had an improved growth rate compared with premature infants fed pooled,
mature, donor milk (Gross 1983
). This was largely
thought to be due the higher protein content of preterm breast milk
compared with milk from term mothers during the first few weeks of
lactation. Although this work led to a resurgence in the use of
mother’s own milk for preterm infants, even in Gross’s study, the
infants did not achieve the intrauterine rate of growth.
Since the 1940s, it had been known that human milk was deficient in
protein, calcium, phosphorus, sodium, iron, vitamins and trace minerals
and would not satisfy the intrauterine requirements of the growing
premature infant. The 1941 edition of Hess’s textbook recommended
supplemental vitamins for both breast-fed and formula-fed
premature infants. Heird and Anderson (1977)
pointed out
these deficiencies in their review on this topic, but also noted that
at this time, infants fed human milk grew as well as those receiving
formula, and that it remained to be demonstrated that the ideal rate of
weight gain for premature infants ex utero was the in utero rate of
weight gain. Despite this, in 1977, in its first statement on the
nutritional needs of LBW infants, the American Academy of Pediatrics
(AAP) concluded that "the optimal diet for the LBW infant may be
defined as one that supports a rate of growth approximating that of the
third trimester of intrauterine life, without imposing stress on the
developing metabolic or excretory systems" (AAP 1977
).
The 1980s saw the commercial development of special
formulas3for very-low-birth-weight (VLBW) infants (birth weight 
1000 g ).
Compared with standard formulas, these contained more protein (2.2
g/dL), Na (1.5 mEq/dL), Ca (150 mg/dL), P (80 mg/dL) and vitamins per
100 mL, which more adequately met the needs of the premature infant who
required smaller total volumes of feedings with higher concentrations
of nutrients compared with larger premature infants. These formulas
allowed for the delivery of 
3 g/(kg · d) protein and 6.5
g/(kg · d) fat with an intake of 150 mL/(kg · d). They also
contained 50% of the fat as medium-chain triglycerides. Clinical
studies with these formulas designed for the needs of the VLBW infant
clearly showed the advantages of improved growth compared with human
milk without the metabolic abnormalities reported with previous
formulations (Cooper et al. 1984
, Greer and McCormick 1988
, Gross 1983
, Schanler and Oh 1985
, Tyson et al. 1983
). In the 1980s and
1990s, with the development of commercially available human milk
fortifiers for preterm infants, such fortification of human milk become
the standard of care for the LBW infant. Even so, comparative studies
continued to show that infants fed the special formulas for VLBW
infants grew faster than those fed fortified human milk
(Atkinson et al. 1981
, Schanler and Garza 1987
, Schanler et al. 1999
). These human milk
fortifiers contain protein, vitamins and minerals that in theory will
meet the intrauterine needs for growth in these infants when added to
human milk.
In the last 25 y, two other clinical issues had a great effect on
the feeding of VLBW infants. The first of these is a disease of the
intestinal tract, necrotizing enterocolitis. Although the term was
first used in the early 1950s by Quaiser (1952)
, it
really became a clinical problem with the remarkable overall
improvements in neonatal intensive care of the 1960s and 1970s. No
other single disease has a greater effect on the enteral nutrition of
premature infants because it is the fear of this disease by care givers
that typically governs when feedings are started, how rapidly they are
advanced, what kind of feeding is used and when they are interrupted.
In the 1990s it was argued that feedings of human milk, even with
fortification, may decrease the incidence of this disease in LBW
infants (Schanler et al. 1999
).
The second issue was the high fluid intakes that were recommended for
VLBW infants in the 1970s, after the long period of time in which
starvation and very low fluid volumes in the first days of life were
the norm. This was the result of increasing concerns about the very
high insensible water loss rates in VLBW infants. They were treated in
overhead warmers to maintain body temperature, often with phototherapy,
and in a relatively low humidity environment. There was also the need
to increase energy intake during a time in which it was difficult to
give concentrated solutions of glucose parenterally. Those providing
care were also concerned about the immaturity of the renal glomerulus
in which the glomerular filtration rate was lower in the preterm than
the term infant, and the inability of the premature kidney to
concentrate urine. Others were concerned about the need to increase the
renal excretion of the solute load associated with increasing
nutritional intakes. All of this led to a large overestimation of the
water needs of the premature infant, and it was not uncommon for the
total fluid volume to exceed 200 mL/(kg · d) in the smallest
infants (Roy and Sinclair 1975
). These high fluid
intakes compromised administration of other nutrients and were
ultimately associated with an increased incidence of patent ductus
arteriosus, congestive heart failure and even necrotizing enterocolitis
(Bell et al. 1980
, Stevenson 1977
). This
led to a gradual reduction in the initial fluid rates for premature
infants in the 1980s to reflect more accurately true fluid needs.
Environmental changes were made as well, with improvements in isolettes
and humidification of ventilators, which lowered insensible water
losses.
Any history of the feeding of the premature infant in the 20th century
would be incomplete without mentioning the advances made in total
parenteral nutrition (TPN), which became available with the use of
catheters for central fluid administration only in the 1960s. The
technical advancement of this practice continued into the 1990s, with
perfection of the technique for placing very fine central catheters
(28-gauge) percutaneously through peripheral veins. Dudrick et al. (1968)
were the first to maintain an infant with small
bowel atresia via a hypertonic mixture of protein hydrolysate and
glucose through an indwelling intravenous catheter for 44 d. The
availability of intravenous lipid emulsions for use in LBW infants in
the late 1970s finally permitted adequate growth in VLBW infants who
were given these solutions. Today, it is routine to manage infants with
a birth weight <1500 g with the use of TPN solutions, which provide
necessary energy as well as vitamins and minerals (AAP
1998
). This greatly facilitated the ability to approach the
"intrauterine requirements for growth" in these VLBW infants in the
early days of life.
Table 1
outlines the major changes in the feeding of the premature infant in
the 20th century. By way of conclusion, the following statement
summarizes the current thinking about nutrition for the premature
infant at the beginning of the 21st century: "Optimal nutrition is
critical in the management of small preterm infants. No standard has
been set for the precise nutritional needs of infants born prematurely
that is comparable to the breast milk standard for term infants.
Present recommendations are designed to provide nutrients to
approximate the rate of growth and composition of weight gain for a
normal fetus of the same postconceptional age and to maintain normal
concentrations of blood and tissue nutrients. Initially after birth,
the management of acute neonatal illnesses and gradual advancement of
feeding to minimize the risk of feeding-related complications, such
as necrotizing enterocolitis, may conflict with the nutritional goal of
obtaining rapid growth in preterm infants" (AAP 1998
).
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FOOTNOTES |
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2 Abbreviations used: AAP, American Academy of
Pediatrics; LBW, low birth weight; TPN, total parenteral nutrition;
VLBW, very-low-birth-weight.
3 The interest of formula companies in the
nutritional requirements of the premature infant was not new; as early
as 1939, the Borden Company produced a booklet on the care and feeding
of premature infants [The Care and Feeding of Premature
Infants (1939), The Borden Company, New York (from the
historical collection of the University of Wisconsin Health Sciences
Library)], which promoted an evaporated milk formula "especially
suited" for the premature infant (Biolac) because of its protein
content and added vitamins and iron.
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REFERENCES |
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TOPABSTRACTINTRODUCTIONREFERENCES |
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1.
American Academy of Pediatrics, Committee on Nutrition Nutritional needs of low-birth-weight infants. Pediatrics 1977;60:519-530
2.
American Academy of Pediatrics, Committee on Nutrition Nutritional needs of low-birth-weight infants. Pediatrics 1985;75:976-985
3. American Academy of Pediatrics Pediatric Nutrition Handbook 1998:75-79 American Academy of Pediatrics Elk Grove Village, IL.
4. Atkinson S. A., Bryan M. H., Anderson G. H. Human milk feeding in premature infants: protein, fat and carbohydrate balance in the first two weeks of life. J. Pediatr. 1981;99:617-624[Medline]
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7. Benjamin M. H., Gordon H. H., Marples E. Calcium and phosphorus requirements of premature infants. Am. J. Dis. Child. 1943;65:412-425
8. Berthod P. La Couveuse et le Gavage a la Maternité de Paris 1887 Doctoral thesis. G. Rougier Paris, France.
9. Budin, P. (1907) The Nursling: The Feeding and Hygiene of Premature and Full-term Infants (translated by W. J. Maloney). Caxton Publishing Co., London, UK.
10. Cooper P. A., Rothberg A. D., Pettifor J. M., Bolton K. D., Davenhuis S. Growth and biochemical response of premature infants fed pooled preterm milk or special formula. J. Pediatr. Gastronenterol. Nutr. 1984;3:749-754
11. Davies D. P. The first feed of low birthweight infants. Changing attitudes in the twentieth century. Arch. Dis. Child. 1978;53:187-192
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14. Gordon H. H., Levine S. Z., Deamer W. C., McNamara H. Respiratory metabolism in infancy and in childhood. XXIII. Daily energy requirements of premature infants. Am. J. Dis. Child. 1940;59:1185-1202
15. Gordon H. H., Levine S. Z., McNamara H. Feeding of premature infants. A comparison of human and cow’s milk. Am. J. Dis. Child. 1947;73:442-452
16. Greer F. R., McCormick A. Improved bone mineralization and growth in premature infants fed fortified own mother’s milk. J. Pediatr. 1988;112:961-969[Medline]
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Hansen J.D.L., Smith C. A. Effects of withholding fluid in the immediate postnatal period. Pediatrics 1953;12:99-113
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21. Hess J. H. Premature and Congenitally Diseased Infants 1922:107-204 Lea & Febiger Philadelphia, PA.
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24. Lundeen E., Kunstadter R. H. Care of the Premature Infant 1958:87-145 J. B. Lippincott Philadelphia, PA.
25. Nichols B. L. The evolution of research techniques in premature infant nutrition. Salle B. L. Swyer P. R. eds. Nutrition of the Low Birthweight Infant 1993:31-41 Vevy/Raven Press New York, NY.
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Raiha N. C., Heinonen K., Rassin D. K., Gaul G. E. Milk protein quantity and quality in low-birthweight infants, I: metabolic responses and effects on growth. Pediatrics 1976;57:659-684
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32. Silverman W. A. Dunham’s Premature Infants 3rd ed. 1961:151-179 Paul B. Hoeber New York, NY.
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34. Tyson J. E., Lasky R. E., Mize C. E., Richards C. J., Blair-Smith N., Whyte R., Beer A. E. Growth, metabolic response and development in very low birth weight infants fed banked human milk or enriched formula: 1. Neonatal findings. J. Pediatr. 1983;103:95-104[Medline]
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