CARE OF THE INFANT 0031-3955/94 $0.00 + .

20

CLINICAL ASSESSMENT OF
NUTRITIONAL STATUS AT BIRTH
Fetal Malnutrition and SGA Are Not
Synonymous

Jack Metcoff,t MS, MO, MPH

Fetal malnutrition (FM) and the terms small for gestational age (SGA)
and intrauterine growth retardation (IUGR) are not synonymous; one may
occur without the other.26,28, 35, 36 FM indicates a clinical state that may be
present at almost any birth weight. SGA is weight for gestational age
based on population norms and some predetermined weight cutoff ( - 2
SO, 5%, 10%).4, 28, 62, 64 IUGR refers to a multiplicity of adverse effects
limiting the fetal growth potential~ An infant who is classified IUGR
may, or may not, also be classified SGA.28 Likewise, an infant who is
IUGR and/or SGA may, or may not, have FM.26, 36, 40 FM affects body
composition and impairs brain development and behavior in experimen-
tal animals.2 Its effect on the brain and mental development in humans
remains controversial,* confounded by many factors including failure to
differentiate between SGA and malnutrition in the newborn. Hill,26 in a
previous study, found that perinatal problems and/or central nervous
system sequelae occurred primarily in fetally malnourished (PM) babies,
whether appropriate for gestational age (AGA) or SGA, but not those
who were simply SGA but not malnourished. For example, in 33 mal-
nourished term infants, IQ scores were significantly lower and needs for
special education higher than in 13 SGA but well-nourished infants,

This study was done at the University of Oklahoma Health Sciences Center and
presented in part at FASEB and American Society of Pediatrics in 1987.
*References 14, 16-18, 25, 26, 35, 44, 50, 58-60.

From the Department of Pediatrics, Biochemistry, and Molecular Biology, University of

Oklahoma Health Sciences Center, Oklahoma City, Oklahoma
tDeceased

PEDIATRIC CLINICS OF NORTH AMERICA

VOLUME 41 • NUMBER 5· OCTOBER 1994 875

876 METCOFF

when followed and tested 12 to 14 years later.26 Forty-five percent of the

malnourished infants had a birth weight for gestational age greater than
the 10th percentile, and their malnutrition would have been missed if
only infants with birth weights less than the 10th percentile were consid-
ered as FM. Thirty-nine percent of the malnourished infants had neuro-
logic handicaps, mental retardation, learning disorders, or seizures later
in childhood.26
The perinatal and later developmental effects of FM often are seri-
ous. The present study was undertaken to develop a practical, system-
atic, easy, and rapid clinical method to identify term babies with, and
classify the degree of, FM. Although FM adversely affects body compo-
sition, including reduced muscle mass and protein content,! organ struc-
ture and composition/I, 42 bone,52,69 chemical composition,! and metabolic
and enzyme functions,s, 24 FM is clinically characterized by obvious intra-
uterine loss of, or failure to acquire, normal amounts of subcutaneous fat
and muscle. Weight, length, and head circumference may, or may not,
be affected. A simple, clinically applicable scoring system was developed
to differentiate malnourished from appropriately nourished babies, irre-
spective of birth weight or clinical classification as IUGR, SGA, or AGA.
Usually, the clinical classification of SGA is based on observed birth
weight below the 10th percentile for gestational age, estimated by the
use of nomograms, such as that developed in Denver,33 or below the 5th
percentile if the nomogram of the National Center for Health Statistics22
is used; and/or by the Rohrer index based on weight/length3 X 10047 as
used by Miller and Hassanein41 or by serial ultrasound exams with com-
puter assisted data analysis. 48 These measures do not identify FM, nor
do they adjust for common confounding factors, such as race, stature of
mother, prepregnant weight, parity, altitude, smoking, and other fac-
tors,35 which are known to influence birthweight. The Brenner et a16
nomogram does take some of these factors into account and adjusts
observed birth weight not only for gestational age, but also for parity,
race, and sex of the baby to derive an "expected" birthweight. This
method was used in this study. Gestational age was estimated indepen-
dently by the Dubowitz exam. 15 Our scoring system rated clinical evi-
dences of malnutrition in term babies determined by inspection and
hands-on estimates of loss of subcutaneous tissues and muscle. This
simple, rapid, quantifiable examination was considered a clinical assess-
ment of nutritional status (CANS) and the score, a CANSCORE. The
differentiation between SGA and FM was achieved by applying both the
Brenner estimate of adjusted birth weight and CANSCORES to 1661
babies.

Subjects and Methods

CANS was developed as a systematized extension of the observa-

tions of McLean and Ushe~ and Scott and Usher,53 and the system
originally developed by Reba Michels Hill (personal communication,
 -
CLINICAL ASSESSMENT OF NUTRITIONAL STATUS AT BIRTH 877

1982). Nine superficial, readily detected signs of malnutrition in the

newborn (including the hair, silky versus straight; "staring," or flag sign;
buccal fat in the cheeks; sharply defined thin or fat double chin, which
usually obscures the neck in well-nourished neonates; a thin clearly
evident neck with loose, wrinkled skin; "accordion" pleating of the skin
of arms and legs with loose, easily lifted skin over knees, elbows, and
anterior femur; sunken intercostal spaces on the chest, and loss of sub-
cutaneous fat on back with loose skin easily lifted; minimal fat and
wrinkled skin on abdomen (which may be distended); and buttocks with
deep folds. These signs were rated 1 (worst, severe FM) to 4 (best, well
nourished). The CANSCORES ratings were 36 (highest) and 9 (lowest).
A single page form on which the observations and relevant data in the
nursery were recorded, with cartoons illustrating the rating of the signs,
is shown in Figure 1. Demographics, gestational age, observed and ex-
pected birth weights, and CANSCORE were recorded on the form for
each baby. Figure 2 shows photographs of babies illustrating some ex-
amples of the clinical signs of FM. These examples of individual signs
were taken for illustration purposes from several different term babies
whose observed birth weights ranged from 1800 to 3400 g.
Only 1382 singleton term babies (38 to 42 weeks) were included in
this study, the others being premature (gestational age [GA] < 38 weeks).
The assessments were, however, made on virtually all babies in the
newborn nursery within 24 to 48 hours of birth during a 3 to 4 month
period each year. Frequency distributions of all the term babies had a
"break point" at 24 (Fig. 3). Therefore, scores less than or equal to 24
were taken as clinical evidence of malnutrition, which must have oc-
curred in utero, for example, "fetal malnutrition." After brief instruction
and supervision, the assessments on some babies were made and re-
corded on the CANS form by house staff and medical students. The
variability between measures of the same babies by different observers
was less than 10%. When a baby was classified as malnourished by the
nursing staff, house staff, or medical student, the Dubowitz, Brenner,
and CANSCORE assessments were checked. At that time, other babies
in the nursery were inspected to find whether an FM baby had been
missed. The deviations observed from expected weight (WDIFF), using
the Brenner nomogram,6 were done independently and were made be-
tween 2 to 12 hours postnatally. GA also was estimated independently
of dates by the Dubowitz examination,I5 done between 12 to 36 hours
postnatally. A baby was classified SGA if WDIFF was more than 500 g
below expected weight (>500 g below), otherwise the baby was consid-
ered AGA, or if more than 500 g above expected weight, large for gesta-
tional age (LGA). Five hundred grams was approximately 1.5 times the
standard deviation of mean birth weight (3290 g ± 390 SD) of this
sample in our nursery, which differed slightly from a previous report in
a much smaller sample (348 singleton births).40
Dubowitz, Brenner, CANS, and demographic data were recorded on
the appropriate forms when the observations were made and entered
into a computer database shortly thereafter. Preceding data analysis, all
data were subject to screening for errors, exotic values were checked,
878 METCOFF

Name

Chan. No.: _ _ __

Binhdate:
/ /
MO DAY YEAR

BinhData: _ __

Weight (g): _ __

Length (em)·,-_ _

FOC(em): _ __

GA(wks): _ __

Sex: M(1)_F(2l_

Date of CANS:
/ /
MO DAY YEAR

Brenner Expected Weight:

(g)

Foot Length (em): _

SCORE: _ _

Examiner's InitiaJs:C---_

Figure 1. See legend on opposite page.

 CLINICAL ASSESSMENT OF NUTRITIONAL STATUS AT BIRTH 879

and outliers detected by univariate frequency distributions. Errors were

corrected. The outlier on the extreme tails of the distribution, less than
1% of all values, were moved closer to the median but were kept 1% to
2% above the highest or lowest sequential series of values in each of the
tails. No data were deleted. Data were analyzed by analysis of variance
(ANOVA), chi square, and analysis of covariance (COVA) using the
Statistical Analytic System (SAS) programs51 on an IBM 3081 computer.
Only babies with complete data were used. Comparisons were made in
three different ways: (1) according to the usual classification of AGA
depending on weight for gestational age less than - 500 g from expected
weight (WOlFF), and SGA greater than - 500 g below expected weight;
(2) by nutritional status (CANSCORE), nourished (NOUR) or malnour-
ished (FM); or (3) by combinations of both measures: as AGA (WOlFF
< - 500 g) and nourished (NOUR), or SGA (WOlFF > - 500 g) but
NOUR with CANSCORE greater than 24, SGA or AGA with CAN-
SCORE less than 25 but malnourished (FM).
Of the 1661 singleton babies with Dubowitz, Brenner, and CANS
assessments, 1382 were born at term (gestational age greater than 37
completed weeks) and 279 (16.8%) were preterm, less than 37 completed
weeks' gestational age. Ninety-five percent (1161) of AGA babies had a
score greater than 24, but 46% (70) of 153 SGA babies also had a score
greater than 24. More than 54% (83/153) of the SGA babies were mal-
nourished, as were 5% (68/1229) of the AGA babies (Table 1). Thus, 46%
of the SGA babies were small but not malnourished, and 5.5% of AGA

Figure 1. The nine signs for clinical assessment of nutritional status (CANS) in newborn
term infants. Each of the signs is rated from 4 (best, no evidence of malnutrition) to 1 (worst,
definite evidence of malnutrition in utero [FM]). Hair: Large amount, smooth, silky, easily
groomed (4); thinner, some straight "staring" hair (3); still thinner, more straight "staring"
hair which does not respond to brushing (2); and straight "staring" hair with depigmented
stripe (flag sign) (1). Cheeks: Progression from full buccal pads and round face (4); to
significantly reduced buccal fat with narrow, flat face (1). Neck and Chin: Double or triple
chin fat-folds, neck not evident (4); to thin chin, no fat folds, neck with loose, wrinkled skin
very evident (1). Arms: Full, round, can't elicit "accordion" folds or lift folds of skin from
elbow or triceps area (4); to striking "accordion" folding of lower arm elicited when examin-
er's thumb and fingers of the left hand grasp the arm just below the elbow of the baby and
thumb and fingers of the examiner's right hand circling the wrist of the baby are moved
toward each other; skin is loose and easily grasped and pulled away from the elbow. Back:
Difficult to grasp and lift skin in the interscapular area (4); to skin loose, easily lifted in a thin
fold from the interscapular area (1). Buttocks: Full, round gluteal fat pads (4); to virtually no
evident gluteal fat and skin of the buttocks and upper, posterior thigh loose and deeply
wrinkled (1). Legs: Like arms. Chest: Full; round ribs not seen (4), to progressive prominence
of the ribs with obvious loss of intercostal tissue (1). Abdomen: Full, round, no loose skin (4)
to distended or scaphoid, but with very loose skin, easily lifted, wrinkled and "accordion"
folds demonstrable (1). Demographics: Self-explanatory. Actual measurements are made in
the nursery (which often differ from those made at delivery). GA (gestational age) refers to
the Dubowitz assessment. Brenner expected weight is adjusted birthweight from use of the
Brenner nomogram. Foot length (not used in the CANSCORE) is proportional to the length
of gestation (e.g., 8.2 to 8.5 cm in a term, 39 weeks baby). Score: Sum (total) of the ratings
of the nine CANS signs = The CANSCORE.
880 METCOFF

Table 1. DISTRIBUTION OF SMALL FOR GESTATIONAL AGE AND FETAL

MALNUTRITION DIAGNOSES IN 1382 NEONATES
CANSt

Brenner" FM Nourished Total

AGA 68 1161 1229

(5.5%) (94%) (89%)
SGA 83 70 153
(54%) (46%) (11%)
Total 151 1231 1382
(10.9%) (89.1%) (100%)

Note that 68 (5.5%) of AGA and 83 (54%) of SGA babies, or 10.9% of 1382 term neonates, were
malnourished in utero (FM). However, 70 (46%) of 153 SGA babies, 11% of the total sample, were not
malnourished.
'Brenner: adjusts observed birth weight for gestational age, parity, sex, and race = "expected"
weight. If observed expected weight> 500 g below = SGA.
tCANS: clinical assessment of nutritional status scores, max = 36; <25 = FM.
CANS versus Brenner: X' = 0.000, Fisher's exact t·test P = 0.000.
FM = fetal malnutrition, AGA = appropriate for gestational age, SGA = small for festational age.

babies were fully grown but were malnourished. Obviously, a large error
in classification (greater than 50%) would occur if SGA or IUGR were
considered synonymous with fetal malnutrition, and if all AGA babies
were considered adequately nourished.

DISCUSSION

Fetal Malnutrition

The most rapid period of normal fetal growth is in the 20 weeks

between 12 and 36 weeks of gestation (i.e., postconceptual age). Between
32 and 36 weeks, the rate of fetal weight gain reaches its peak at 200 to
225 g/wk and declines thereafter. 6 During a 40-week gestational period,
the normally growing human fetus accumulates about 400 g of protein
beginning at conception, and 475 g of fat (most in the last 8 weeks), as
well as 2700 g of water and contained minerals. 54,66 In disagreement with
Naismith's hypotheses,43 the fetus is not a parasite; it only extracts about
2% to 4% of the nutrients reaching it from the placenta,36 96% to 98%
being returned to the placenta and maternal circulation, and utilizes the
nutrients it extracts. It can be underfed or overnourished, depending on
extraction and nutrient composition of the umbilical blood and the flow
rate and capacity to utilize the extracted nutrients.3, 31, 50 Food restriction
in pregnant versus nonpregnant rats causes equivalent weight loss and
changes in body composition of both groups, but the fetuses of the
pregnant rats are significantly smaller than fetuses of normally fed
rats. 29,30
The clinical manifestations of fetal malnutrition depend, in part, on
when it began during gestation. Babies whose length, head circumfer-
ence, and weight are significantly reduced probably were exposed to
Text continued on page 885
 CLINICAL ASSESSMENT OF NUTRITIONAL STATUS AT BIRTH 881

Figure 2. Photographs of some examples of the CANS signs in several newborn, term FM
babies. A, Mexican baby with a full head of hair but obvious malnutrition evidenced by a
score of 1 for the other 8 signs. B, Straight "staring" thin hair with "flag" sign, rated 4. C,
Thin chin without fat folds and thin, very evident neck with loose, wrinkled skin (1).
882 METCOFF

Figure 2 (Continued). D, "Accordion" folding of skin of lower arm and elbow (1). E, Loose,
thin skin, with minimal subcutaneous fat, easily lifted from elbow (1). F, Buttocks with minimal
gluteal fat and loose, deeply wrinkled skin (2).
 CLINICAL ASSESSMENT OF NUTRITIONAL STATUS AT BIRTH 883

Figure 2 (Continued). G, Back with loose skin, minimal subcutaneous tissue, easily lifted
from the interscapular area (2). H, "Accordion" folding of skin of the lower leg (1). I, Very
loose skin, easily lifted from the anterior tibial area (1).
!

120j
110

.. 100
90
" 80
E
Q
U
E 70
N
C 60
'(
50
C
0 40
U
N 30
T
20
10
0
10 20 30 40
SCORE

Figure 3. Clinical assessment of nutritional status (CANS). Frequency distributions of CANS scores for malnourished
and normal newborns. Malnourished = birthweight more than 500 g below expected weight (e.g., Brenner, adjusted
for gestational age, parity, race, and sex). ARM score less than 3. Type A = *, type S = O·
 CLINICAL ASSESSMENT OF NUTRITIONAL STATUS AT BIRTH 885

malnutrition beginning early in the second trimester. Those whose length

and head circumference are less affected but are small and underweight
with some loss of subcutaneous tissues and muscle probably became
malnourished beginning early in the third trimester. For babies who are
significantly underweight for gestational age with obvious loss of sub-
cutaneous tissues, but with length and head circumference within the
normal range, an insufficient or unbalanced nutrient supply most likely
occurred in the late third trimester (after 36 weeks' gestation).20, 28, 6! For
the last two categories, weight, that is, total tissue mass, may be above
the tenth percentile for gestational age; however, signs of malnutrition
may be obvious. Such an infant's expected weight might have been at
the 50th to 75th percentile in utero, whereas observed birthweight is at
the 10th to 15th percentile at birth,
If the fetus does not receive or fails to utilize sufficient nutrient
substrates, the amounts of protein and fat synthesized are reduced; this
is reflected by decreased body content of these nutrients.! If the nutrient
supply is limited acutely after the period of rapid fetal growth (20 to 36
weeks) or if gestation is prolonged and more than 42 weeks, the fetus
cannibalizes some of its previously deposited fat and protein.36, 50, 56 When
this occurs, plasma amino acids and other nutrient concentrations in the
fetus may be sustained at nearly normal concentrations by nutrients
derived from the baby's own catabolized cells.
The umbilical venoarterial concentration differences for amino acids,
except for glutamine, are not significantly different in SGA infants, al-
though levels of the branched chain amino acids were significantly lower
in both umbilical venous and arterial blood. 7 Intracellular amino acid
concentrations, however, are abnormal and the rate of protein synthesis
is decreased. 37,38

Clinical Assessment of Nutritional States

Neither SGA nor IUGR are synonymous with FM. FM is a clinical

diagnosis and is independent of birth weight for gestational age. Fetal
malnutrition, a term coined by Scott and Usher,52 can be identified on
the basis of typical clinical features. Clifford lO considered babies with
obvious malnutrition as "dysmature." Pick in 195446 recognized malnu-
trition in 3 babies. Each of these babies was term, weighed less than 2.2
kg at birth, and was 48.3 to 53.3 cm in length. All had significant placen-
tal abnormalities and/or marked thickening of the walls of the umbilical
arteries and narrowing of the lumens, later described as placental
insufficiency.IO,2! Postnatally, these babies had very rapid growth with
high caloric feedings, more than doubled their birth weight by 4 months,
and had developmental progress that was normal thereafter. Their mal-
nutrition probably began late in the third trimester and was probably
related to insufficient delivery of nutrients from an abnormal placenta.
In FM, the subcutaneous tissue and underlying muscle are diminished and
the skin of arms, legs, elbows, knees, and interscapular regions is very
886 METCOFF

loose. In severe FM, the neonate may look "emaciated" or "marasmic,"

as described by Pick. The skin appears several sizes too large for the
baby. The decreased subcutaneous fat and muscle are evident by more
quantitative measures, such as upper arm circumference, and triceps and
interscapular skin fold measurements/a' 28,34,40,52,62 with estimate of arm
muscle area.19, 20, 40 Buccal and buttock fat pads are reduced, and the scalp
hair may be coarse, patchy, or "straight and staring," as in marasmus, or
even have a "flag sign," as in severe protein-calorie malnutrition (kwa-
shiorkor).
Differentiation of FM neonates from adequately nourished neonates,
whether AGA or SGA, provided the basis for development of our CANS
score. The comparison of various modalities, for example, reduced
growth, neurologic handicaps, later learning difficulties, poor school per-
formance, low IQ tests4 of SGA versus AGA, with the latter considered
the "control group," and using observed birth weight for gestational age,
as in most reported studies, were based on the presumption that SGA is
synonymous with FM. Failure to identify FM confounds both the test
and control groups by inclusion of undiagnosed FM babies among the
AGA controls, and NOUR but not FM babies in the SGA test groups,
thus underestimating the effects of FM on physical and mental develop-
ment. In our study, 46% of SGA infants were not malnourished (based
on adjusted birthweight and CANSCORES) and 5% of AGA infants were
fetally malnourished. If, as observed by Hill/6 39% of later neurologic
and intellectual handicaps occur predominantly in PM babies, they
would have been missed if only a birthweight of less than the 10th
percentile was used. Thus, about half of the SGA and at least 5% of the
AGA malnourished babies are at risk. For example, in the studies by
others,14, 16-18, 32, 44 it is likely that half the SGA babies did not have FM
and therefore were at significantly reduced risks for later developmental
disabilities, whereas at least 5% of the AGA (control) babies had FM,
thereby confounding the comparison group. Stein and Susser's retrospec-
tive epidemologic study8-60 failed to find reduced mental performance
at age 19 in young men who had intrauterine (last trimester) and post-
natal exposure to undernutrition during the Dutch famine of 1944 to
1945. Their study has been widely cited as evidence that malnutrition
during pregnancy does not affect mental development. Fetally malnour-
ished babies, however, may have been underrepresented among the male
army recruits 19 years later. The intelligence tests at induction centers
were confined to survivors, noninstitutionalized and competent individ-
ual males. 35 More than twice the number of individuals classified as mild
mental retardation (borderline intelligence, morons) were conceived dur-
ing the food shortage compared with individuals conceived before or
born during the famine. The incidence of stillbirths (36.5/1000 livebirths),
perinatal deaths (65/1000 livebirths), and deaths during the first year of
life from central nervous system malformations (2.2-2.5/1000 livebirths)
was markedly increased compared with the period before or 4 to 5
months after the food shortage.67
In the study by Hill et a1/6 of 33 malnourished babies, birth weights
of 15 babies (45%), lengths of 21 babies (66%), and head circumferences
 CLINICAL ASSESSMENT OF NUTRITIONAL STATUS AT BIRTH 887

of 29 babies (79%) were more than the 10th percentile for gestational age.
Overall, 32.6% of FM infants would have been misclassified as AGA.
Follow-up for 12 to 14 years after birth revealed that FM babies had
significantly lower IQ (verbal, performance, and full-scale65 ) scores than
well-nourished infants. Thirty-nine percent of FM infants with handi-
caps, including spastic diplegia, seizures, visual problems, learning dis-
abilities, or mental retardation, had birth weights greater than the 10th
percentile on the Denver fetal growth curves. FM would not have been
recognized as a probable cause of later neurologic or mental disabilities.
Our data, like Hill's, indicate that when classification into SGA and AGA
groups is based on growth curves alone, and all SGA babies are consid-
ered at risk, then comparison of the two groups would be biased, because
45% are likely to be SGA/NOUR and 5% of AGA/FM babies likely
would be considered as the AGA "control" (presumably NOUR) group.
Perina tally, about one third of term SGA babies are at risk for hy-
poglycemia and increased lactatemia, possibly because of delayed ontog-
eny of critical enzymes, for example, phosphoenolpyruvate carboxyki-
nase in the gluconeogenic path,s, 24, 67 and/or prenatal exhaustion of
hepatic glycogen reserves. 55 These biochemical deficits are also evident
in experimental animals with FM.27, 45, 57, 68 Because less than one half of
SGA babies develop hypoglycemia, it seems possible that an SGA infant
with FM is more likely to be affected than a non-FM SGA baby.
In utero nutritional support to supplement fetuses of ewes on pro-
tein-calorie restricted diets, either by intragastric infusion8 or intravenous
administration, ameliorates the development of placental embolization-
induced growth retardation in sheep.9 This work clearly demonstrates
that the effects of the circumstances that limit fetal growth may be re-
versible with nutritional support. For example, mothers who smoke dur-
ing pregnancy are known to deliver babies with birth weight at least 200 \
g below expected weight. If such women received a nutritional supple-
ment (WIC) from mid-pregnancy, however, their babies were signifi-
cantly (P = 0.017) heavier (168 g) than babies of unsupplemented smok-
ing mothers.39 When SGA can be detected in utero, during the second or
early third trimester using ultrasound and prediction of fetal growth,
such as that devised by Rossavik,49 Deter et al,l1-13 and cordocenteses
used to obtain umbilical blood for concentrations of nutrients in plasma
and cells/' 23, 57 specific intrauterine nutrition therapies for the human
malnourished infant could be developed to prevent malnutrition at birth,
which might prevent some later developmental problems. Numerous
investigators have used chronic infusions of glucose and/or amino acids
given to pregnant women to augment impaired fetal growth or have
added nutrients to the amniotic fluid, with apparent improvement of
fetal growth. 23
The association of SGA with FM might account for the observation
that only about one third of SGA babies fail to exhibit catch-up growth
postnatally, have congenital anomalies, perinatal hypoglycemia, hypo-
calcemia, and/ or polycythemia, and develop neurologic and mental def-
icits by school age as judged from reports by Eaves,16 Fancourt,17 Fitz-
hardinge and Steven/ 8 Hill,26 and others.
 888 METCOFF

CONCLUSION

To summarize, in a large sample of 1382 term neonates, a simple,

brief clinical assessment of nutritional status (CANS) revealed that 151
(10.9%) were FM, including 5.5% of 1229 AGA and 83 (54%) of 153 SGA
babies. Nearly half (45.8%) of the SGA infants were not malnourished in
utero.
Hopefully, some investigators will, in the future, relate our CAN-
SCORE identification to distinguish malnourished FM babies from non-
malnourished SGA and IUGR babies with Rossavik's intrauterine predic-
tions49 similar to the studies by Deter et al,12 then follow up the later
physical and mental development of the babies like those reported by
Hill et aU6 Further, if maternal malnutrition is a probable cause of fetal
malnutrition36, 39, 40, 42 and the nutritional state of the mother is appropri-
ately evaluated at mid-pregnancy to predict births of small babies some
20 weeks later/6, 39, 40 coupled with cordocentesis to assess fetal, placental,
and maternal nutrient metabolism3, 7, 8, 57 with serial ultrasound evalua-
tions, the diagnosis of a FM fetus might be made in the second trimester
and nutritional therapy for mother and fetus could be carried out in
utero to correct FM before birth.
About 20 million babies are born per year with birth weights less
than 2500 g worldwide, and 30% to 40% of these infants are born at term
gestation and therefore are SGA. Our observations suggest that at least
one half of these (about 3 million) babies are fetally malnourished. With
fetal and maternal nutritional therapy starting at mid-pregnancy, FM
might be prevented or corrected and thousands of babies in the United
States and millions worldwide would be spared a bleak future and have
a better chance for a normal, productive life as competitive citizens.
I

ACKNOWLEDGMENT
The author is grateful to Andrew Cucchiara, PhD, for assistance with the statistical
analysis; and to the Pediatric House staff and Nursing staff in the Newborn Nursery at the
Oklahoma Memorial Teaching Hospital at OUHSC who contributed to this study; and to
Esther Werre, Department of Pediatrics, Evanston Hospital, for superior help in preparation
of the manuscript.

References

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Joseph Hagemann, MD
Division of Neonatology
Department of Pediatrics
Evanston Hospital
2650 Ridge Avenue
Evanston, Illinois 60201