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age, months figure 2-8 Centiles of daily weight increments of normal infants. (Source: Drawn from data in Roche SG, Fomon S. Reference data on gains in weight and length during the first two years of life. J Ped. 1991;119:355-362.)

A short child may or may not be ill at the time of measurement: He may have a late sequelae from a process occurred in the past. On the contrary, if a child is not growing at a normal rate, then we are certainly facing a pathological condition, occurring during the period in which she was measured. Growth velocity provides excellent information of the dynamic condition of the growth process. For example, Figure 2-6 (point c) shows the attained height of a malnourished child 2 years old. We can say there is a marked height deficit. If the following measurement was point z, it would mean that the growth rate is abnormally slow and the child is progressively deteriorating and at high risk. On the contrary, if the following measurement was point v, then growth rate is higher than normal and we can assume the child is in the process of catching up and recovering from malnutrition.

Some Considerations of Pediatric Value

Both growth delay or small size are quite common causes for consultation in pediatric practice. However, they are unspecific clinical signs, because growth impairment may have a great variety of underlying causes. The majority of the causes of growth problems at the primary care level can be identified without the use of sophisticated tests or studies.

In general, the clinical approach to growth problems in the first 1 or 2 years of life should be a different approach than to growth problems appearing later. In the first year of life, small size or short stature frequently is related to the pre- or perinatal period. In other cases, especially growth delay during the first year, they are secondary to causes of multifactorial origin. In case of growth delay in the school years, if the child is asymptomatic, we can take more time to search for the underlying cause. For example, we could evaluate the growth velocity over a period of 6 or 12 months without seriously affecting the prognosis. However, if the patient is an infant, we cannot wait such a long time. Growth problems presenting during infancy should be investigated and diagnosed as early as possible.

The long-term consequences of growth delay in infancy may be serious. The obvious result of growth retardation during this period of life is short stature. The risk of the final height being adversely affected as a consequence of growth delay is higher if the delay takes place during infancy, because the child is growing very quickly at this time. There are also other possible consequences of early growth delay. Martorell et al.19 have described educational and functional impairment in adulthood as a result of stunting at 3 years of age in a sample of impoverished Guatemalan children. Studies carried out in the United Kingdom in the last 20 years suggest that growth retardation during prenatal life and the first year of postnatal life may be associated with a variety of adult conditions including cardiovascular disease, stroke, hypertension, non-insulin-dependent diabetes mellitus, and low bone mineral density. The mechanisms underlying this association may be related to early metabolic changes in hormone interactions and modalities of tissue responses to these hormones, with persisting and long-term consequences in adult life. This phenomena of early metabolic changes being associated with late consequences are referred to as fetal or metabolic programming.20-22

In childhood, growth problems have an important impact on the child's psychosocial adjustment. The problem itself, and the accompanying clinical and laboratory studies directed to the identification of the problem, may interfere with school performance, sports, and social integration.

As happens in other phases of growth,9 the chance of experiencing complete catch-up depends on the duration of the factors causing growth delay, their intensity, the age at which they occur, and as stated by McCance, the "individual thrive to grow."23

Causes of Short Stature

The description of the causes of short stature varies according to the auxolog-ical diagnosis. If we want to describe causes of small size (weight or length), the picture is different to the description of the causes of growth delay. Taking into account that, in a clinical setting, this problem is usually presented as smallness, we describe causes of short stature defined as height below the third centile of appropriate height-for-age (distance) charts.

Malformations, Deformations, or Alteration of Body Proportions

In these cases, short stature is only a part of the clinical picture. This group includes children with skeletal dysplasias, some of neonatal onset (e.g., achon-droplasia), some others detected after the second year of life or even later in childhood (e.g., hypochondroplasia, dyschondrosteosis); dysmorphic syndromes, either of genetic origin (e.g., Noonan's syndrome), chromosomal alterations (e.g., Turner's syndrome), or due to prenatal infections (e.g., congenital rubella syndrome); and teratogenic malformations (e.g., fetal hydantoin syndrome, fetal alcohol syndrome). Some syndromes evolve with a normal growth velocity in childhood, such as Silver-Russell syndrome, but others with a slow growth velocity, such as Turner's syndrome.

Dysmorphic syndromes and chromosomal disorders are well described in books specially dedicated to their clinical identification.24 Searching devices built on information databases may be helpful in the diagnosis.25 Some syndromes are quite frequent (for example, Turner's syndrome has an incidence of 1 in every 2500 female births), and others are rarer, such as achondroplasia (one case in every 26,000 births), see Chapters 10 and 11.

In the Absence of Dysmorphism, with Normal Body Proportions

Extreme Variations of Normality

Extreme variation of normality includes two conditions: familial short stature and delayed maturation. Both are normal conditions and the most frequent diagnosis made in clinical practice.

A diagnosis of familial short stature (FSS) is made in normal children older than 2 years, with no underlying disease, normal physical examination, and normal growth velocity. Height is usually within -2.0 and -3.0 SD (standard deviation) scores, or Z-scores, and the height of the child adjusted to that of the parents is within normal limits (-2.0 and +2.0 Z-scores). The parental adjustment can be calculated by subtracting the average of the parents Z-scores from the child's Z-score. For example, in a child whose height Z-score is -2.5 (less than the third centile and perhaps indicative of abnormal short stature), the father's height is -0.98 Z-score and the mother's height is -1.66 Z-score, the child's adjusted Z-score for height (AHZ) is AHZ = -2.50 - {[(-0.98) + (-1.66)]/2} = -1.18 SD, which is within normal limits.

Much care should be taken, however, when a parent's height is below normal limits for population standards, for the parent may have a pathological condition and, in turn, this condition may have been inherited by the child. Also, when the child's height deficit is below -3.00 Z-scores, the diagnosis of FSS should be put in doubt. In FSS, predicted final height using the most common methods26 is within the genetical range. This range (10th and 90th centiles) is within ±7.5 cm of the corrected mid-parental height. Mid-parental height is "corrected" for the sex of the child under consideration by adding 13 cm to the height of the mother if the child is a boy or subtracting 13 cm from the height of the father if the child is a girl (13 cm is used because this is the average difference in adult stature between the sexes). If both mother and son were on the 50th centile (0 Z-score) as adults, we would expect the son to be 13 cm taller than his mother. A 50th centile daughter would be expected to be 13 cm smaller than her 50th centile father. For example, for a boy, whose father and mother's heights are 167.0 and 158.0 cm, respectively, the genetic range is [167.0 + (158.0 + 13)]/2 = 169.0 ± 7.5 cm. The height of the parents should be actually measured in the clinic, since parental height by hearsay has proven to be quite unreliable,27 and consequently, the estimated genetic range is expected to be wider.

A diagnosis of delayed maturation is made in children with late onset of puberty, delayed skeletal maturation, or both with no other abnormal feature and normal height velocity. Both conditions usually are present but not always, since bone age does not correlate well with pubertal events with the exception of menarcheal age. There is usually a family history of delayed puberty that is more evident by a mother's late menarcheal age than by evidence from the father. Predicted height is within the normal parental height, however, it is very common that, during puberty, the acceleration of bone age is below the predicted one. On average, children with delayed maturation attain a height some distance below their genetic target. Physical examination is normal, and growth velocity is also normal during childhood. This diagnosis is more frequently made in boys than in girls, which may be a reflection of problems in self-esteem and psychosocial integration, especially in puberty.

Perinatal Problems

Intrauterine growth retardation (IUGR)28 is diagnosed when the weight or length at birth is low for the infant's gestational age. Birth length is related more to the height the child attains in childhood or at maturity, whereas birth weight is strongly related to neonatal mortality and morbidity. A proportion of children who have growth retardation catch up in postnatal life, either during the first years or even during childhood. Approximately 20% of all IUGR children do not catch up at all.

The possibility of catching up depends on the type or nature of the IUGR experienced in prenatal life, including the nature of the damaging agent, its timing of occurrence, and duration. If the impairment took place in the first trimester, as happens in congenital rubella, then the probability of catching up is almost nonexistent, and at school age, the child will have the same growth deficit as at birth.29 In the case of mild growth impairment experienced in the last trimester, as happens with many cases of twin pregnancy or minor diseases of short duration suffered by the mother, then catch up is feasible, and it is usually detected in the first few postnatal months. In between these two extreme situations are many intermediate conditions.

Preterm babies born with normal weight for their gestational age can also be small during the first year of life, but due to a different mechanism;30 growth delay after birth. The growth assessment of preterm babies should include the use of a chart that allows for an age calculation based on gestational age. Figure 2-7 shows an example of such chart, where the X-axis indicates the age, in terms of postconception age.31 This is calculated counting the time in completed weeks elapsed from the first day of the last menstrual period up to the day of birth. The menstrual period is an indicator of the time of conception, which is why this age is called the postconception age. This age is marked in the chart until 92 weeks, exactly 1 year after term (i.e., 40 weeks of full-term gestation plus 52 postnatal weeks).

Curve a of Figure 2-7 shows the postnatal growth of a baby born at 32 weeks gestation with a birth weight of 1200 g. This birth weight is located on the 25 th centile, hence, the child has an adequate weight for gestational age. This baby spent 3 months in an incubator, during which time he had many complications (feeding, respiratory, and metabolic problems). His growth curve could not be kept within the centile lines in which he was born, and his growth rate was slower than normal during the period 28-41 weeks postconception. Afterward, when he became easier to feed, he started recovering weight and finally experienced a complete catchup growth. In this baby (as in many others), three phases of growth can be iden-tified:32 the first period with a growth retardation, followed by a second period of catch-up, and then a third period with a normal growth rate. Not all preterm babies grow this way. Some of them, like curve b, may not catch-up and remain with a height deficit during the rest of their infancy and childhood. These children may present at later ages for short stature. Their clinical examination and growth velocity at later ages is normal, and unless a careful perinatal history is taken, the cause of their short stature may remain obscure.

Immediate postnatal growth of newborn groups in institutions is a good indicator of the quality of perinatal care, and in my view, standard and comparable ways of evaluating it should be developed as positive indicators of perinatal care and as an important complement to neonatal mortality.


Primary malnutrition is consequence of reduced nutritional intake (either predominantly proteins, predominantly calories, or both), strongly associated with unfavorable socioeconomic conditions. Kwashiorkor (predominantly protein deficiency)

and marasmus (predominantly calorie deficiency) are perhaps the most frequent causes of growth impairment in the world. They are frequently observed in developing countries33 and in inner cities and marginal groups of developed countries. The severity of the growth deficiency is proportional to the severity of the nutritional deficit.

Depending on the duration and quality of protein and energy deficiency and the relative impact on growth in weight and height, two main types of malnutrition can be recognized: stunting and wasting.34 Wasting, assessed by the weight-for-height index, is the expression of present nutritional state and near past food intake; it is also associated with a high risk of disease and death. Stunting, assessed by the height-for-age index, is an indicator of past nutrition. It is not necessarily associated with a higher risk of disease and death.

Recent research has suggested that body composition in late childhood may be associated with the relative intake of energy and proteins in early life. A high-protein/low-energy intake in infancy is associated to a higher degree of fatness in late childhood. This association may in turn be related to the influence of the early diet on hormone secretion.35

Psychosocial Deprivation

Type 1 psychosocial deprivation (PD) applies to infants with nonorganic failure to thrive. Maternal deprivation, lack of adequate nutrition, and other factors may intervene in this entity, in combination with deficit in the swallowing function, deficiency of micronutrients, and the like. There may be reduced growth velocity in weight, height, or both. Type 2 PD applies to children older than 3-4 years of age, in whom nutritional deficiencies are not apparent, and the underlying mechanism is thought to be growth hormone deficiency.3

Chronic Disease

Practically any chronic disease may have an impact on physical growth. The most frequent entities seen in practice are severe asthma, malabsorption (e.g., celiac disease, chronic inflammatory disease, cystic fibrosis), congenital heart disease (especially with right to left shunt or cardiac failure), chronic renal failure, chronic anemia, metabolic acidosis of any origin, chronic pulmonary disease, and chronic infections (e.g., tuberculosis, AIDS). The mechanisms underlying growth delay in these entities are varied, such as reduced nutritional intake (secondary to anorexia, malabsorption, volume-limited intake), metabolic disbalance, hypoxia, chronic metabolic acidosis protein loss, and not infrequently, the treatment itself.

With the progress of therapeutic resources in medicine and the consequent reduction in mortality, the impact of the chronic disease on growth is becoming more and more important. From the point of view of the health care team, this becomes an indicator of treatment quality, and from the patient's point of view, an indicator of quality of life. In the case of acute lymphoid leukemia, for example, currently more than 90% of children survive after 8 years of treatment. After this and many other important advancements achieved in the last years, we could say,

"children do not die anymore, but . . . how do they grow?" There is thus a new challenge for the clinical management of children surviving diseases that were lethal in the near past.36


Some drugs are well known for their negative impact on growth. A major one is adrenal steroids, widely used in asthma, nephrotic syndrome, lupus, and many other chronic diseases. Any dose greater than the physiological one may delay growth, and the magnitude of the retardation is proportional to the dose and the duration of the treatment. Doctors know that sometimes a high price is paid for achieving a successful treatment, and in these cases, a continuous balance between the need to maintain the patient in an asymptomatic state and allow a normal pattern of growth has to be permanently maintained.

Other drugs, such as cytostatics, can affect growth. Cranial irradiation used in the treatment of tumors of the central nervous system and leukemia can damage the hypothalamic functions. Such damage has implications for the release of both hypothalamic and pituitary hormones, not the least of which is growth hormone.

Endocrine Conditions

These problems are discussed in Chapter 10.


Physical growth is the very substance of pediatric practice, modern pediatric knowledge reverberates along its axes. It provides a longitudinal, sequential, and prospective view of the human being during the most evolving and dynamic period in human life.


I am grateful to Dr. Nidia Escobal and Virginia Fano for their valuable suggestions to the manuscript.


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