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EVALUATION OF CHILDREN PHYSICAL DEVELOPMENT

June 26, 2024

EVALUATION OF CHILDREN nPHYSICAL DEVELOPMENT. SEMIOTICS OF DISORDERS OF PHYSICAL nDEVELOPMENT

Growth and development represent a continuous interaction of biologic nprocesses that begin at birth and terminate at death. The integrity and the nquality of these processes are influenced by a myriad of variables, including ngenetic, physiologic, biochemical, psychological, and socio-economic factors. nPhysicians are uniquely responsible for safeguarding and enhancing growth and ndevelopment. The traditional medical role focuses on preventing, detecting, and ntreating the noxious influences that can impair these processes.

Among physicians the challenge is particularly demanding for the npediatricians because much of growth and development is completed during the nfirst few years of life. Professionals providing health care for children must nbe aware of the various genetic, nutritional, hormonal, emotional, and economic nimpediments (among others) that can severely disturb the milieu for normal ngrowth and development. Failure to recognize antecedent high-risk factors and nsignals that herald disturbed patterns of growth and development may result iserious and permanent disabling sequel. Students of pediatrics, regardless of ntheir level of training, should be familiar with the complex processes that nconstitute growth and development.

Knowledge of the normal growth and development of children is essential nfor preventing and detecting disease by recognizing overt deviations from nnormal patterns, Although the processes of growth and development are not ncompletely separable, it’s convenient to refer to “Growth” as the increase ithe size of the body as a whole or the increase in its separate parts, and to nreserve “development” for changes in function, including those influenced by nthe emotional and social environments. The development of the human organism is na large, complex topic. To identify and treatment underlying disorders, all who ncare for children must be familiar with normal patterns of growth and ndevelopment so that they can recognize abnormal variations.

Within the broad limits that characterize nnormal development, every individual’s path of growth and development through nthe life’s cycle is unique, with a range of complex, interrelated changes noccurring from the molecular to the behavioral level. One goal of pediatrics is nto help each child achieve his or her individual potential for growth and ndevelopment and thus become a mature adult. Periodically nmonitoring each child for the normal progression of growth.

Physical ndevelopment is a dynamical process of ngrowth and biological maturation of a child nusually referred to as a unit, express the sum of the numerous changes nthat take place during the different periods of childhood.

The main criterions of assessment of physical development are:

• nweight;

• nheight (stature, nhead-to-heel length);

• nhead circumference (HC); •

nchest circumference;

• nproportionality of these measurements.

To ndetermine whether or not growth and development have taken place, the child can be compared to a representative ngroup of children at the same point in time (cross-sectional method), or the same nchild can be measured and compared at different npoints in time (longitudinal method). Standards or norms for the study of developmental progress have been established by nthese two contrasting methods. The nmost commonly employed technique for assessment of child’s physical development is measurement of height and weight. nWhen compared with standardized nnorms, a child’s developmental progress can be determined with a high degree of confidence.

The maximum growth in length nand weight occurs before birth in prenatal period. Body weight of fetus of 25 to 42 weeks of gestation can be ncalculated according to the empirical formula: in average the body nweight of 30-weeks fetus is 1300 g, for each previous week minus 100 g, for each nnext add 200 g.

For nexample:

• nBody weight of n26-weeks fetus equals 1300 – 100×4 = 900 g;

• Body weight of 35-weeks fetus nequals 1300 + 200×5 = n2300 g.

Body length of fetus of 25 to 42 weeks of ngestation can be calculated according to formula:

L = gestation age (in weeks) + 10 cm;

Or body nlength of fetus of first 5 months of gestation equals:

nL = (gestation age (in months))².

For fetus of 6 to 9 months of gestation:

L= gestation age (imonths) x 5.

For nexample:

· nBody length of 32-weeks fetus equals n32+10=42 cm;

· nBody length of 3 months fetus equals 3²=9 ncm;

· nBody length of 7 months fetus equals n7x5=35 cm.

· n

Newborns. At birth weight is more variable than height and to a ngreater extent is a reflection of the nintrauterine environment.

The average newborweighs 3200 to 3400 g (7 to 7.5 npounds).

Admissible limits of nthe norm ranges from 2700 to 4000 g. Babies, which birth weight equals more nthan 4000 g, are called huge. Birth nlength is influenced considerably by the prenatal environment and gestatioage. It is of great value as a sign of maturity of newborn organism. Its normal nrate ieonate is 50 to 52 cm. nAdmissible limits of the norm ranges from 46 to 56 cm.

Head circumference at nbirth is equal 34 to 36 cm.

Chest circumference nequals 32 to 34 cm.

Anthropometrical measurements and their assessment

Weight.

Technique nof procedure.

Weigh ninfants nude on platform-type scale; protect infant by placing hand above body to prevent falling off scale. Weigh young childre(by 2 years) nude on platform-type scale in sitting position. Weigh older nchildren in underwear (no shoes) ostanding-type upright scale. Check that scale is balanced before weighting. nCover scale with cleaapkin or sheet of paper for each child. Measure to the nearest 10 ng or 0.5 ounce for infants and 100 g or 0.25 pound for children. To have exact results weigh children in the morning nbefore first meal, after nurination and defecation.

platform-type scale

During first days of nchild’s life there appears to be a small decrease of body weight that is called nphysiological loss of weight. The maximum weight decrease is 6 to 8 % of birth nweight. After the third day of life an increase begins, and the renewal of birth weight is observed by the seventh (eighth) day of nlife. But only 20 % of childreshow this ideal type of physiological weight loss. For others it takes more time (approximately till 10-th to 14^th day of nlife) to regain birth weight. This physiologic weight loss represents a loss of nexcessive extracellular fluid and meconium, in addition to relative lack of nfood and fluids intake. The rate of nweight gain increases rapidly for a shot time after birth but soon decreases markedly. By the time the individual reaches nmaturity the birth weight has only increased about 20 times (to 68 kg). Igeneral the birth weight doubles by 4 to n4.5 months of age and triples by the end of the first year (See Table 3.1). By the end of the second year it usually quadruples. After nthis point the “normal” rate of nweight gain, just as the growth in height, assumes a steady annual increase of napproximately 2 to 2.75 kg per year until the adolescent grows spurt. Boys may add 20 kg and girls 15 kg during the growth spurt n(See Table 3.2).

Weight gain is usually nconsidered to be an indication of satisfactory growth progress in a child and is probably the best index of nnutrition and growth. However, it may be difficult to ndetermine if this increase in weight is caused by healthy tissue development or by an unhealthy deposition of tat or naccumulation of fluid.

General Trends in Weight nand Height Gain During Infancy

Age	Weight gain (grams)		Height gain (cm)
Age	Monthly	For the whole period	Monthly	For the whole period
1.	600	600	3	3
2.	800	1400	3	6
3.	800	2200	3	9
4.	750	2950	2.5	11.5
5.	700	3650	2.5	14
6.	650	4300	2.5	16.5
7.	600	4900	2	18.5
8.	550	5450	2	20.5
9.	500	5950	2	22.5
10.	450	6400	1-1.5	23.5-24
11.	400	6800	1-1.5	24.5-25
12.	350	7150	1-1.5	25.5-27

Height

Technique of procedure.

Measure recumbent length in children below 12 months. Place supine with head in midline, pinna of the ear must nbe on an imaginary vertical line with lower eyelid of the eye. Grasp knees and push gently toward table to nfully extend legs. Measure from vertex (top) of head to heels of feet (toes npointing upward).

Measure standing height (stature) in children over 12 nmonths. Remove nsocks and shoes. Have child nstand as tall as possible, back straight, head in midline, lower eyelid nand pinna of the same side ear on one imaginary horizontal line. Check for flexion of knees, slumping shoulders, rising of nheels. Measure from top of head to standing surface. Measure to the nearest cm or n1/8 inch.

Linear growth occurs nalmost entirely as a result of skeletal growth and is considered nto be a stable measure of general growth. Growth in height is not uniform throughout life, but when maturation of nthe skeleton is complete, linear growth nceases. The maximum growth in length occurs before birth, but the newborn continues to grow at a rapid, though nslower, rate (See Table.3.1). As the month npass, the growth rate rapidly decelerates. By 2 years of age the child normally nhas achieved 50 % of his adult height. In average yearly height gain at age 2 nor 3 years is 8 cm.

Table 3.2

General Trends in Weight and Height Gain During Childhood

Age	Weight	Height
Toddlers (1-4 years)	Birth weight quadruples by age 2.5 years Yearly gain: 2 kg	Height at age 2 is approximately 50 % of eventual adult height Yearly gain: 8 cm
Preschoolers (4-6 years)	Yearly gain: 2 kg	Birth length doubles by age 4 Yearly gain: 6 cm
School-age children	10 years old child weighs in average 30 kg Yearly gain: 2 kg	Yearly gain: 6 cm Birth length triples by about age 13
Pubertal growth spurt
Females – 10-14 years	Yearly gain: 4 kg	Height gain: 16 cm
Males – 11-16 years	Yearly gain: 4 kg	Height gain: 20 cm
Empirical formulas:	2 -10 years: W=10+2n; 10-16 years: W=30+4(n-10), or W=2n+8 (kg), where- age of child in years	1-4 years: H=100-8(4-n); 5-15 years: H= 100+6(n-4), or H=6n+80 (cm), where- age of child in years

Thus by age 4 birth length has usually doubled and is equal nto 100 cm. Then the child begins a relatively stable and steady growth rate of n5 to 6 cm per year that continues for the next 7 to 8 years. (Occasionally a nchild will exhibit a transitory midgrowth height nincrease at age 6 or 7). This long midgrowth period nis ended by a sudden and marked acceleration – the adolescent growth spurt. nAlthough there is wide variation, this increase, which begins about 10.5 to 11 nin girls and 12.5 to 13 in boys, lasts approximately 2 to 2.5 years. During nthis time a boy may add 20 cm to his height and a girl 16 cm. Usually, 98 % of the terminal height is reached by age 16.5 nin girls but not until age 17.5 in boys.

Head ncircumference.

Technique nof procedure.

Measure nhead circumference (HC) with paper or steel tape at greatest circumference, from nslightly above the eyebrows and pinna of the ears to occipital prominence of nskull.

General trends in head ncircumference gain during childhood are the next:

Age HC

Infants n Birth-6 months Monthly gain: 1.5 cm

6-12 months Monthly gain: 0.5 cm

Children 1-5 years Yearly ngain: 1 cm

6-15 nyears Yearly ngain: 0.6 cm

If anthropometrical nmeasurements at birth are unknown it is comfortably to use such nempirical formulas:

· nHead circumference for children from nbirth till 6 months:HC=43-1.5x(6-n), where- age of child in months.

· nHead circumference for children from 6 ntill 12 months:

HC=43+0.5x(n-6), where- age nof child in months.

· nHead circumference for children from 1 ntill 5 years:

HC=50-lx(5-n), where- age of nchild in years.

· nHead circumference for children from 5 ntill 15 years:HC = 50+0.6x(n-5), where n-age of child in years.

Chest ncircumference

Technique of procedure.

Measure chest circumference with paper or steel tape around chest nat nipple line and under tips of scapulas at back. Ideally, take nmeasurements during inhalation and expiration; record the average of the two nvalues.

General trends in chest circumference gain during nchildhood are the next:

Age Chest circumference

Infants Birth – 6 months Monthly gain: 2 cm

6-12 months Monthly ngain: 0.5 cm

Children 1 n- 10 years Yearly gain: 1.5 cm

11-15 years Yearly gain: 3 cm

If anthropometrical nmeasurements at birth are unknown it is comfortably to use such nempirical formulas:

· nChest circumference for children from nbirth till 6 months:ChC=45-2x(6-n), where- age of child in months.

· nChest circumference for children from n6 till 12 months:ChC=45+0,5x(n-6), where- age of child in months.

· nChest circumference for children from n1 till 10 years:ChC=63-l .5x(10-n), where- age of child in years.

· nChest circumference for children from n10 till 15 years:ChC=63+3x(n-10), where- age of child in years.

It is nnecessary to compare head circumference and chest circumference. At birth HC nexceeds chest circumference by 2 to 3 cm. At age 4 months HC equals chest ncircumference. Later, the rate of chest circumference increases rapidly, at the nsame time HC continues to grow nat a slower rate. So, during childhood chest circumference exceeds HC by about 1 to 7 cm.

Assessment of physical ndevelopment of the child

To value the proportionality and harmony of nphysical development of a child anthropometrics indexes are used.

1. nThe index of fatness by Chulitska ncan be calculated for children of first 8 years of life.

I=3´shoulder circumference+thigh circumference+shicircumference-height (stature) (cm)

Normal data according to age:

Infants	20-25 cm
Toddlers	20 cm
Preschoolers	10-15 cm
8 year child	Decreases to 6 cm

Decrease of this index shows on hypothrophia, exhaustion or great height. nIts increase shows on paratrophy (obesity) or considerable delay of growth.

2. nThe index by Erismann can be ncalculated for children by 15 years.

IE=chest circumference-½ nheight (cm)

Normal ndata according to age:

Infants	13,5 – 10 cm
Toddlers	9 –6 cm
Preschoolers	4 – 2 cm
School-age children	0 cm
Teenagers	1 – 3 cm

Decrease of this index, especially its negative meanings is the sign of ndysproportionality of physical growth (excessive linear growth). Considerable increase nof this index shows on dwarfism or small stature.

Growth

The growth data must remain generally nwithin the same percentile, except during rapid growth periods. In this case nphysical development is evaluated as proportional.

Serial measurements of growth are plotted nperiodically on standard growth charts to determine the pattern of ngrowth and to compare the individual child growth with the norm for that nparticular age group (See Growth Charts). The growth chart is a presentation of nnormal growth in terms of curves plotted along percentile levels. The true ngrowth pattern is reflected in the velocity curve, which is derived from nmeasurements at regular intervals from the distance curve. For example, a child nmay fall below the 3^rd percentile on a distance curve, whereas the nchild’s rate of gain over time may actually be withiormal limits. Childredo not have as strong tendency to remain in the same percentile position ovelocity curves as they do on distance curves. There is a pattern of moving nfrom outer percentile positions toward more central positions. During nadolescence the “typical” distance curves are misleading because the percentile nranges of growth vary remarkably. If the child matures early, he moves to a nhigher percentile before dropping back to his preadolescent percentile. nConversely, if a child matures late, he moves to a lower percentile before nregaining at maturity his preadolescent percentile.

If body length appears disproportional, nmeasurement of sitting height is required.

Body mass index is defined as the nindividual’s body mass divided by the square of his or her height. The formulae nuniversally used in medicine produce a unit of measure of kg/m2. BMI can also nbe determined using a BMI chart, which displays BMI as a function of weight n(horizontal axis) and height (vertical axis) using contour lines for different nvalues of BMI or colors for different

For evaluating of physical development percentile ntables or Z-scores tables are used (See nTables).

Measurements of length, weight and betweethe 25^th and 75^th percentiles are likely to represent nnormal growth.

Measurements between the 10^th nand 25^th percentiles represent less than average data and betweethe 75^th and 90^th – bigger than average data.

These measurements may or may not be nnormal, depending on previous and subsequent measurements and on genetic and nenvironmental factors. Measurements between the 10^th and 3d, and the n90^th and 97^th percentiles belong to low and high data, nwhich require further examination. Measurements below the 3^rd and nabove the 97^th percentiles are extremely low and nextremely high and reflect pathological deviations of physical development.

Overweight: >+1SD (equivalent to BMI 85-95 percentiles)

Obesity: >+2SD

(equivalent to BMI n> 95 percentiles)

Thinness: <-2SD

Severe thinness: <-3SD (equivalent to nBMI < 5 percentiles)

All charts of physical development assessment nare present of WHO page http://www.who.int/childgrowth/en/

BIOLOGICAL nACCELERATION

From measurements and observations recorded nover than past century, especially its second half, there appears to be a nsignificant worldwide trend in the rate and age of maturation. Children from nwidely different populations are maturing earlier and becoming larger at each nage.

Look through some examples:

· n25 to 30 years ago students used to learn such quarterly nbody length gain in infants: 3 cm, 2.5 cm, 1.5 cm and 1 cm per month. Nowadays ndata are 3 cm, 2.5 cm, 2 cm, and 1.5 cm per month.

· nAt present the birth weight doubles at age 4 to 4½ nmonths and triples by 10 to 11 months, while in the past it used to happen by nthe end of 6 months and at 12 months accordingly.

· nIn 1960s the body length of 100 cm was showed in average by na 5 years old children and its yearly gain reached 5 cm till 9 years. At npresent time average 4 years child is 100 cm tall, and then he grows on 6 cm nannually.

· nThe average size increase since 1900 is near 1 cm per decade nin height and 1 kg in weight in preschool children and 2.5 cm and 2.5 kg per ndecade during puberty.

· nAt the beginning of last century chest circumference equals nhead circumference by 9 to 10 months, and nowadays by the end of 4 months.

· nIn girls the age of menarche has advanced progressively.

There also appears to be a slight but not so marked increase in average nadult height, since although children are growing faster they also stop growing nsooner. The average young man reaches his full height at approximately age 20, nwhereas in 1900 he did not reach his final height until about 25 years. The ntrend appears to reach a plateau in populations with optimum environments, nwhich suggested that there is a maximum end point.

Many theories have been advanced to explaithis phenomenon. Improved environmental factors, such as nutrition and nsocioeconomic conditions, are important factors as well as the sharp decrease nin infant mortality during this century. Since body size is an inherited trait, nthe tendency toward the selection of mates from wider geographic areas and ndifferent races is an important factor. The influences of sun radiation, as nwell as the admission of vitamin D3 for prevention rachitis nare also of great importance, as they accelerate the maturation of skeletobones.

Semiotics of deviation of childrephysical development

The main disorders of nchildren’s physical development are:

Hypotrophy

Paratrophy

Obesity

Nanism (dwarfism)

Small stature

Gigantism

Hydrocephalus

Microcephalia

Hypotrophia

It nis delay of physical development of a child of first 2 years of life mainly due nto deficiency of real weight in comparison to ideal weight.

Hypotrophia can be ncongenital, acquired or of mixed genesis.

Congenital nhypotrophia nmust be diagnosed immediately after child’s birth. Informative index for this nis weight-length coefficient (WLC).

WLC = Weight of newborn (g) / Length of newbor(cm)

Normal nWLC=60-64.

Idependence on WLC the stage of hypotrophia can be nestablished:

I stage	WLC=59-56
II stage	WLC=55-50
III stage	WLC=49 and less

For example: the newborn child weighs 3200g, her body length nis 58 cm. WLC=3200:58=55. The diagnosis: Congenital hypotrophia nof II stage.

If the deficiency of body weight is observed othe 2^nd month of child’s life and later, the hypotrophia nis acquired. There are 3 stages of acquired hypotrophia ndepending on the stage of weight deficiency.

Stage	Deficiency of body weight (%)
I	11-20
II	21-30
III	31 and more

The clinical signs of hypotrophia nare decrease of subcutaneous fat on the abdomen (at the I nstage), on extremities (at the II stage), on the face (at the III stage). At nthe III stage of hypotrophia the child’s face looks nlike the face of old man (“Volter’s face”). Besides nthis, the decrease of skin elasticity, turgur and nbody length, delay of neuropsychological development and weakness of immune nsystem take place.

In case when child was born with hypotrophia nand the body weight does not normalize during some first months of his (her) nlife the hypotrophia is of mixed genesis.

Paratrophy

It is enlargement of body weight more than for 10 % of ideal nweight. The main course of it is overfeeding of a baby.

Stage of paratrophy	Excessive weight (%)
I	11-20
II	21-30
III	31 and more

According to clinical signs paratrophy nis divided into 2 types: lipomatic and lipomatic-pastose.

In case of lipomatic type the nchild looks healthy (skin and mucous membranes are of nature colour, turgur is normal, etc); nlaboratory tests are normal. The child gets ill rarely and for a shot period.

In case of lipomatic-pastose paratrophy skin is pale, flabby and edematic, turgur is decreased, signs of nanemia are present. The child is dull mood and not active. On the first year of nlife such children often have allergic reactions, rickets, weakened nimmune system.

Obesity

The presence of excessive weight in child older than 1 year nis called obesity.

Stages of obesity	Excessive weight (%)
I	10-29
II	30-49
III	50-99
IV	100 and more

Nanism (dwarfism)

It is a disorder of physical development, which ndeals with the delay of height.

The dwarf height in adult persons of white race nis considered the height below 130 cm for male and below 120 cm for female.

Classification:

dwarfism nwith proportional constitution;

dwarfism nwith disproportional constitution.

Etiology of nanism is congenital disorders of nendocrine system (hypofunctions nof hypophysis or thyroid) or metabolism.

The main symptom of dwarfism is delay of growth nin height. Other clinical signs depend on the course of the disease. As a rule nsuch children at birth have normal body length; at the age 2-4 years they fall nbelow the third percentile on the height velocity curve but the measurements of nhead and chest circumference and, sometimes, weight lies within the first npercentiles. Late symptoms of dwarfism are dry, wrinkled and pale skin, nchildish face, poorly developed muscles, excessive development of subcutaneous nfat on the chest (pseudo mammas), low blood pressure, fertilessness. n

Small stature

It is the equal delay of height and weight gain in childrein comparison to the average data. The height-weight velocity curves of such nchildren are within the 2^nd and the 3^rd percentiles.

Etiology of small stature is heredity, lack of protein and nvitamins intake during prenatal period and the 1^st year of life.

Gigantism

It’s a clinical syndrome, which develops as a result of hyperproduction of somatotropine nhormone of hypophysis that leads to remarkable growth nin height.

The first manifestation of gigantism takes place during prepubertal or pubertal periods. Other complaints are nweakness, often headaches, extremity or cardiac pains. Physical development of nsuch children is disproportional: the height velocity goes up over the 3^rd npercentile, weight lies within the 2^nd and 3^rd npercentiles and other measurements within “normal curves”.

EMBRYONIC PERIOD. n

Milestones of prenatal ndevelopment are presented in Table 6-4 . By 6 days postconceptual age, as nimplantation begins, the embryo consists of a spherical mass of cells with a ncentral cavity (the blastocyst). By 2 wk, implantation is complete and the nuteroplacental circulation has begun; the embryo has 2 distinct layers, nendoderm and ectoderm, and the amnion has begun to form. By 3 wk, the 3rd nprimary germ layer (mesoderm) has appeared, along with a primitive neural tube nand blood vessels. Paired heart tubes have begun to pump.

nTABLE 6-4 — Milestones of Prenatal nDevelopment

WK	DEVELOPMENTAL EVENTS
1	Fertilization and implantation; beginning of embryonic period
2	Endoderm and ectoderm appear (bilaminar embryo)
3	First missed menstrual period; mesoderm appears (trilaminar embryo); somites begin to form
4	Neural folds fuse; folding of embryo into human-like shape; arm and leg buds appear; crown-rump length 4–5 mm
5	Lens placodes, primitive mouth, digital rays on hands
6	Primitive nose, philtrum, primary palate; crown-rump length 21–23 mm
7	Eyelids begin
8	Ovaries and testes distinguishable
9	Fetal period begins; crown-rump length 5 cm; weight 9 g
10	External genitals distinguishable
20	Usual lower limit of viability; weight 460 g; length 19 cm
25	Third trimester begins; weight 900 g; length 25 cm
28	Eyes open; fetus turns head down; weight 1,000 g
38	Term

During wk 4–8, lateral nfolding of the embryologic plate, followed by growth at the cranial and caudal nends and the budding of arms and legs, produces a human-like shape. Precursors nof skeletal muscle and vertebrae (somites) appear, along with the branchial narches that will form the mandible, maxilla, palate, external ear, and other nhead and neck structures. Lens placodes appear, marking the site of future neyes; the brain grows rapidly. By the end of wk 8, as the embryonic period ncloses, the rudiments of all major organ systems have developed; the average nembryo weighs 9 g and has a crown-rump length of 5 cm.

FETAL PERIOD.

From the 9th wk on (fetal period), nsomatic changes consist of increases in cell number and size and structural nremodeling of several organ systems. Changes in body proportion are depicted iFigure 6-6 . By 10 wk, the face is recognizably human. The midgut returns from nthe umbilical cord into the abdomen, rotating counterclockwise to bring the nstomach, small intestine, and large intestine into their normal positions. By n12 wk, the gender of the external genitals becomes clearly distinguishable. nLung development proceeds, with the budding of bronchi, bronchioles, and nsuccessively smaller divisions. By 20–24 wk, primitive alveoli have formed and nsurfactant production has begun; before that time, the absence of alveoli nrenders the lungs useless as organs of gas exchange.

The Preschool Years Susan Feigelman

The ages between 2 and 5 yr are governed nby the emergence of language and exposure of children to an expanding social nsphere. As toddlers, children learn to walk away and come back to the secure nadult or parent. As preschoolers, they explore emotional separation, nalternating between stubborn opposition and cheerful compliance, between bold nexploration and clinging dependence. Increasing time spent in classrooms and nplaygrounds challenges a child’s ability to adapt to new rules and nrelationships. Preschool children know that they can do more than ever before, nbut they are also very aware of the constraints imposed on them by the adult nworld and their own limited abilities.

PHYSICAL DEVELOPMENT n

By the end of the 2nd nyear, somatic and brain growth slows, with corresponding decreases iutritional nrequirements and appetite, and the emergence of “picky” eating habits (see nTable 14-1 ). Expect a gain of approximately 2 kg (4–5 lb) in weight and 7–8 cm n(2–3 in) in height per year. Birthweight quadruples by 2½ yr of age. Aaverage 4 yr old weighs 40 lb and is 40 in tall. The head will grow only aadditional 5 cm between ages 3 and 18 yr. Current growth charts, with growth nparameters, can be found on the Centers for Disease Control website (www.cdc.gov/nchs) nand in Chapter 14 . Children with early adiposity rebound (increase in body nmass index) are at increased risk for adult obesity.

Growth of sexual norgans is commensurate with somatic growth. The preschooler has genu valgum n(knock-knees) and mild pes planus (flatfoot). The torso slims as the legs nlengthen. Physical energy peaks, and the need for sleep declines to 11–13 hr/24 nhr, with the child eventually dropping the nap (see Fig. 8-1 ). Visual acuity nreaches 20/30 by age 3 yr and 20/20 by age 4 yr. All 20 primary teeth have nerupted by 3 yr of age (see Table 8-3 ).

Gross and fine motor nmilestones are presented in Table 9-1 . Most children walk with a mature gait nand run steadily before the end of their 3rd yr. Beyond this basic level, there nis wide variation in ability as the range of motor activities expands to ninclude throwing, catching, and kicking balls; riding on bicycles; climbing oplayground structures; dancing; and other complex pattern behaviors. Stylistic nfeatures of gross motor activity, such as tempo, intensity, and cautiousness, nalso vary significantly. Although toddlers may walk with different styles, toe nwalking should not persist.

The effects of such nindividual differences on cognitive and emotional development depend in part othe demands of the social environment. Energetic, coordinated children may nthrive emotionally with parents or teachers who encourage physical activity; lower-energy, nmore cerebral children may thrive with adults who value quiet play.

Handedness is usually established by the 3rd nyr. Frustration may result from attempts to change children’s hand preference. nVariations in fine motor development reflect both individual proclivities and ndifferent opportunities for learning. Children who are seldom allowed to use ncrayons, for example, develop a mature pencil grasp later.

Bowel and bladder ncontrol emerge nduring this period, with “readiness” for toileting having large individual and ncultural variation. Girls tend to train faster and earlier than boys. nBed-wetting is normal up to age 4 yr in girls and age 5 yr in boys (see nChapters 22.3 and 543 ). nMany children master toileting with ease, particularly once they are able to nverbalize their bodily needs. For others, toilet training can involve a nprotracted power struggle. Refusal to defecate in the toilet or potty is nrelatively common and can lead to constipation and parental frustration. nDefusing the issue with a temporary cessation of training (and a return to ndiapers) often allows toilet mastery to proceed.

IMPLICATIONS FOR PARENTS AND PEDIATRICIANS. n

The normal decrease iappetite at this age often arouses worry about nutrition. The growth charts nshould reassure parents that the child’s intake is adequate. Childreormally nmodulate their food intake to match their somatic needs according to feelings nof hunger and satiety. Daily intake fluctuates, at times widely, but intake nduring the period of a week is relatively stable. Parental attempts to control nthe child’s intake interfere with this self-regulatory mechanism as the child nmust either accede to or rebel against the pressure. The result may be either novereating or undereating.

Highly active children face increased nrisks of injury, and parents should be counseled about safety precautions. nParental concerns about possible hyperactivity may reflect inappropriate nexpectations, heightened fears, or true overactivity. Children who engage ireckless, uncontrollable activity with no apparent regard for personal safety nshould be evaluated further.

PHYSICAL DEVELOPMENT n

Growth during the nperiod averages 3–3.5 kg (7 lb) and 6–7 cm (2.5 in) per year (see Figs. 9-1 and n9-2 ). Growth occurs discontinuously, nin 3–6 irregularly timed spurts each year, with each growth spurt lasting, oaverage, 8 wk. The head grows only 2–3 cm in circumference throughout the nentire period, reflecting a slowing of brain growth. Myelinization is complete nby 7 yr of age. Body habitus is more erect than previously, with long legs ncompared with the torso.

Growth of the midface nand lower face occurs gradually. Loss of deciduous (baby) teeth is a more ndramatic sign of maturation, beginning after eruption of the 1st molars around n6 yr of age. Replacement with adult teeth occurs at a rate of about 4 per year, nso that by age 9 yr, children will have 8 permanent incisors and 4 permanent nmolars. Premolars erupt by 11–12 yr of age. Lymphoid tissues hypertrophy, oftegiving rise to impressive tonsils and adenoids.

Muscular strength, ncoordination, and stamina increase progressively, as does the ability to nperform complex movements, such as dancing or shooting baskets. Such nhigher-order motor skills are the result of both maturation and training; the ndegree of accomplishment reflects wide variability in innate skill, interest, nand opportunity.

There has been a ngeneral decline in physical fitness among school-aged children. Sedentary nhabits at this age are associated with increased lifetime risk of obesity and ncardiovascular disease. The number of overweight children and the degree of noverweight are both increasing. Most youth do not participate in any organized nphysical activity outside of school; ¼ do not engage in any free-time nphysical activity.

Prior to puberty, the nsensitivity of the hypothalamus and the pituitary changes, leading to increased ngonadotropin synthesis. For most children, the sexual organs remain physically nimmature, but interest in gender differences and sexual behavior remains active nin many children and increases progressively until puberty. Although this is a nperiod when sexual drives are limited, masturbation is common, and children may nbe interested in differences between genders.

Puberty may be noccurring at younger ages. Early-developing girls may feel uncomfortable, nparticularly if expected to behave as an older child would. Girls may worry nthat they are overweight, and many engage in unhealthy dieting to achieve aabnormally thin cultural ideal.

IMPLICATIONS FOR PARENTS AND PEDIATRICIANS

Middle childhood is ngenerally a time of excellent health. However, children have variable sizes, nshapes, and abilities. Children of this age compare themselves with others, neliciting feelings about their physical attributes and abilities. Fears of nbeing “defective” can lead to avoidance of situations in which physical ndifferences might be revealed, such as gym class or medical examinations. nChildren with actual physical disabilities may face special stresses. Medical, nsocial, and psychologic risks tend to occur together.

Children should be asked about nregular physical activity. Participation in organized sports or other organized nactivities can foster skill, teamwork, and fitness, as well as a sense of accomplishment, nbut pressure to compete when the activity is no longer enjoyable has negative neffects. Prepubertal children should not engage in high-stress, high-impact nsports, such as power lifting or football, because skeletal immaturity nincreases the risk of injury.

EARLY ADOLESCENCE n

BIOLOGIC DEVELOPMENT. n

While adolescence is ndefined as a period of development, puberty is the biologic process in which a nchild becomes an adult. These changes include appearance of the secondary nsexual characteristics, increase to adult size, and development of reproductive ncapacity. Adrenal production of androgen (chiefly dehydroepiandrosterone nsulfate [DHEAS]) may occur as early as 6 yr of age, with development of nunderarm odor and faint genital hair (adrenarche). Levels of luteinizing nhormone (LH) and follicle-stimulating hormone (FSH) rise progressively nthroughout middle childhood without dramatic effect. Rapid pubertal changes nbegin with increased sensitivity of the pituitary to gonadotropin-releasing nhormone (GnRH); pulsatile release of GnRH, LH, and FSH during sleep; and ncorresponding increases in gonadal androgens and estrogens. The triggers for nthese changes are incompletely understood, but may involve ongoing neuronal ndevelopment throughout middle childhood and adolescence. Contemporary childrein the United States may enter puberty earlier than the published norms n(although reports of dramatically earlier puberty are controversial), perhaps nrelated to increased weight and adiposity (see Chapters 563 and 564 ). The nresulting sequence of somatic and physiologic changes gives rise to the sexual nmaturity rating (SMR), or Tanner stages. Figures 12-1 and 12-2 [1] [2] depict nthe somatic changes used in the SMR scale; Tables 12-2 and 12-3 [2] [3] ndescribe these changes in words. Table 12-4 lists mean ages and normal ranges nfor stages of pubic hair, breast, and genital development. Note that the SMR nstages are not perfectly synchronized (e.g., SMR2 genital development may precede SMR2 pubic hair ndevelopment). Figures 12-3 and 12-4 [3] [4] depict the typical sequence of npubertal changes in boys and girls, respectively. The range of normal progress nthrough sexual maturation is wide.

TABLE n12-2 n — Classification of Sex Maturity States iGirls

SMR STAGE	PUBIC HAIR	BREASTS
1	Preadolescent	Preadolescent
2	Sparse, lightly pigmented, straight, medial border of labia	Breast and papilla elevated as small mound; diameter of areola increased
3	Darker, beginning to curl, increased amount	Breast and areola enlarged, no contour separation
4	Coarse, curly, abundant, but less than i adult	Areola and papilla form secondary mound
5	Adult feminine triangle, spread to medial surface of thighs	Mature, nipple projects, areola part of general breast contour

From Tanner JM: Growth at Adolescence, 2nd ed. nOxford, England, Blackwell Scientific Publications, 1962. SMR, sexual maturity nrating.

nTABLE 12-3 — Classification of Sex nMaturity States in Boys

SMR STAGE	PUBIC HAIR	PENIS	TESTES
1	None	Preadolescent	Preadolescent
2	Scanty, long, slightly pigmented	Minimal change/enlargement	Enlarged scrotum, pink, texture altered
3	Darker, starting to curl, small amount	Lengthens	Larger
4	Resembles adult type, but less quantity; coarse, curly	Larger;glans and breadth increase in size	Larger, scrotum dark
5	Adult distribution, spread to medial surface of thighs	Adult size	Adult size

From Tanner JM: Growth at Adolescence, 2nd ed. nOxford, England, Blackwell Scientific Publications, 1962. SMR, sexual maturity nrating.

nTABLE 12-4 — Mean Age in Years and nSE for Sexual Maturation Stage in Girls (Pubic Hair and Breast Development) and nBoys (Pubic Hair and Genital Development) by Race

	AGE IN STAGE
	NON-HISPANIC WHITE		NON-HISPANIC BLACK		MEXICAN-AMERICAN
STAGE	Mean	SE	Mean	SE	Mean	SE
GIRLS
Pubic Hair
PH2	10.96^[*]	0.23	10.25^[*]	0.15	11.17^[*]	0.21
PH3	12.41^[*]	0.19	11.37^[*]	0.23	12.84^[*]	0.18
PH4	15.11^[*]	0.18	13.69^[*]	0.31	14.61^[*]	0.26
PH5	16.53^[*]	0.17	16.05^[*]	0.14	16.61^[*]	0.12
Breast Development
B2	11.05^[*]	0.18	10.25^[*]	0.20	10.70	0.21
B3	12.80^[*]	0.19	11.94^[*]	0.22	12.61^[*]	0.20
B4	15.16^[*]	0.32	13.61^[*]	0.34	14.03^[*]	0.27
B5	16.25^[*]	0.18	15.78^[*]	0.14	16.21^[*]	0.12
BOYS
Pubic Hair
PH2	11.81	0.16	11.48^[*]	0.13	12.20^[*]	0.24
PH3	13.03	0.27	12.79^[*]	0.19	13.44^[*]	0.26
PH4	14.89	0.18	15.21	0.26	15.25	0.16
PH5	16.84	0.13	16.67^[*]	0.08	17.14^[*]	0.10
Genital Development
G2	11.08	0.18	10.79	0.13	11.09	0.17
G3	12.55	0.29	12.03^[*]	0.28	12.97^[*]	0.28
G4	15.29	0.19	15.07	0.33	15.38	0.19
G5	16.64	0.15	16.42^[*]	0.09	16.85^[*]	0.13

Adapted from Tables 3 and 5 in Sun SS: National nestimates of the timing of sexual maturation and racial differences among US nchildren. Pediatrics, 2002;110(5):911–919. Note: For sample sizes, refer to ntables in original article.

SE, standard error.

^*	Significant pair-wise racial difference, p < 0.05.

In girls, the first visible sign of puberty and nthe hallmark of SMR2 is the appearance of breast buds, between 8 and 12 yr of nage. Menses typically begins 2–2½ yr later, during SMR3–4 (median age, n12 yr; normal range, 9–16 yr), around the peak height velocity (see Fig. 12-4 n). Less obvious changes include enlargement of the ovaries, uterus, labia, and nclitoris, and thickening of the endometrium and vaginal mucosa.

In boys, the first visible sign of puberty nand the hallmark of SMR2 is testicular enlargement, beginning as early as n9½ yr. This is followed by penile growth during SMR3. Peak growth occurs nwhen testis volumes reach approximately 9–10 cm³ nduring SMR4. Under the influence of LH and testosterone, the seminiferous ntubules, epididymis, seminal vesicles, and prostate enlarge. The left testis nnormally is lower than the right. Some degree of breast hypertrophy, typically nbilateral, occurs in 40–65% of boys during SMR2–3 due to a relative excess of nestrogenic stimulation. Gynecomastia sufficient to cause embarrassment and nsocial disability occurs in fewer than 10% of boys. Breast swelling <4 cm idiameter has a 90% chance of spontaneous resolution within 3 yr. Gynecomastia npresenting later in puberty, occurring in the prepubertal period, or occurring nin the absence of signs of pubertal development may be pathologic and requires na work-up, including a thorough medication (e.g., H₂-blockers, npsychotropics), drug (e.g., anabolic steroids), and medical history (e.g., nKlinefelter syndrome, testicular failure, thyroid disease, tumor).

For both sexes, growth nacceleration begins in early adolescence, but peak growth velocities are not nreached until SMR3–4. Boys typically peak 2–3 yr later than girls, begin this ngrowth at a later SMR stage ( Fig. 12-5 ), and continue their linear growth for napproximately 2–3 yr after girls have stopped. The asymmetric growth spurt nbegins distally, with enlargement of the hands and feet, followed by the arms nand legs, and finally, the trunk and chest, giving young adolescents a gawky nappearance. Rapid enlargement of the larynx, pharynx, and lungs leads to nchanges in vocal quality, typically preceded by vocal instability (voice ncracking). Elongation of the optic globe often results iearsightedness. nDental changes include jaw growth, loss of the final deciduous teeth, and eruptioof the permanent cuspids, premolars, nd finally, molars (see Table 8-3 ). nOrthodontic appliances may be needed.

COGNITIVE AND MORAL DEVELOPMENT. n

According to Piagetiatheory, adolescence marks the transition from concrete operational thinking to formal nlogical thinking (abstract thought). This includes the ability to nmanipulate algebraic expressions, reason from known principles, weigh many npoints of view, and think about the process of thinking itself. Some early nadolescents demonstrate abstract thought, others acquire the capability later, nand others never fully acquire it. Young adolescents may be able to apply nformal logical thinking to schoolwork, but not to personal dilemmas. Wheemotional stakes are high, adolescents may regress to more concrete operational nand/or magical thinking. This can interfere with higher-order cognition and nultimately affect the nability to perceive long-term outcomes of current decision-making.

Some theorists argue nthat the transition from concrete to formal operations follows from nquantitative increases in knowledge, experience, and cognitive efficiency nrather than from a qualitative reorganization of thinking. Consistent with this nview are data showing a steady rise in cognitive processing speed from late nchildhood through early adulthood, associated with a reduction in synaptic nnumber (pruning of less-used pathways) and continued myelination of neurons. nAdolescents also experience the development of the dorsolateral prefrontal ncortex and the superior temporal gyrus, areas responsible for higher-order nassociations, including the ability to inhibit impulses, weigh the consequences nof decisions, prioritize, and strategize. It is unclear whether the hormonal nchanges of puberty directly affect cognitive development. Related to nneurobehavioral maturation, adolescents may experience an increased intensity nof emotion and/or greater inclination to seek experiences that create such nhigh-intensity emotions. Cognitive development also differs by gender, with ngirls developing at earlier ages than boys.

The development of moral nthinking roughly parallels cognitive development. Whereas younger childreview relationships with adults in terms of power and fear of punishment, preadolescents nbegin to perceive right and wrong as absolute and unquestionable. Punishments nand rewards must be fair; otherwise, the adolescent may complain or become nangry.

SELF-CONCEPT. n

Self-consciousness nincreases exponentially in response to the somatic transformations of puberty. nSelf-awareness at this age centers on external characteristics, in contrast to nthe introspection of later adolescence. It is normal for early adolescents to nbe preoccupied with their body changes, scrutinize their appearance, and feel nthat everyone else is staring at them (Elkind’s imaginary audience).

The media, with its noverrepresentation of sex, violence, and substance use, has a profound ninfluence on cultural norms and an adolescents’ sense of identity. Adolescents nuse, on average, 7 hr of media per day (e.g., television, Internet). Half of nall high school students have a television in their bedrooms, 70% live in homes nwith a personal computer, and the proportion with Internet access is napproximately 75%.

This exposure may ncause girls to develop a distorted sense of femininity, and they may be at risk nfor viewing themselves as overweight, leading to eating disorders and ndepression ( Chapter 27 ). Similarly, boys may have difficulties with nself-image. Images of masculinity may be confusing, leading to self-doubt, ninsecurity, and misleading conceptions about male behavior. Adolescents who ndevelop earlier than their peers, especially girls, may have higher rates of nschool difficulty, body dissatisfaction, and depression. These adolescents look nlike adults and may have adult expectations placed on them, but are not ncognitively or psychologically mature.

RELATIONSHIPS WITH nFAMILY, PEERS, AND SOCIETY.

In early adolescence, nyoung teens become less interested in parental activities and more interested nin the peer group, typically with peers of the same sex. A symbolic expressioof this shift is to renounce family norms of dress and grooming in favor of the npeer group “uniform,” such as hair, clothes, and body ornamentation. Such stylistic nchanges may spark conflicts that are truly about power or difficulty accepting nseparation. Adolescents also seek more privacy, which may contribute to family ndiscord.

The trend toward nseparation from family often involves selecting adults outside of the family as nrole models and developing close relationships with particular teachers or the nparents of other children. Organizations such as scouting or sports teams caalso provide an important sense of extrafamilial belonging.

Early adolescents noften socialize in same-sex peer groups. Scatological jokes, teasing directed nagainst the other gender, and rumor mongering about who likes whom attest to nburgeoning sexual interest. Belonging is all important. In one-to-one nfriendships, boys and girls differ in important ways. Female friendships may ncenter on sharing confidences, whereas male relationships may focus more oshared activities and competition.

An early adolescent’s nrelationship to society centers on school. The shift from elementary school to nmiddle school or junior high school entails giving up the protection of the nhomeroom in exchange for the additional stimulation and responsibility involved nin moving from class to class. This change in school structure mirrors and nreinforces the changes involved in separating from the family.

SEXUALITY. n

Sexuality includes not nonly sexual behaviors but also interest and fantasies, sexual orientation, nattitudes toward sex, and awareness of socially defined roles and mores. nAnxiety and interest in sex and sexual anatomy increase during early puberty. nIt is normal for young adolescents to compare themselves with others. In boys, nejaculation occurs for the first time, usually during masturbation and later as nnocturnal emissions, and may be a cause of anxiety. Early adolescents sometimes nmasturbate together; mutual sexual exploration is not necessarily a sign of nhomosexuality. Sexual behavior, other than masturbation, is less common iearly puberty, although 31% of an urban sample reported sexual intercourse nbefore 14 yr of age. The relationship between hormonal changes and sexual ninterest and activity is controversial; no consistent links between hormones nand sexual arousal, age of first intercourse, or frequency of intercourse have nbeen found.

IMPLICATIONS FOR PEDIATRICIANS nAND PARENTS.

Parents may have nconcerns that they are hesitant to discuss. Parents can be interviewed before nthe adolescent to avoid undermining the ado lescent’s trust. Wheinterviewing and examining an adolescent, health care providers should keep imind that physical maturation correlates with sexual maturity, whereas npsychosocial development correlates more closely with chronological age. Early nadolescents typically need reassurance that the somatic changes they are nexperiencing are common and normal.

The pediatriciaeeds nto help parents differentiate between the normal discomforts of the age and ntruly concerning behaviors. Bids for autonomy, such as avoiding family nactivities, demanding privacy, and increasing argumentativeness, are normal; nextreme withdrawal or antagonism may be dysfunctional. Bewilderment and ndysphoria at the start of junior high school are normal; continued failure to nadapt several weeks to months later suggests a more serious problem. nRisk-taking is limited in early adolescence; escalation of risk-taking nbehaviors is problematic. Parents must adapt discipline measures to the nchanging abilities of the adolescent, who can think through problems, assess nconsequences, and problem solve. Thus, the development of negotiation strategies nis critical. Children and adolescents raised by parents who use negotiating as npart of child rearing have more positive outcomes than those raised by parents nwho use more authoritarian or permissive styles.

MIDDLE ADOLESCENCE n

BIOLOGIC DEVELOPMENT. n

In middle adolescence, ngrowth accelerates above the prepubertal rate of 6–7 cm (3 in) per year. In the naverage girl, the growth spurt peaks at 11.5 yr at a top velocity of 8.3 cm n(3.8 in) per year and then slows to a stop at 16 yr (see Fig. 12-4 ). In the naverage boy, the growth spurt starts later, peaks at 13.5 yr at 9.5 cm (4.3 in) nper year, and then slows to a stop at 18 yr. Weight gain parallels linear ngrowth, with a delay of several months, so that adolescents seem first to nstretch and then to fill out. Muscle mass also increases, followed napproximately 6 months later by an increase in strength; boys show greater ngains in both. Lean body mass, approximately 80% in the average prepubertal nchild, increases to 90% in boys and decreases to 75% in girls as subcutaneous nfat accumulates.

Bone maturatiocorrelates closely with SMR because epiphyseal closure is under androgenic ncontrol ( Table 12-5 ). Boys with SMR3 pubic hair and SMR4 genitals normally nhave their peak growth spurts ahead of them; girls at the same SMR are usually npast their peaks (see Figs. 12-3 and 12-4 [3] [4]). Widening of the shoulders nin boys and the hips in girls is also hormonally determined. Other changes ninclude a doubling in heart size and lung vital capacity. Blood pressure, blood nvolume, and hematocrit rise, particularly in boys. Androgenic stimulation of nsebaceous and apocrine glands results in acne and body odor. Physiologic nchanges in sleep patterns and requirements may be mistaken for laziness; nadolescents have difficulty falling asleep and waking up, especially for early nschool start times as opposed to typical self-regulated or preferred sleep nschedules.

nTABLE 12-5 — Modal Age at nOnset and Completion of Fusion in Skeletal Areas in Adolescence

BOYS MODAL AGE BETWEEN (Yr)	AREA	GIRLS MODAL AGE BETWEEN (Yr)
ELBOW
13.0–13.5	Onset in humerus	11.0–11.5
15.0–15.5	Complete in ulna	12.5–13.0
FOOT AND ANKLE
14.0–14.5	Onset in great toe	12.5–13.0
15.5–16.0	Complete in tibia, fibula	14.0–14.5
HAND AND WRIST
15.0–15.5	Onset in distal phalanges	13.0–13.5
17.5–18.0	Complete in radius	16.0–16.5
KNEE
15.0–15.5	Onset in tibial tuberosity	13.5–14.0
17.5–18.0	Complete in fibula	16.0–16.5
HIP AND PELVIS
15.5–16.0	Onset in greater trochanter	14.0–14.5
After 18.0	Complete in symphysis	17.5–18.0
SHOULDER AND CLAVICLE
15.5–16.0	Onset in greater tubercle of humerus	14.0–14.5
After 18.0	Complete in clavicle	17.5–18.0

Menarche is achieved nby 30% of girls by SMR3 and by 90% by SMR4 (95% of girls reach menarche at n10.5–14.5 yr of age). Menarche usually follows approximately 1 yr after the growth nspurt begins. It is very common for cycles to be anovulatory during the first 2 nyr after menarche (approximately 50%). The timing of menarche, which is not ncompletely understood, appears to be determined by genetics as well as by nfactors such as adiposity, chronic illness, and exercise. In developed ncountries, the average age at menarche has decreased in the past century, nperhaps in response to better nutrition and less physical activity. Before nmenarche, the uterus achieves a mature configuration, vaginal lubricatioincreases, and a clear vaginal discharge appears (physiologic leukorrhea). Iboys, the phallus lengthens and widens during SMR3, and sperm are usually napparent in semen.

COGNITIVE AND MORAL nDEVELOPMENT.

With the transition to nformal logical thinking, middle adolescents start to question and analyze nextensively. Young people now have the cognitive ability to understand the nintricacy of the world they live in, to see beyond themselves, and to begin to nunderstand their own actions in a moral and legal context. Questioning of moral nconventions fosters the development of personal codes of ethics, which may be nsimilar to or different from those of their parents. An adolescent’s new nflexibility of thought can have pervasive effects on relationships with the nself and others.

SELF-CONCEPT. n

Middle adolescents are nmore accepting of their own body changes and become preoccupied with idealism nin exploring future options. Affiliation with a peer group is an important step nin confirming one’s identity and self-image. It is normal for middle nadolescents to experiment with different personas, changing styles of dress, ngroups of friends, and interests from month to month. Many philosophize about nthe meaning of life and wonder, “Who am I?” and “Why am I here?” Intense nfeelings of inner turmoil and misery are common. Girls may tend to characterize nthemselves and their peers according to interpersonal relationships (“I am a ngirl with close friends.”), whereas boys may focus on abilities (“I am good at nsports.”). Adolescents of both genders, but especially boys, who develop later nthan their peers may experience poorer self-image and have higher rates of ndifficulty in school.

RELATIONSHIPS WITH nFAMILY, PEERS, AND SOCIETY.

Middle adolescence nrefers to “stereotypical adolescence.” Relationships with parents become more nstrained and distant due to redirected energies toward peer relationships and nseparation from the family. Dating can become a lightning rod for parent-child nbattles, in which the real issue may be the separation from parents rather thathe particulars of “with whom” or “how late.” The majority of teenagers nprogress through adolescence with minimal difficulties rather than experiencing nthe stereotypical “storm and stress.” It is the large minority of adolescents n(approximately 20–30%) who do experience stress and struggle through nthis period who require support. Adolescents with visible differences are also nat risk for problems, such as not developing adequate social skills and nconfidence and having more difficulty establish ing satisfying relationships.

As part of middle nadolescents’ exploration of future options, they begin to think seriously about nwhat they want to do as adults, a question that formerly had been comfortably nhypothetical. The process involves self-assessment and exploration of available nopportunities. The presence or absence of realistic role models, as opposed to nthe idealized ones of earlier periods, can be crucial.

SEXUALITY. n

Dating becomes a nnormative activity as middle adolescents assess their ability to attract nothers. The degree of sexual activity and its onset vary widely. At age 16 yr, napproximately 33% of girls and 42% of boys report having oral or vaginal sex. nMost adolescents have kissed by age 14 yr (71%). French kissing is more commoby age 15 yr, and petting is more common among teen boys at age 16 yr (75%), nbut it catches up with teen girls by age 17 yr (76%). Homosexual nexperimentation is common and does not necessarily reflect a child’s ultimate nsexual orientation. Many adolescents worry that they might be homosexual and ndread being found out. Homosexual adolescents face an increased risk of nisolation and depression. Fear of stigmatization may keep them from discussing ntheir concerns with pediatricians or other potentially helpful adults (see Chapter 13 ).

In addition to sexual norientation, middle adolescents begin to sort out other important aspects of nsexual identity, including beliefs about love, honesty, and propriety. nRelationships at this age are often superficial and emphasize attractiveness nand sexual experimentation rather than intimacy. Adolescents tend to choose one nof three sexual paths: celibacy, monogamy, or polygamous experimentation. Most nhave some knowledge of the risks of pregnancy, HIV, and other sexually ntransmitted diseases, but knowledge does not consistently control behavior. nFewer than 70% of adolescents consistently use condoms, and approximately 26% nof girls do not use any method of contraception at their first intercourse.

IMPLICATIONS FOR nPEDIATRICIANS AND PARENTS.

Middle adolescence is na time when the opportunity to talk confidentially with a nonjudgmental, ninformed adult can be particularly appreciated and helpful in the midst of nsignificant psychologic and biologic change.

Adolescents vary ngreatly in their rate of physical and social progress and in the resolution of ncentral conflicts about autonomy and self-esteem. Questions about family and npeer relationships can help locate a child along the developmental continuum nand facilitate individualized counseling. Early- and late-maturing adolescents nare at risk for psychologic problems. Anticipatory guidance with parents or nguardians and appropriate referral to mental health professionals of these nadolescents may be warranted.

In asking about dating nand sex, do not assume heterosexuality; this approach increases the likelihood nthat concerns about sexual orientation will surface. Intention to have sex and nwhether close friends are sexually active are good indications that a youth may nbe initiating sexual activity shortly. Parental connectedness and close nsupervision or monitoring of the youth’s activities and peer group can be nprotective against early onset of sexual activity and involvement in other nrisk-taking behaviors, and can foster positive youth development. Parents nshould also assume an active role in their adolescent’s transition to adulthood nto ensure that their child receives appropriate preventive health services.

LATE ADOLESCENCE n

BIOLOGIC DEVELOPMENT. n

The somatic changes ithis period are modest by comparison to earlier periods. The final stages of nbreast, penile, and pubic hair development occur by 17–18 yr of age in 95% of nmales and females. Minor changes in hair distribution often continue for nseveral years in males, including the growth of facial and chest hair and the nonset of male pattern baldness in a few. Acne occurs in the majority of nadolescents, particularly males.

PSYCHOSOCIAL nDEVELOPMENT.

Slowing physical nchanges permit the emergence of a more stable body image. Cognition tends to be nless self-centered, with increasing thoughts about concepts such as justice, npatriotism, and history. Older adolescents are more future-oriented and able to nact on long-term plans, delay gratification, compromise, set limits, and think independently. nOlder adolescents are often idealistic, but may also be absolutist and nintolerant of opposing views. Religious or political groups that promise nanswers to complex questions may hold great appeal.

With emancipatiocomplete, older adolescents begin the transition to adult roles in work and ntheir relationships.

They also have more nconstancy in their emotions. The peer group and peer values recede iimportance. Individual, particularly intimate relationships take precedence, nproviding an important component of identity for many older adolescents. Icontrast to the often superficial dating relationships of middle adolescence, nthese relationships increasingly involve love and commitment. Career decisions nbecome pressing because an adolescent’s self-concept is increasingly bound up nin his or her emerging role in society.

IMPLICATIONS FOR PEDIATRICIANS AND PARENTS. n

Erikson identified the crucial task nof adolescence as the establishment of a stable sense of identity, including nemotional and physical separation from the family of origin, initiation of nintimacy, and realistic planning for economic independence. The relationship nchanges from one of parent-child to an adult-adult model. Continued difficulty nin any of these areas may constitute an indication for referral for counseling. nAdolescents who become parents may have the added difficulty of achieving nappropriate developmental milestones prior to assuming adult responsibilities.

Constitutional Growth Delay

Background

Children with constitutional growth delay (CGD), the most ncommon cause of short stature and pubertal delay, typically have retarded nlinear growth within the first 3 years of life. In this variant of normal ngrowth, linear growth velocity and weight gain slows beginning as young as age n3-6 months, resulting in downward crossing of growth percentiles, which oftecontinues until age 2-3 years. At that time, growth resumes at a normal rate, nand these children grow either along the lower growth percentiles or beneath nthe curve but parallel to it for the remainder of the prepubertal nyears.

At the expected time of puberty, the height of children with nconstitutional growth delay begins to drift further from the growth curve nbecause of delay in the onset of the pubertal growth spurt. Catch-up growth, nonset of puberty, and pubertal growth spurt occur later than average, resulting niormal adult stature and sexual development. Although constitutional growth ndelay is a variant of normal growth rather than a disorder, delays in growth nand sexual development may contribute to psychological difficulties, warranting ntreatment for some individuals. Studies have suggested that referral bias is nlargely responsible for the impression that normal short stature per se is a ncause of psychosocial problems; nonreferred childrewith short stature do not differ from those with more normal stature in school nperformance or socialization. A recent study determined that constitutional ngrowth delay was the most common cause of short stature in children.

Pathophysiology

Constitutional growth delay is a global delay in development nthat affects every organ system. Delays in growth and sexual development are nquantified by skeletal age, which is determined from bone age radiographic nstudies of the left hand and wrist. Growth and development are appropriate for nan individual’s biologic age (skeletal age) rather than for their chronologic nage. Timing and tempo of growth and development are delayed in accordance with nthe biologic state of maturity. Constitutional growth delay may be inherited as nan autosomal dominant, recessive, or x-linked trait.

Epidemiology

Frequency

United States

Approximately 15% of patients with short stature referred nfor endocrinologic evaluation have constitutional ngrowth delay. Individuals with constitutional growth delay and familial short nstature represent another 23%. The frequency of constitutional growth delay may nbe underestimated because individuals with milder delays and those who are not npsychologically stressed may not be seen by subspecialists. In a study of 555 n(out of 80,000) schoolchildren below the third percentile in height for age nwith growth rates below normal (< 5 cm/y), twice as many boys as girls were naffected. Constitutional growth delay was found in 28% of boys and 24% of ngirls, and another 18% of boys and 16% of girls had familial short stature icombination with constitutional growth delay.

Mortality/Morbidity

Constitutional growth delay is not associated with increased nmortality because it is a variant of normal growth rather than a disease. nHowever, in some affected individuals, it can be associated with significant npsychological stress, resulting in poor self-image and social withdrawal. nResearchers have also found that individuals with constitutional growth delay nmay be at increased risk for reduced bone mass in adulthood because of the ndelay in sex steroid influence on bone accrual during adolescence.

A recent study compared associations between bone formatiomarkers and resorption and bone mineral density ihealthy children and in children with constitutional growth delay. The study nconcluded that parathyroid hormone was a valuable marker in bone mineralizatioduring puberty and that accelerated bone mineralization was reflected by high nserum parathyroid hormone levels during puberty.

Race

No racial bias has been identified.

Sex

Although the epidemiologic data indicate that all variants nof normal growth are twice as common in boys as in girls, referrals for short nstature reflect an even more divergent sex ratio. This likely reflects greater nconcern about males who are shorter than their peers or who have delayed sexual ndevelopment.

Age

Patterns of growth consistent with constitutional growth ndelay occur in infants as young as 3-6 months. However, individuals often do nnot seek medical attention until puberty, when lack of sexual development nbecomes a concern and discrepancy in height from peers is magnified by the ndelay in pubertal growth spurt.

Growth and Development After nTransplantation

Background

Growth and development are important challenges to nphysicians caring for children with end-stage organ (ie, nkidney, heart, liver) failure.Transplantation may nsuccessfully reverse the growth impairment in these children, for whom it nremains the most physiologic treatment for growth retardation. Nutritional nstatus improves after transplantation, and most children have the potential to nexperience accelerated growth, to obtaiormal height, and to improve ncognitive and developmental skills, including behavioral, motor, and social nfunctions. Appropriate neurologic development can be expected after ntransplantation, and children have the potential to perform at levels that are nadequate for their ages.

Many neuropsychological deficits, as well as physical impairments nand growth failure, however, may still occur and persist. In one study, npediatric recipients of liver transplants, when compared with other groups of nchronically ill children, scored lower in many motor and psychological tests nand obtained fewer academic achievements.A mild nfunctional impairment was present in 79% of children after liver ntransplantation, when the children were compared with a reference population.

This article discusses general principles of growth and ndevelopment in children after transplantation, with a special focus orecipients of kidney and liver transplants.

Pathophysiology

Pathophysiology of growth failure in children with chronic ndisease

Linear growth is one of the most important differences nbetween adults and children. A multitude of factors affect somatic growth, such nas the hypothalamic-pituitary axis, growth hormones, insulinlike ngrowth factors, and binding proteins. Thyroid and adrenal hormones, the sex nsteroid hormones released during puberty, are also under the central control of nthe hypothalamic-pituitary axis and play an important role in achieving optimal ngrowth potential.

Growth retardation is a hallmark of chronic illnesses such nas chronic kidney disease (CKD) in children, and it is associated with nincreased morbidity and mortality. Growth retardation is assessed by the nstandard-deviation score (SDS) or height-deficit score (Z-score). These scores nmeasure the patient’s height in relation to that of unaffected children of nsimilar age. Children with congenital CKD exhibit a relative loss in the nnutrient-dependent infant phase and the gonadal hormone–dependent pubertal nphase, as well as reduced percentile-parallel growth in the mainly growth nhormone–dependent growth period in mid-childhood.

Classification of the stages of CKD (as per the National nKidney Foundation–Kidney Disease Outcomes Quality Initiative [NKF-K/DOQI]) nusing glomerular filtration rate (GFR) measurements (mL/min/1.73 m) are nprovided:

· ne90 GFR – Kidney damage with nnormal or increased GFR

· n60-89 GFR – Kidney damage with nmild reduction of GFR

· n30-59 GFR – Kidney damage with nmoderate reduction ofGFR

· n15-29 GFR – Kidney damage with nsevere reduction of GFR

· n< 15 GFR – Kidney failure

The severity of growth retardation is directly related to nthe age of onset of renal failure—the earlier the onset, the more severe the ngrowth disturbance. Because one third of a child’s growth occurs during the nfirst 2 years of life, any disturbance of the rapid growth during infancy nreduces height potential more than a growth disturbance in later childhood. CKD nresults in marked height deficit in this age group. The main contributing nfactor to growth retardation in infants is inadequate nutritional intake and nwater and electrolyte losses. Additional factors include metabolic acidosis, nrenal osteodystrophy, and catabolic states associated nwith infections.

The mid-childhood period of growth is characterized by a nrelative constant growth rate of 5-7 cm/y and is mainly regulated by growth nhormone, thyroid hormone, and adequate nutrition. The growth pattern of a child nwith congenital CKD often follows the percentile achieved at the end of ninfancy. In children who develop CKD after age 2 years, growth usually follows nthe percentile achieved after stabilization of the disease. Growth retardatioin this age group is mainly determined by the degree of renal insufficiency. nRelative height tends to decrease in patients with GFR below 25 nml/min/1.73m²; growth is usually stable when the GFR is above that nthreshold.

Growth failure in patients with CKD is largely caused by nperturbations in the growth hormone–insulinlike ngrowth factor–I (GH-IGF-I) axis.The IGF system plays na critical role in all phases of mammalian growth. The prenatal contribution of nthe IGFs is independent of GH. Shortly after birth, GH-dependent IGF-I nproduction becomes the critical regulator of skeletal growth. The relatively nstable growth in childhood is principally under the control of the GH-IGF-I naxis and thyrotropin. Twenty percent of adult height nis attained during puberty, which is modulated both by the GH-IGF-I axis and nsex hormones. GH is the most potent secretagogue for nIGF-I, which mediates most of the action of GH. GH levels are reported to be nhigh normal or elevated in children with CKD. Despite the GH levels, somatic ngrowth is not stimulated, because the bioactivity of IGF-I is decreased iuremia.

IGF-I is transported in plasma bound to IGF-binding proteins n(IGFBPs), mostly to IGFBP-3. Only about 1% of plasma IGF-I occurs in the free nbioactive form. There are 6 main IGFBPs in the circulation, two of which, nIGFBP-1 and IGFBP-2, have inhibitory effects on IGF action. Children with CKD nhave normal levels of intact IGFBP-3 but elevated levels of other IGFBPs iproportion to the degree of renal failure, leading to an inhibition of IGF nactivity and a GH-resistant state. CKD also reduces the expression of IGF-I by nreducing postreceptor signaling. Treatment with supraphysiologic doses of recombinant human GH (rhGH) increases the bioactivity of serum IGF-I, thus novercoming the inhibitory effects of excess IGFBPs. Children who have the nlowest growth velocity before treatment benefit the most from rhGH.

The effects of chronic metabolic acidosis on growth may be npartially mediated by the GH-IGF-I axis. Animal studies have shown aanti-anabolic effect of acidosis in bone growth centers, which is partly nrelated to a state of resistance to GH and IGF. This may be a contributing nfactor in the development of delayed longitudinal growth and may contribute to nrenal osteodystrophy in patients with CKD.

The onset of puberty is delayed in adolescents with CKD, nwith an average delay of about 2 years for the appearance of clinical signs of npuberty. Thus, children with chronic renal insufficiency enter puberty with ngrowth retardation. The pubertal growth spurt is delayed, shortened, and nassociated with a reduced growth velocity. The mean pubertal height gain is nonly 50% that of normal late-maturing children, and the loss of growth npotential may be irreversible.

Growth retardation is preventable and can be reversed ipatients who develop CKD in infancy and in mid-childhood. Measures include ncorrection of the metabolic acidosis, optimization of nutrition and water and nelectrolyte balance, correction of renal osteodystrophy, nand treatment with rhGH.

Growth failure in end-stage liver disease (ESLD) is a nsignificant problem, especially in patients younger than 5 years. Multiple nfactors are involved, such as anorexia, deficiencies of fat-soluble vitamins nand trace elements, fat malabsorption, decreased nhepatic protein synthesis, and increased energy requirements. One must consider npsychological factors and acquired dietary behavior, particularly in patients nwith a history of prolonged tube feeding and long hospitalization.

Imbalance of growth-promoting hormones also plays aimportant role. The endocrinologic network nof GH, IGF (somatomedins), nand IGFBP is altered in patients with ESLD, as well as in liver transplant patients.Children with cirrhosis have nnormal or elevated hormone levels but develop resistance to the hormone’s nbiologic activities, which is reversed by liver transplantation.

Most pediatric heart transplant recipients have suboptimal ngrowth parameters before transplantation. Some of the contributing factors are npoor intestinal perfusion leading to nutrient malabsorption, ninadequate renal perfusion, and hemodynamic instability leading to ischemic ninjury to the hypothalamic-pituitary axis. Poor feeding, which may be mandated nor caused by poor appetite, coupled with increased energy expenditure, may lead nto negative nitrogen balance and growth deceleration.

Growth and development after kidney transplantation

The optimal goal of renal transplantation is attainment of ntarget final adult height. Even though growth velocity improves after renal ntransplantation, most children do not have catch-up growth; height deficit is nnot compensated, so the standard-deviation score does not improve. Englund et al have shown that the growth increment nfollowing transplantation is maximal for the most growth-retarded children and nthat the growth is most marked in the first 3 years after transplantation. nThus, growth after transplantation is affected by the degree of stunting at ntransplantation and by renal function after transplantation.

The greatest growth retardation is seen in younger children; ntherefore, age of onset of disease and duration of disease are important ndeterminants. Recipients who receive an allograft before age 6 years may nmanifest acceleration in growth velocity (catch-up growth). The majority of nallograft recipients who are older than 6 years at the time of transplantatiofail to demonstrate catch-up growth and manifest a negative change (delta) istandardized height (Z-score) following transplantation. Both allograft ndysfunction and steroid use may impair growth after transplantation. Renal ntransplantation in the most growth-retarded children younger than 6 years has nthe greatest beneficial effect on growth potential. A large number of patients nmay still not achieve ideal adult height. This is likely related to renal osteodystrophy, which is exclusive to patients with CKD.

Chronic renal failure is known to have adverse effects oneurodevelopment. The two critical periods of brain development occur at 15-20 nweeks of gestation, involving neuronal proliferation, and at 25-30 weeks after nbirth, with focus on glial proliferation. Thus, any developmental problem during nthe first year of life may result in irreversible brain damage. Studies have nsuggested that developmental delay of 60-85% occurs in infants with renal ninsufficiency, related to the early onset and longer duration of the renal ndisease. Tube feedings have become an important component in the care of these nchildren because malnutrition has repeatedly been implicated as a detrimental ninfluence on development.

A study by Valanne et al (2004) of n33 renal transplant patients younger than 5 years revealed that 54% (18 npatients) had ischemic lesions in the vascular border zones, with good ncorrelation to pretransplant hemodynamic crises. nThose patients with border-zone infarcts were older at time of transplantatioand had received dialysis for a longer period, suggesting that most of the nlesions in these patients could have been prevented by careful monitoring and nearly transplantation.

Successful renal transplantation during infancy is nassociated with improvement of developmental outcome. Children with renal ntransplants have been shown to achieve a level of cognitive function similar to nthat of healthy children. In recent studies of pretransplantation nand posttransplantation development, up to 80% of nchildren attended normal school and had normal motor skills, providing nadditional benefit of early transplantation (Qvist et nal, 2002).

Growth and development after liver transplantation

Approximately 20% of pediatric liver transplant recipients nare estimated to experience growth impairment at some point after ntransplantation. A recent suggestion was that a pretransplantation ngrowth defect may not be completely corrected in liver transplant recipients, nalthough an increasing percentage of children are demonstrating catch-up ngrowth. Growth may initially worsen after transplantation (during the initial 6 nmonths), but catch-up growth begins afterward.

The SPLIT 2000 (Studies of Pediatric Liver Transplantation) nannual report demonstrated that growth failure was more significant in patients nyounger than 5 years but that these same patients also manifested the greatest nimprovement 18 months after transplantation. According to the report, some nimportant pretransplantation factors affecting posttransplantation growth are age at transplantation (patients nyounger than 2 years had the greatest catch-up growth), Z-score at ntransplantation, and primary diagnosis (patients with biliary atresia seem to nhave the most catch-up growth).A proper recognition of children with nnutritional and growth deficits before solid-organ transplantation is therefore nfundamental.

Posttransplantation nfactors that may impact growth include graft function and the need for retransplantation, steroid use, and occurrence of posttransplant lymphoproliferative ndisease (PTLD). Corticosteroids influence the GH-IGF axis by suppression of npituitary GH production, inducing IGF inhibitors in serum and increasing nIGFBPs. Steroids also cause direct inhibition of skeletal matrix production by ndecreasing synthesis of type1 collagen, chondrocyte proliferation, and bone nmatrix production. GH counteracts the catabolic activity through increased nprotein and collagen synthesis. Endogenous cortisol levels appear to be reduced nin liver transplant patients and correlate with growth impairment. An increase nin the percentage of liver transplant patients who demonstrate catch-up growth nhas been attributed to steroid withdrawal and supplemental use of growth nhormone. Liver transplant recipients have been shown to have more catch-up ngrowth than kidney transplant recipients, especially aftersteroidwithdrawal.Acareful nmultispecialty approach is therefore necessary to decrease the incidence of ngrowth failure after solid-organ transplantation in children. Pretransplantation nutritional therapy can be optimized; nthe most appropriate timing of surgery can be selected; and the best nimmunosuppressive regimen can be determined.

Cognitive and emotional difficulties have been shown to noccur more often in liver transplant patients than in age-matched controls. nVisual spatial deficits seem to occur in children with liver transplants, but nmotor abilities are generally not affected. Studies have shown that infants who nundergo liver transplantation in the first year of life can achieve healthy nneurodevelopment. In the first year after transplantation, however, language nskills may be blunted, probably because of nasogastric tube feeding.

Psychoneurologic nscores were maintained during 4 years of follow-up observation, although a ntransient reduction in social skills and eye-hand coordination occurred during nthe same period, when the children spent longer times in the hospital. In older nchildren, neurologic deficits that are established at the time of ntransplantation are more difficult to overcome. Liver transplant recipients seem nto experience greater psychosocial problems than kidney transplant recipients, nwhich is likely related to body image, especially in the adolescent age group.

Growth and development after small bowel transplantation

Small bowel transplantation poses specific nutritional problems.Small bowel transplant patients may commonly have nmacronutrient and micronutrient deficiencies because of high stomal output and diarrhea. Decreased intestinal motility nand malabsorption may also be present. Chronic ndependence on parenteral nutrition may lead to food aversion; however, npreliminary data demonstrate that growth is normal in 50% of recipients, and n15% may experience catch-up growth. Studies have shown that most patients ncontinue to experience cognitive delays several years after small bowel ntransplantation. Children who receive small bowel transplants when they are ninfants may also demonstrate motor delays.

Growth and development after heart transplantation

Growth outcomes in pediatric heart transplantation patients nhave been encouraging. Some reports have suggested that growth delay may be nless of a problem for heart transplant recipients than for liver and kidney ntransplant recipients. This difference may be due to the fact that childrewith congenital heart disease receive heart transplants at a very young age and nthose with acquired conditions are much older when they receive transplants, nthus bypassing the critical periods of growth.

Studies of growth after heart transplantation reveal varied nresults:

· nChinnock nand Baum (1998) reported on 66 infants younger than 6 months who received heart ntransplants and did not receive maintenance steroid therapy. Catch-up growth nfor these patients was almost universal in the first year after heart ntransplantation.

· nCohen et al performed a nretrospective analysis of the effects of cardiac transplantation on skeletal nmaturation and linear growth. Bone age delays as great as 3-4 years were seein the years before transplantation. Bone age delay greater than 12 months was nseen in 38.5% of patients at the time of transplantation. Children who received nheart transplants before age 7 years and those with a pretransplantation ndiagnosis of cardiomyopathy experienced the greatest decrease in skeletal ngrowth.

· nThe seventh pediatric report of nthe Registry for the International Society for Heart and Lung Transplantation (Boucek, 2004) reveals that adolescent heart transplant nrecipients had no major changes in growth Z-score after transplantation and no ndramatic changes when stratified for steroid use. The patients did have aincrease in weight Z-scores, again with no stratification for steroid use.

Important factors that affect growth after transplantatioinclude age at transplantation, etiology of cardiac failure, graft function, nchronic renal dysfunction after heart transplantation, and steroid use. nChildren initiated on a steroid-free protocol almost universally demonstrate ncatch-up growth. Evidence suggests that the growth-suppressive effects of steroids ncan be overcome by exogenously administered growth hormone. Recent data suggest nthat growth hormone modulates cardiac growth independent of somatic growth. nChildren who have growth hormone deficiencies have subnormal left ventricular nmass.

Very few studies have been performed oeurocognitive ndevelopment after heart transplantation in pediatric patients, but the data nsuggest that patients do not suffer major deficits in mental or psychomotor ndevelopment. Wray et al demonstrated that though the overall mean developmental nscore of infants and young children was withiormal range after heart ntransplantation, scores were significantly lower than those of healthy nchildren. Patients with congenital heart disease had a significantly lower ndevelopmental quotient and lower scores in locomotor nability, speech and hearing, eye-hand coordination, and performance than those npatients with cardiomyopathy.

Researchers at Loma Linda University Medical Center found nthat infants with hypoplastic left heart syndrome who nreceived heart transplants before age 6 months had ultimately normal growth and ndevelopmental outcomes withiormal limits.

Growth and development after lung transplantation

Few lung transplants are performed in the pediatric npopulation, with cystic fibrosis being the primary indication for lung ntransplantation in children. Malnutrition in pediatric patients with cystic nfibrosis is multifactorial (eg, pancreatic ninsufficiency causing fat malabsorption, diabetes nmellitus, anorexia, poor appetite, and intestinal obstruction). Some of these npatients are severely malnourished before transplantation. Decreased bone ndensity due to vitamin D deficiency and long-term steroid use can further erode nbone mass. At some adult transplant centers, patients who are below 80% of nideal body weight are not considered good candidates for lung transplantation. nBody mass index is an important indicator of good nutritional status before and nafter transplantation.

Osteoporosis is another important risk factor, especially because nbone mineral density may worsen after transplantation as a result of long-term nsteroid use. Daily administration of steroids, which is the rule in pediatric nlung transplantation, unlike in other solid-organ transplantations, further ndecreases bone growth. Long-term survival after lung transplantation is not as nencouraging as that seen after heart transplantation; graft half-life in lung ntransplantation is approximately 3.5 years.

Epidemiology

Frequency

United States

A review of the 2005 North American Pediatric Renal Trials nand Collaborative Studies (NAPRTCS) database of kidney recipients demonstrated nthat at time of transplantation, the mean height deficits for all patients is n-1.85; that is, the average patient is nearly 2 standard deviations below the nappropriate age- and sex-adjusted height level, or is shorter than the third npercentile of their peers.At the time of ntransplantation, linear growth is impaired more often in recipients of livers nthan in those who receive kidneys. However, the frequency of catch-up growth iliver recipients can be greater than that in kidney recipients, probably nbecause of decreased administration of corticosteroids.

Exact incidence of catch-up growth varies according to ndifferent groups and immunosuppressive regimens. In 294 unselected candidates nfor liver transplants, Bartosh et al (1999) reported nthe mean height Z-score at the time of transplantation to be -1.6 ± 1.8, with n39% of patients below 2.0. As many as 47% of patients demonstrated catch-up ngrowth after transplantation.In infants who receive nheart transplants, 88% reach a normal height after 5 years, mainly because of ngood catch-up growth.

International

Sarna et al nfrom Finland reported 79% of liver recipients as being below the reference nrange for height at 3 years after transplantation.In nthe same series, the catch-up growth after transplantation was reported to be n26% in the first year, 47% in the second year, and 56% in the third year.In 1999, Viner et al from England reported severe ngrowth retardation in 20% of patients at the time of liver transplantation.

Mortality/Morbidity

Nutritional status and growth failure are directly ncorrelated with overall mortality and morbidity after liver and renal ntransplantation. Children with weight less than -1 standard-deviation score nhave a lower survival rate at 2 years after transplantation (57%) than those nwith weight greater than -1 standard-deviation score (95%). The same is true nfor height.

Race

Growth impairment after renal ntransplantation appears to be greater in black and Hispanics than in whites.

Sex

In the NAPRTCS 2005 report of kidney transplant patients, nmean height deficits is greater for males (-1.90) than females (-1.77). Most nstudies do not report an association between sex and growth retardation after ntransplantation.

Age

Age is usually correlated directly with growth retardatioat the time of transplantation; however, age is inversely correlated with the nrate of growth after transplantation.

· nOf pediatric patients receiving nkidney transplants, only those patients younger than 6 years demonstrate nsignificant recovery, with catch-up growth of 47% in patients younger than 2 nyears and 43% in those aged 2-5 years. Children older than 5 years have, as a ngroup, not been shown to experience catch-up growth.

· nAlthough liver transplantatioin persons younger than 2 years was initially associated with poor height noutcome, later results did not confirm such findings. The current view is that ntransplantation in infancy better preserves the height potential of the patient nand prevents growth retardation before transplantation. The greatest catch-up ngrowth has been seen in patients younger than 2 years.

· nPatients with early onset of nliver disease but older age at the time of transplantation have an increased nincidence of neuropsychological impairment because of the prolonged neurotoxic neffect of liver toxins on brain development. Infants who receive transplants nbefore any damage is established may be expected to experience healthy nneuropsychological development.

Growth Failure

Background

Short stature may be the normal expression of genetic npotential, in which case the growth rate is normal, or it may be the result of na condition that causes growth failure with a lower-than-normal growth rate.Growth failure is the term that describes a growth nrate below the appropriate growth velocity for age (see image below).

A child is considered short if he or she has a height that nis below the fifth percentile; alternatively, some define short stature as nheight less than 2 standard deviations below the mean, which is near the third npercentile. Thus, 3-5% of all children are considered short. Many of these nchildren actually have normal growth velocity. These short children include nthose with familial short stature or constitutional delay in growth and nmaturation. In order to maintain the same height percentile on the growth nchart, growth velocity must be at least at the 25th percentile. Wheconsidering all children with short stature, only a few actually have a specific ntreatable diagnosis. Most of these are children with a slow growth velocity.

Pathophysiology

The most rapid phase of human growth is intrauterine. nFollowing birth, a gradual decline in growth rate occurs over the first several nyears of life. The average length of an infant at birth is about 20 inches, the nlength at age 1 year is approximately 30 inches, the length at age 2 years is napproximately 35 inches, and the length at age 3 years is approximately 38 ninches. After age 3 years, linear growth proceeds at the relatively constant nrate of 2 inches per year (5 cm/y) until puberty.

Normal growth is the result of the proper interaction of ngenetic, nutritional, metabolic, and endocrine factors. To a large extent, ngrowth potential is determined by polygenic inheritance, which is reflected ithe heights of parents and relatives. Secretion of growth hormone (GH) by the npituitary is stimulated by growth hormone–releasing hormone (GHRH) from the nhypothalamus. Another signal, which is stimulated by certain growth nhormone–releasing peptides (GHRPs), may be present; the receptor for the GHRPs nhas been identified, and a possible natural ligand for these receptors has beedetermined. Somatostatin secreted by the hypothalamus ninhibits growth hormone secretion.

When growth hormone pulses are secreted into the systemic ncirculation, insulinlike growth factor (IGF)–1 is nreleased, either locally or at the site of the growing bone. Growth hormone ncirculates bound to a specific binding protein (GHBP), which is the extracellular nportion of the growth hormone receptor. IGF-1 circulates bound to one of nseveral binding proteins (IGFBPs). The IGFBP that most depends on growth nhormone is IGFBP-3.

A peptide hormone that stimulates growth hormone release, nnamed ghrelin (from the word ghre, a root word nin proto-Indo-European languages meaning grow), has been described. This nhormone is unique in that it is a small polypeptide modified at the third amino nacid (serine) by esterification of n-octanoic acid. nGhrelin appears to be made in the stomach and stimulates growth hormone nsecretion by binding with its own receptor, which had previously been known to nbind synthetic GHRPs. Ghrelin may play a role in regulation of growth hormone nat the hypothalamic level, permitting an adequate energy supply for nmaintenance, growth, and repair.

Epidemiology

Frequency

United States

In 1994, Lindsay et al studied 114,881 school children in Utah.After 1 year, 79,495 of the original group were available nfor evaluation. Of these, 555 (0.7%) had heights that were below the third npercentile and a growth rate that was less than 5 cm/y. When examined further, ncauses for short stature within this group of children included familial short nstature (37%), constitutional delay (27%), a combination of familial short nstature and constitutional delay (17%), other medical causes (10%), idiopathic nshort stature (5%), growth hormone deficiency (3%), Turner syndrome (3% of ngirls), and hypothyroidism (0.5%).

International

Several studies have been conducted to determine the nfrequency of various causes of short stature. In 1974, Lacey and Parkin evaluated children in Newcastle upon Tyne in England.They studied 2256 children, 111 of whom were below nthe third percentile in stature. Of the 98 children that they were able to nexamine, only 16 had evidence of organic disease causing their short stature. nDiagnoses included Down syndrome, cystic fibrosis, chronic renal insufficiency, ngrowth hormone deficiency, juvenile rheumatoid arthritis (treated with nglucocorticoid), and Hurler syndrome.

Mortality/Morbidity

Short stature has been thought to have far-reaching effects non psychological well-being, including poor academic achievement (despite nnormal intelligence, healthy family dynamics, and high socioeconomic status) nand behavioral problems (eg, anxiety, nattention-seeking actions, poor social skills).

Morbidity related to the underlying cause of the growth nfailure may also be observed. Some studies involving children who have not beeseen in a clinic that treats short stature (and, therefore, may represent a ndifferent patient population) have challenged the notion that short stature has npsychological implications. At the present time, this issue is not completely nresolved.

Mortality rates in children with growth failure relate to nthe underlying cause of the growth failure. Mortality is not related to growth nfailure itself; rather, it is related only to the cause of the growth failure.

Sex

The sex distribution of children treated with growth hormone nis about 3 boys for every girl. Recent work in this area suggests that this is nmostly due to a referral bias, either from parents themselves or from the nreferring physician.

Hyposomatotropism

Background

Remarkable research over the past 4 decades has advanced our nknowledge of the physiology of the growth hormone (GH) axis.

Human pituitary-derived growth hormone

More than 40 years have elapsed since humapituitary-derived growth hormone (pit-hGH) was npurified and the first patient, a 17-year-old male adolescent with growth nhormone deficiency (GHD), was treated successfully with pit-hGH. nFor many years, pituitary glands harvested from human cadavers provided the nonly practical source of GH with which to treat GHD. Worldwide, more tha27,000 children with GHD received pit-hGH from the n1950s to the mid 1980s.

Pit-hGH was a suboptimal therapy nfor 3 reasons.

1. The nshortage of pit-hGH limited its use and the dosages nadministered.

2. The nbiopotency of preparations varied. Strict diagnostic ncriteria for GHD were used to address these problems (eg, npeak plasma immunoreactive GH levels of more tha3.5-5 ng/mL after provocative stimuli).

3. Treatment nwas often interrupted. The mean age for starting treatment with pit-hGH was often 12-13 years (late in childhood), and severe ngrowth failure (height Z score -4 to -6) was required. As a result, pit-hGH therapy was often discontinued when girls attained a nheight of 60 inches and when boys attained a height of 65 inches.

Nonetheless, pit-hGH had dramatic neffects. Among patients with isolated GHD, final height standard deviatioscores increased to approximately -2 in boys and -2.5 to -3 in girls. For nchildren with multiple pituitary-hormone deficiencies, height standard ndeviation scores increased to between -1 and -2.

The number of patients with GHD who were treated with pit-hGH increased from approximately 150 to more than 3000 by n1985. However, in 1985, studies indicated that pit-hGH nwas the likely source of contaminated material (prions) responsible for nCreutzfeldt-Jakob disease (a slowly developing, progressive, fatal neurologic ndisorder) in 3 young men. As a consequence, production and distribution of pit-hGH for therapy was discontinued.

Recombinant human growth hormone

The commercial introduction of recombinant human growth nhormone (rhGH) in 1985 dramatically changed the field nof therapy for GH. Since then, rhGH has beeadministered to more than 50,000 children worldwide, making it one of the most nextensively studied therapies in the pediatric pharmacopoeia.

US Food nand Drug Administration (FDA)–approved indications for the administration of rhGH in children include treatment of the following nconditions:

· nGrowth failure associated with nGHD (approved in 1985)

· nChronic renal failure (approved nin 1993)

· nTurner syndrome (approved i1996-1997)

· nPrader-Willi nsyndrome (approved in 2000)

· nSmall size for gestational age, nwith failure to catch up (approved in 2001)

· nIdiopathic short stature n(approved in 2003)

· nSHOX ngene deficiency (approved in 2006)

· nNoonan syndrome (approved i2007)

Achievement of final adult height consistent with a child’s ngenetic potential remains the primary therapeutic endpoint for rhGH therapy in the pediatric population. In addition to nits effects on bone mass, GH regulates muscle mass, muscular strength, body ncomposition, lipid and carbohydrate metabolism, and cardiac function. Patients nwith GHD typically have hyperlipidemia, increased body fat, premature natherosclerotic plaques, delayed bone maturation, and impaired cardiac nfunction.

At present, GHD in adults is recognized as a distinct nclinical syndrome that encompasses reduced psychological well-being and nspecific metabolic abnormalities. Such abnormalities, including hypertension, ncentral obesity, insulin resistance, dyslipidemia, and coagulopathy, closely nresemble those of metabolic insulin resistance syndrome. The increased rates of ncardiovascular morbidity and mortality reinforce the close association betweethe syndromes.

Replacement of GH in adults with GHD markedly reduces ncentral obesity and substantially reduced total cholesterol levels but has nproduced little change in other risk factors, particularly, insulin resistance nand dyslipidemia.For these patients, concerns are the npersistent insulin resistance and dyslipidemia, together with the elevated nplasma insulin and lipoprotein(a) levels observed with GH replacement. nLong-term follow-up data are required to assess the effect of GH replacement ocardiovascular morbidity and mortality in adults with GHD.

The large commercial supply of rhGH nfuels research and debate over the proper indications for this potent and nexpensive therapy. Few disagree that many patients with childhood-onset GHD nrequire continuous GH replacement therapy into adulthood. However, the ndiagnostic criteria for GHD in patients of any age remain controversial. This nambiguity stems from the wide variability in current tools used to diagnose nGHD, as discussed below (see Workup).

Clinicians and researchers alike will continue to grapple nwith these dilemmas in the foreseeable future. However, commercial interests nand patient advocates continue to pressure the medical community to expand the naccepted indications for rhGH. Therefore, the nclinician and the clinical researcher must examine published data critically nand must educate individual patients and their families about the risk-benefit nratio of rhGH therapy for them.

Pathophysiology

Anatomy

Most of the pituitary gland is dedicated to synthesizing and nsecreting GH from somatotrophs of the adenohypophysis (anterior pituitary). See the image below.

The adenohypophysis derives from nthe Rathke pouch, a diverticulum of the primitive noral cavity. The adenohypophysis consists of 3 lobes, nnamely, the pars distalis, the pars intermedia (which is vestigial in humans), and the pars tuberalis. The pars distalis is nthe largest lobe and contains most of the somatotrophs. nThe pituitary gland lies within the sella turcica, covered superiorly by the diaphragma nsellae and the optic chiasm.

Growth hormone

The hypothalamus communicates with the anterior pituitary ngland by releasing of hypothalamic peptides, which are subsequently transported nin the hypophyseal portal circulation (ie, the blood supply and communication between the nhypothalamus and the adenohypophysis). GH is secreted nin a pulsatile pattern as a single-chain, 191-amino acid, 22-kDa protein.

Two specific hypothalamic peptides play major regulatory nroles in GH secretion: growth hormone-releasing hormone (GHRH) and somatotropin-releasing factor. Amplitudes and frequencies nfor release of GHRH and somatotropin-releasing nfactor, as well as GH, differ between boys and girls and may partially account nfor differences in the phenotypes between the sexes.

Several neurotransmitters and neuropeptides also control GH nsecretion by directly acting on somatotrophs or by nindirectly acting by means of hypothalamic pathways. These neurotransmitters ninclude pituitary adenylate cyclase nactivating polypeptide (PACAP), galanin, npituitary-specific transcription factor-1 (Pit-1), prophet of Pit-1 (PROP1), nHESX1, serotonin, histamine, norepinephrine, dopamine, acetylcholine, gamma-aminobutyric acid, thyrotropin-releasing nhormone, vasoactive intestinal peptide, gastrin, neurotensin, nsubstance P, calcitonin, neuropeptide Y, vasopressin, and corticotropin-releasing nhormone.

Insulinlike ngrowth factors

Insulinlike growth nfactors (IGFs) are a family of peptides that partially depend on GH and that mediate nmany of its anabolic and mitogenic actions.

Two theories have been proposed regarding the relationship nbetween GH and IGFs: the somatomedin hypothesis and nthe dual-effector hypothesis. According to the somatomedin nhypothesis, IGF mediates all of the anabolic actions of GH. Although this ntheory is partially correct, GH also has various other independent metabolic nactions, such as enhancement of lipolysis, stimulation of amino acid transport nin the diaphragm and the heart, and enhancement of hepatic protein synthesis. nThe attempt to resolve this discrepancy lies in the dual-effector model. nAccording to this theory, GH stimulates precursor cells to differentiate and nsecrete IGF, which, in turn, exerts mitogenic and nstimulatory effects.

Insulinlike ngrowth factor binding proteins

Six high-affinity insulinlike ngrowth factor binding proteins (IGFBPs) bind IGFs in the circulation and ntissues, regulating IGF bioavailability to the IGF receptors. Under most nconditions, IGFBPs appear to inhibit the action of IGFs by competing with IGF nreceptors for IGF peptides. However, under specific conditions, several IGFBPs ncan enhance IGF actions or exert IGF-independent actions.

Relative concentrations of the IGFBPs vary among biologic nfluids. IGFBP-3 is the most abundant IGFBP species in human serum and ncirculates as part of a ternary complex consisting of IGFBP-3, an IGF molecule, nand a glycoprotein called the acid-labile subunit. IGFBP-3 is the only IGFBP nthat clearly demonstrates GH dependence. Therefore, IGFBP-3 is a clinically nuseful tool for the diagnosis of GHD and the follow-up care of patients.

Sex steroids

Androgens and estrogens substantially contribute to growth nduring the adolescent growth spurt. Children with GHD lack the normal growth nspurt despite adequate amounts of exogenous or endogenous gonadal steroids. The nrelationship among the sex steroids, GH, and skeletal maturation is not clearly nunderstood. However, GH secretion is lower in frequency and higher in amplitude namong males than in among females.

Androgen and estrogen receptors have been identified in the nhypothalamus and are suspected to play an important regulatory role in the nrelease of somatostatin, the hypothalamic hormone nthat inhibits GH secretion. Somatostatin regulatiois believed to direct the frequency and amplitude of GH secretion. Therefore, nit may be one of the sources of the differences between male and female nindividuals.

Thyroid hormone

Thyroid hormone is essential for postnatal growth. Growth nfailure, which may be profound, is the most common and prominent manifestatioof hypothyroidism. The interrelationships between the thyroid and the npituitary-GH-IGF axis are complex and not yet fully defined. Hypotheses include na direct effect of thyroid hormone on the growth of epiphyseal cartilage and a npermissive effect on GH secretion. Proof of the permissive effect on GH nsecretion derives from studies revealing that spontaneous GH secretion is ndecreased and that the response to provocative GH testing is blunted ipatients with hypothyroidism (see Workup).

In addition, growth velocity is markedly decreased among rhGH-treated patients with GHD and hypothyroidism until nthyroid hormone replacement is begun. Downregulation nof GH receptors and decreased production of IGF-1 and IGFBP-3 have beereported in the hypothyroid state. An unexplained relationship exists betweethe treatment of patients with GHD by using rhGH and nthe development and unmasking of hypothyroidism.

Epidemiology

Frequency

United States

The prevalence is 1 case per 3480 children or adolescents naged 4-15 years.

International

No strong data about the international prevalence of hyposomatotropism are available.

Mortality/Morbidity

Sequelae of hyposomatotropism include the following:

· nBehavioral and educational ndifficulties

· nPeripheral vascular disease and nreduced myocardial function

· nLean body mass, reduced nmuscular strength, and reduced exercise capacity

· nReduced thermoregulation

· nAbnormal metabolism of thyroid nhormone

· nImpaired psychosocial nwell-being

· nDecreased bone mineral content

The overall crude mortality rate for patients with ntumor-related, trauma-related, or iatrogenic GHD is 2.7%.

Clinicians must be cognizant of the increased incidence of nmortality among patients with multiple pituitary hormone insufficiency nsecondary to adrenal crisis.

Race

A racial ascertainment bias may be noted. Demographic and ndiagnostic features of GHD in children in the United States reveal that black nchildren with idiopathic GHD are shorter than white children are at the time of ndiagnosis. The low overall representation of black children in the populatiowith GHD (6%) compared with their representation in the at-risk populatio(12.9%) also suggests an ascertainment bias between the races.

Sex

A male ascertainment bias may be observed. The predominance nof GHD diagnosed in boys in the United States and the observation that girls nwith idiopathic GHD are comparatively shorter than boys at the time of ndiagnosis suggest a sex-based ascertainment bias.

Age

The age of patients with GHD is depends on the etiology of nthe disease.

Nutritional Considerations in Failure to Thrive

Background

Failure to thrive (FTT) is both a descriptive term for nvarious entities and a diagnosis. It is defined as a significant interruptioin the expected rate of growth during early childhood. Because sequential nmeasurements of growth are vital aspects of preventive pediatrics, failure to nthrive is a concern for all pediatric heath care providers. All standard npediatric textbooks have sections on this topic,and numerous review articles have been written.However, ndespite significant attention, a meta-analysis of studies on industrialized nchildren with this condition failed to demonstrate any significant adverse noutcomes in this cohort.Still, failure to thrive cabe a prelude to significant morbidity and mortality in the developing world, iimpoverished children, and in children with various chronic illnesses.

Although specific anthropometric criteria to define failure nto thrive vary, all describe children with inadequate or worsening growth over ntime. The most common definition is weight less than the third to fifth npercentile for age on more than one occasion or weight measurements that fall 2 nmajor percentile lines using the standard growth charts of the National Center nfor Health Statistics (NCHS).

Some authors have included height measurements as part of nthe definition; however, height measurements more precisely describe short nstature. If weight parameters are significantly compromised, height can also be nsecondarily affected in individuals with failure to thrive. A European study nexamined a large cohort of children using various terms associated with npediatric growth compromise and documented a wide variance in the prevalence of nthis condition.Although serial measurements of head ncircumference are important in the evaluation of infants and toddlers, isolated nfailure of the head to grow should not suggest the typical failure to thrive ndifferential.

In the developed world, the published literature indicates nthat although the differential diagnosis of failure to thrive is comprehensive, nmost children with this problem are diagnosed with predominantly psychosocial nor nonorganic problems. However, because speech and feeding evaluations have nbecome more commonplace and are more sophisticated, psychosocial compromise is nnow recognized as more likely to yield failure to thrive in those with subtle nswallowing dysfunction or other organic conditions.As nthis fundamental paradigm is reconsidered,the practicing child care provider must make every effort nto identify simultaneous pathophysiology, regardless of how deprived the child nwith failure to thrive may appear.

Conversely, the contributions of dysfunctional familial ndynamics, oppositional behavior, and depression to the failure to thrive noted nin chronic illnesses must also be appreciated. Some authors have substituted a nnonorganic failure to thrive paradigm for the organic failure to thrive nparadigm, with individual children lying closer to one extreme or the other.

Normal growth and growth charts of term and premature ninfants, as well as the etiology, evaluation, management, and outcome of nfailure to thrive are discussed in this article. For information on energy nmalnutrition, see the article Marasmus.

Pathophysiology

Although failure to thrive has historically been considered nto be organic or nonorganic, a new view attempts to identify all contributing nfactors, often finding contributors from both categories in a single child. nNonorganic failure to thrive is almost always the result of inadequate energy nintake. In addition to that problem, organic failure to thrive may also be the result of compromised use of ingested ncalories (usually vomiting or malabsorption and/or nexcessive losses [ie, protein-losing enteropathy]) and excessive metabolic demands. Prior to nanalyzing these entities, normal growth is reviewed.

Normal growth in term infants

The average birth weight for a term infant is 3.3 kg. Weight ndrops as much as 10% in the first few days of life, secondary to loss of excess nfluid. By 10-14 days of life, birth weight should be regained. Breastfed ninfants who are fed smaller volumes of colostrum for the first few days regaibirth weight a little later than bottle-fed infants.

On average, infants gain 1 kg/mo nfor the first 3 months, 0.5 kg/mo from age 3-6 nmonths, 0.33 kg/mo from age 6-9 months, and 0.25 kg/mo from age 9-12 months. Term infants double their birth nweight by age 4-6 months and triple their weight by age 12 months. Aalternative schema to use is that term infants gain almost 30 g (1 oz) per day for 3 months and then almost 15 g (0.5 oz) per day for the next 6 months. From age 9 months until nthe child is a toddler, the average weight gain is roughly 0.25 kg/mo (or 0.5 lb/mo). nAfterwards, the weight gain is about 2 kg/y through early school age.

Caloric intake to assure adequate intake in a normal infant nis 100-110 kcal/kg/d for the first half year and 100 kcal/kg/d nfor the second half of the first year. Beyond 10 kg, 50 nkcal/kg/d is required until 20 kg. Beyond 20 kg, 20 nkcal/kg/d are necessary.

Term infants grow 25 cm in length during the first year, n12.5 cm in the second year, and then slow down to approximately 5-6 cm betweeage 4 years and the onset of puberty, at which time, growth can increase up to n12 cm per year.

The average head circumference is 35 cm at birth and rapidly nincreases to 47 cm by age 1 year. The rate of growth then slows, reaching an average nof 55 cm by age 6 years.

Also, the upper-to-lower body segment ratio changes with ngrowth. Normally, the ratio at birth is 1.7, the ratio at age 3 years is 1.3, nand the ratio by age 7 years becomes 1. The lower body segment is measured from nthe symphysis pubis to the floor.

Normal growth in premature infants

When plotting growth charts for premature babies, a n”corrected age” should be used. This corrected age can be calculated nby subtracting the number of weeks of prematurity from the postnatal age. nSpecial growth charts based on gestational age rather than chronological age have been developed for infants, beginning at 26 weeks’ ngestational age. However, because these charts represent a compilation of a nrelatively small number of infants, they may not be completely reliable. nWhichever technique is used for premature babies (eg, nadjustment of age, using specific premature growth charts), consistency of nmethodology is essential. Once a method for plotting growth is chosen, that ntechnique should be followed each time plotting occurs. Prior to 40 weeks’ ngestation, some infants may require as much as 120 kcal/kg/d nto ensure adequate weight gain.

Catch-up growth is attained at approximately age 18 months nfor head circumference, age 24 months for weight, and age 40 months for height. nSubsequently, normal growth charts can be used. In some premature babies with nvery low birth-weight, catch-up growth does not occur until early school age.

Growth charts

Growth charts were developed by the NCHS based on data ncollected through the Third National Health and Nutrition Examination Survey nIII. They have been used since 1977 and are available for males and females naged 0-36 months and aged 2-18 years. The growth charts for boys and girls aged n0-36 months include weight and height for age and head circumference; growth ncharts for both age groups include weight for stature.

These charts have been revised and are available from the nCenters for Disease Control and Prevention (2000 CDC Growth Charts: United nStates).The new charts are applicable to infants, children, and adolescents nfrom birth to age 20 years and have 7 percentile curves (5th, 10th, 25th, 50th, n75th, 90th, 95th). Charts are available for use in subspecialty patients (eg, endocrine, gastroenterology), with additional third and n97th percentile curves. Body mass index (BMI) charts, which are available for nindividuals aged 2-20 years, have replaced the nweight-for-stature charts. BMI is calculated by dividing weight in kilograms by nheight in meters squared.

Accurate measurements are essential to the interpretation of ngrowth charts. Scales need to be regularly calibrated; length should be ncarefully measured, and head circumference should be measured using nstandardized techniques.

Alternate growth charts are available for children who are nbreast fed and for children with Down syndrome,Turner syndrome,achondroplasia,meningomyelocele, nlow birth weight, and very low birth weight. No matter which growth chart is nused, the most valuable information is obtained by careful measuring and nplotting on the same chart over time. Infants and children should remain withi1-2 percentile curves over time.

Epidemiology

Frequency

United States

In reports from 1980-1989, failure to thrive accounted for n1-5% of tertiary hospital admissions for infants younger than 1 year. As many nas 10% of children in primary care settings show signs of failure to thrive. nThe incidence is highest in children with prematurity and with other medical nconditions. The proportion of nonorganic failure to thrive among all infants nwith failure to thrive is much higher in the United States and other nindustrialized countries than in the developing nation.

International

In underdeveloped countries, malnutrition manifesting as nfailure to thrive is more common.

Mortality/Morbidity

Ultimate physical growth and cognitive development may be ndecreased in children with long standing failure to thrive, especially with aearly onset. However, efforts to analyze the published data have not yielded nunequivocal confirmation in children in the developing world.Earlier npublications have described more cognitive deficits ionorganic than organic nfailure to thrive.

In developing countries, malnutrition is a significant cause nof mortality, whether directly or secondary to complications (eg, infection). Among children with certain illnesses, nfailure to thrive is an independent risk factor for premature mortality, such nas with HIV infectionand epidermolysis nbullosa.

Race

Failure to thrive can occur in all socioeconomic strata, nalthough it is more frequent in families living in poverty. Studies indicate nincreased incidence in children receiving Medicaid, children living in rural nareas, and children who are homeless.

Sex

Nonorganic failure to thrive is reported more commonly ifemales than in males.

Age

The term is mainly reserved for growth compromise in young nchildren.

References

а) nBasic

1. nManual of Propaedeutic Pediatrics / S.O. Nykytyuk, N.I. Balatska, N.B. Galyash, N.O. Lishchenko, O.Y. Nykytyuk – Ternopil: TSMU, 2005. n– 468 pp.

2. Kapitan T. Propaedeutics nof children’s diseases and nursing of the child : n[Textbook for students of higher medical educational institutions] ; Fourth nedition, updated and translated in English / T. Kapitan n– Vinnitsa: The State Cartographical Factory, 2010. – 808 pp.

3. Nelson Textbook of Pediatrics /edited by Richard E. nBehrman, Robert M. Kliegman; senior editor, Waldo E. nNelson – 19^th ed. – W.B.Saunders Company, n2011. – 2680 p.

b) Additional

1. WHO child growth standards and the identification of nsevere acute malnutrition in infants and children // nhttp://www.who.int/childgrowth/en

2. nwww.bookfinder.com/author/american–academy–of–pediatrics

3. www.bookfinder.com/author/american–academy–of–pediatrics