Growth Flashcards
1
Q
Vital Sign Tips
A
Respiratory rate and heart rate should be counted for a full minute with child calm and at rest
Each degree of Fahrenheit increases the HR 8-10 beats/ minute
Blood pressure When you have difficulty getting a blood pressure from a patient (i.e., it is too “quiet” to hear it), have the patient raise up their arm to help make it louder Sex, age, weight
2
Q
Pubertal Growth Spurt
A
Girls = 8-12cm (3-5in) Boys = 10-14 cm (4-6in)
3
Q
Why are measurements so important?
A
Clinical decisions and clinical interventions are based on physical measurements Accurate and reliable physical measures are used to: - Monitor the growth of an individual - Detect growth abnormalities - Monitor nutritional status - Track the effects of medical or nutritional intervention **IF YOU DO NOT FEEL COMFORTABLE WITH A MEASUREMENT YOU NEED TO REPEAT IT!**
4
Q
Growth Charts – weight for age
A
Reflects body weight relative to age Influenced by recent changes in health or nutritional status. Not used to classify infants, children and adolescents as under or overweight. Used in early infancy for monitoring weight and helping explain changes in weight-for-length and BMI-for-age in older children.
5
Q
Stature/Length-for-age
A
Linear growth relative to age Used to define shortness or tallness
6
Q
BMI for age
A
Anthropometric index of weight and height Used to classify children and adolescents as underweight, overweight, or obese.
7
Q
Weight for length/stature Head circumference
A
Weight-for-length/stature reflects body weight relative to length and requires no knowledge of age. Indicator to classify infants and young children as overweight and underweight Head circumference-for-age is critical during infancy and can be charted up to 36 months of age. Measurements reflect brain size.
8
Q
Head circumference positioning
A
Proper positioning of measuring tape Widest circumference, avoiding ears
9
Q
BMI for age
A
>95th percentile – Obese
>85th and <95th percentile = overweight
10
Q
Weight for length/stature
A
>95th percentile – Obese
<5th percentile = underweight
11
Q
Stature/length for age
A
<5th = short stature
12
Q
Head circumference for age
A
95th percentile = developmental problems
13
Q
BMI
A
Body fatness changes as children grow Girls and boys differ as they mature BMI declines and reaches a minimum around 4-6 years of age before beginning a gradual increase through adolescence and most of adulthood
14
Q
BMI is a Screener
A
BMI is not a direct measure of body fatness.
However, BMI parallels changes obtained by direct measures of body fat such as underwater weighing and dual energy x-ray absorptiometry (DXA).
BMI can be considered a proxy for measures of body fat. BMI will change with age so it must be plotted
15
Q
SGA
A
A birth weight and/or length greater than 2 SD below the mean It is below the 10th percentile in weight, length, or HC
16
Q
LGA
A
babies are those babies who are greater than 2SD above the mean Birth weight (or length, or HC) lies above the 90th percentile for that gestational age
17
Q
STATURAL growth
A
A complex process that is determined by the interaction of Genetics Nutrition Socioeconomic factors
18
Q
Abnormally Rapid Growth Velocity Midparental height
A
Determining heights of biological parents is of critical importance
Girls: Father’s height + Mother’s height - 5 in.//2
Boys: Father’s height + Mother’s height +5 // 2
Target height = midparental height = 2SD
19
Q
Physical exam for growth
A
Dysmorphic features
Midline defects
Skin
Neck
Sexual exam
20
Q
Deciphering Problematic Growth Curves
A
Is the growth rate normal or abnormal? Look at as many points as possible Is there abnormal tempo of growth? Bone age Are there underlying reasons for intrinsic/genetic short stature? History, mid parental height, PE findings Do the answers to these questions fully explain child’s position on the growth curve? Convergence of multiple growth patterns in one child
21
Q
Confounding Factors - Obesity
A
Obese children are taller With endocrinopathies, height is impaired If the child’s ht. is at or greater than mid parental height, an endocrine cause of the obesity is unlikely
22
Q
Genetic Channeling
A
Upward to downward movement toward mid parental range Usually accomplished by 12-15 months
23
Q
Constitutional growth delay - Risk Factors
A
- Family history
- The child is healthy, growing below but parallel to the 3rd percentile line
- Between 6-24 months, the linear growth and weight track downward to the 3rd percentile
- Slow growth rate between 12-30 months
- Delayed onset of puberty and a growth spurt and usually end up with heights in the lower half of the normal range.
- Bone age that is delayed by 2 or more years
24
Q
Confounding Factors in Late Childhood Growth
A
Infrequent measurement opportunities Normal prepubertal growth deceleration Effects of medications for common disorder (ADHD, asthma, depression) Normal variation in onset of puberty
25
Key information required to decipher a child's growth curve
Birth length and weight (SGA vs. prematurity)
Mid parental height
Family growth and pubertal history
Growth rate-normal for age
Bone age (Left wrist)-contributions of delayed vs genetic/intrinsic growth disturbance
Health history – effects of disease on growth
26
Bone age
Bone age is a measure of skeletal maturity.
A conventional X-ray of the left hand and wrist to evaluate bone age may be obtained at the initial visit to assess skeletal maturation, and may be repeated over time if needed
The methods used most commonly for determining bone age are the Greulich and Pyle Atlas and the Tanner- Whitehouse (TW2) method
27
Skeletal Maturation
Occurs under the influence of estrogen, thyroid hormone, androgen and growth hormones Bone are is generally more than 2 years in advance of chronologic age in long-standing precocious puberty because of the action of sex hormones
28
General screening tests in the evaluation of abnormal growth in children (7)
CBC -- anemia, blood dyscrasia, infections
BMP -- rules out renal disease and electrolyte abnormalities that could occur with Barter syndrome, other renal or metabolic disorders and diabetes insipidus
Liver functioning testing Assesses metabolic or infectious disorders associated with liver dysfunction
Urinalysis and urine pH level Assesses kidney function and rules out renal tubular acidosis
Erythrocyte sedimentation rate Evaluates for chronic inflammatory states
GH deficiency IGF-1, IGF binding protein 3 Hypothyroidism -- free thyroxine, TSH
29
Sexual Maturity Rating (SMR; Tanner staging)
Males
Size of the testes
Length of the penis
Hair development
Females Breast development Public hair development
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Body Fat
Body fat continually increases in girls during most of the second decade, while boys tend to decrease fat after age 14. In the lower ranges, BMI-for-age tends to increase more slowly in both adolescent boys and girls. At the 5th percentile, BMI-for-age increases at the rate of about 0.5 unit/year during most of the second decade.
31
Female Puberty
What is first and what percentage
The appearance of breast buds in girls are the earliest signs of pubertal development in 85%
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Puberty and Females (3)
Sexual maturity rating (tanner stage) Breast budding (Thelarche is the first sign in 85%) Public hair growth (Pubarche) is the initial pubertal sign in 15% of girls
33
Menarche occurs an average of ________ after thelarche
2 years Range is 1 to 5 years
34
Peak height velocity reached
at 12 years in girls immediately prior to menarche
35
Early in puberty
Slow their accumulation of total body fat, but during their peak height velocity they accelerate their accumulation of fat and lean body tissue, leading to an increase in weight that peaks just prior to menarche.
After that time, the rate at which weight is added slows, with an inflection point around 13 years of age.
Between the age of 12 and 13, girls at the 5th percentile gain less than 8 lbs. while those at the 95th percentile gain more than 13 lbs.
36
TANNER STAGES BREAST
Tanner 1 = none
Tanner 2 = breast bud diameter = areola width
Tanner 3 = Breast diameter \>areolar width
Tanner 4 = Mounding of areola above plane of breast
Tanner 5 = Adult
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TANNER FEMALE PUBIC HAIR
Tanner 1 = none Tanner 2 = slightly pigmented over mons or labia Tanner 3 = dark, coarse, on mons Tanner 4 = Adult in character, confined to mons Tanner 5 = Adult spread to medial thigh
38
Male Puberty
Testicular volume and prepubescent and pubescent boys
In boys, testicular size should be measured by a Prader orchidometer.
A testicular volume of \> 4 mL in boys indicates puberty is starting
Prepubescent boys testicle equals 2.5 cm in length
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Male puberty
Increase in stature due to \_\_\_\_\_\_\_
PHV?
The increase in stature in males is due to androgens produced by the testes, so the growth spurt in stature is preceded by an increase in the size of the testes.
Androgens also cause the penis to lengthen and widen
Pubertal development is slow to SMR stage III
Accelerate with a total four years between stage II and V PHV is achieved at age l4 years
40
TANNER GENITALIA MALE
Tanner 1 = Prepubertal testis \<2cm
Tanner 2 = prepubertal testis 2.5 cm, volume 4mL
Tanner 3 = Phallus has grown in length; testes \>3cm, volume 6mL, 8mL
Tanner 4 = Phallus has grown in breath; testes \> 4cm Volume 10mL/15mL
Tanner 5 = adult testes \>5cm; volume \>15mL
41
Male Tanner again
GENITAL DEVELOPMENT (MALE)
* Stage Preadolescent
* Testes, scrotum, and penis about same size and proportion as in early childhood
* Enlargement of scrotum and testes
* Skin of scrotum reddens and changes in texture; little or no enlargement of penis
* Enlargement of penis
* First mainly in length; further growth of testes and scrotum (11.5-14
* Increased size of penis with growth in breadth and development of glans
* Further enlargement of testes and scrotum and increased darkening of scrotal skin (13.5-15)
* Genitalia adult in size and shape
42
Adolescence and Alkaline Phosphatase
* With rapid bone growth, alkaline phosphatase levels increase
* Level can be 50-100% above the normal range.
* Peaks at about the peak height velocity in males and females so occurs earlier in females
43
Delayed Puberty Definition
Delayed puberty is defined clinically by the absence or incomplete development of 2nd sexual characteristics by an age at which 95 % of children of that sex and culture have initiated sexual maturation.
44
Delayed puberty ages for upper 95%
The upper 95th % in the U.S. for age is: boys 14 years of age girls 12 years of age
45
Definition of Precocious puberty GIRLS (8)
Breast development
Precocious puberty
* Any sign of puberty in girl less than 8
* Boys less than 9
* Within creases to tanner 3 within a 6-12 month period in a 6-8 year old
* Wait in a girl with 2cm or less of glandular tissue and no increase in growth
* Menarche before age 10 years
* Pubic Hair White: Before age 7 years Black: Before age 6 years
46
Adrenarche (5)
* Increased adrenal androgen secretion
* Occurs between ages 6 to 8 years
* Transient growth spurt
* Some children develop axillary and pubic
* No sexual development occurs
47
Gonadarche: GnRH released Boys vs. Girls
Boys
LH stimulates Testosterone production
FSH stimulates sperm maturation
Girls
FSH stimulates
Estrogen and follicle formation LH stimulates corpus luteum after Ovulation
48
Mean age of Menarche
African America = 12.2 year Caucasian = 12.9 year Boys = precocious puberty less than 9 years
49
Hypergonadotropic hypogonadism vs. Hypogonadotrophic hypogonadism
There are two major categories: Hypergonadotropic hypogonadism (high luteinizing hormone [LH] and follicle-stimulating hormone [FSH]) is secondary to primary gonadal failure. Hypogonadotropic hypogonadism (low or normal LH and FSH) is secondary to constitutional delay or a central gonadotropin deficiency.
50
Precocious Puberty
Any sign of secondary sexual maturation before 8 years in girls and 9 years in boys. More recent data suggests early puberty may not warrant extensive evaluation or intervention if it occurs after 6 years in African-American girls or after 7 years in Caucasian girls (Herman- Giddens, 1997).
51
Red flags for pathologic pubertal development
* Contrasexual development
* Feminization in boys—gynecomastia
* Virilization in girls – Clitoris enlargement, acne Peripheral cause (often asynchronous development)
* Penis enlarges without scrotal enlargement
* Extensive pubic Hair Growth
* Menarche without breast bud development in girls
* Precocious Puberty in boys (50% pathologic)
* Rapid growth in breast development through tanner III in an 8 year old or less
* Enlargement of the penis without enlargement of the testicle
* Documented growth acceleration in a child over 6-12 months in a girl less than 8 or a boy less than 9
* Any virilization signs such as clitoris enlargement, voice deepening or increase in muscle mass.
52
Precocious Puberty TYPES
* Incomplete precocious puberty:
* Premature thelarche
* Premature adrenarche
* GnRH and gonadotropin independent puberty
* FSH and LH suppressed
* True and complete (central precocious Puberty)
* Pseudoisosexual Puberty
53
Pseudo-precocious puberty
Some of the changes of puberty are present But appearance is isolated or out of normal sequence
54
Isosexual puberty
When the changes of puberty are consistent with child's gender
When they are discordant with gender, they are heterosexual
55
True precocious puberty
Early pubertal changes
Normal progression in order of breasts, pubic hair development, growth spurt
For females, menstruation
56
Premature thelarche
* Development of breast buds
* Most common variation
* Usually 1-4 years of age
* Usually benign if not associated with onset of other pubertal events
57
Precocious puberty should be suspected if
* Breast, nipple and areolar development reach tanner 3
* Linear growth accelerates
* Androgenization with pubic and/or axillary hair
58
Premature thelarche or precocious puberty
Premature thelarche 6mo-2yr
Breasts: Usually II, early III regresses in 80%
no pubic hair, axillary hair, apocrine odor, menses, accelerated growth, advanced bone age, considered benign
Precocious puberty 5-8 years
Breasts: II through V; does not fluctuate in size Public hair or axillary hair+breast
YES apocrine odor, menses, accelerated growth, advanced bone age, early puberty = SHORT STATURE
59
NORMAL VALUES
FSH LH Estradiol Bone age
0-2.8
0-1.6
\<25 - estradiol
Bone age -- with age
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Premature Adrenarche + Physical Assessment
* The growth of axillary hair stimulated by androgen
* Look for androgen exposure
* Family history (partial forms of adrenal hyperplasia)
* Look at breasts for female
* Testicular enlargement for male
* Axillary hair is only finding, check in 3-4 months
* Acne
* Enlargement of the clitoris
61
Clinical Eval of Precocious Puberty
Pubertal signs
Age of onset
Rate of progression
Growth pattern
62
Clinical Evaluation of Precocious Puberty: History
Past medical history
* CNS insults
* Exposure to environmental sex hormones
* Serious illnesses
* Any symptoms
Check regarding family history of sexual precocious
Sibling with ambiguous genitalia
Family may consider precocious puberty normal
63
Clinical Eval of Precocious puberty (4) clinical aspects
Plot height, wt., and head circumference (if less than 3 years) Will be rapid if CPP or pseudoisosexual precocious puberty
Height will rise to higher growth percentile than occupied previously
Blood pressure hypertension may suggest Congenital adrenal hyperplasia due to deficiency of 11 beta hydroxylase)
Sexual maturity Are there breast buds? Have they regressed from birth? Is this a new process?
Signs of systemic disease
64
Clinical Eval of PP
Look for evidence of CNS mass
Evidence of androgenic influence
Evidence of any other mass
MASS: Optic fundus; Visual fields
* Acne Facial and axillary hair
* Increased muscle bulk
* Extent of pubic hair
* Penile elongation
* Scrotal rugation increased with thinning
* Clitoris enlargement
Asymmetric testicular enlargement
Hepatomegaly Abdominal mass
65
5 Clinical evals for PP
Cafe au lait spots
Myxedematous face
Thyroid enlargement
Abnormal visual field
Abnormal neuro findings
(hyperreflexia = brain tumor = UMN disease; hyporeflexia = LMN disease
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Evidence of estrogenic influence Evidence of gonadotropic stimulation Pseudoisosexual precocious puberty
Evidence of estrogenic influence
* Size of breast tissue
* Must distinguish breast from soft smooth consistency of increased fat
* Reddish, less moist vaginal mucosa in prepubertal girl
* Pale moist appearance of pubertal vaginal mucosa, elongated clitoris
* Labia minor more visible as puberty progress
Evidence of gonadotropic stimulation
* Measure phallic and testicular dimension: testicles must be =
* Without testicular enlargement, penis enlargement, adrenal pathology
* Testicular volume is greater than phallic size in normal puberty, CPP, and Primary hypothyroidism
Pseudoisosexual precocious puberty
Penile dimension are disproportionately greater than testicular size
67
LAB TESTING FOR PP
Further evaluation should be directed at the possibility of:
* Nutritional disorders
* Occult chronic illness
* Hormonal abnormalities
Initial screening should include:
* Complete blood count
* Erythrocyte sedimentation rate
* Liver function tests
68
LAB TESTING FOR PP If hypothyroidism is suspected...
Thyroid hormone should be assessed TSH, free T4 is vital If growth abnormality is found, do a bone age OF LEFT WRIST
69
The Hormonal eval for PP should include the following tests
Random serum LH and FSH Estradiol (females)/testosterone (males) should be obtained to distinguish between primary and secondary hypogonadism
70
Precocious puberty: Stature
Sexual precocity is more common in girls than boys.
In both cases, linear growth is accelerated during childhood, often with markedly advanced bone maturation.
Because of very early epiphyseal closure, the paradoxically tall child will be short as an adult
71
SUMMARY -- Females
No Menarche 5 years after breast development
No Menses by age 16 years ( Primary Amenorrhea)
Over 50% of delayed puberty is due to constitutional delay (late bloomers)
72
Summary of Puberty findings
Historical clues
Physical findings
Selected lab values
Treatment Males = testosterone Females = estrogen
73
Three Major Patterns in Infants and Children
Normal head circumference, normal height and decreased weight initially and eventually decelerating ht and head as well. (Type 1)
Normal head circumference, disproportionate height and almost normal weight (type 2)
Small head circumference and decreased weight and height (type 3)
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Type 1
Retardation of weight with near normal or slowly decelerating height and HC Suggests under nutrition
75
Type 2
Near proportional retardation of weight and height with normal HC
* Constitutional growth delay
* Genetic short stature
* Endocrinopathies
* Structural dwarfs
76
Type 3
Concomitant retardation of weight height and HC
SGA: in utero and perinatal insult
Chromosomal aberrations
CNS abnormalities
Rarely familial
77
Normal Upper segment to lower segment ratio
Upper segment head to symphysis pubis to lower segment (type 2)
US to LS in infants is 1.7 to 1.8 to 1
As child approaches adolescent .9 to l.0:1
Upper: lower segment ratio is low in Marfan syndrome
Abnormal in bony dysplasia
After spinal irradiation
78
Growth curve
Deceleration of linear growth in a well-nourished child
* Growth hormone deficiency
* Hypothyroidism
* Glucocorticoid excess (causes Cushing's syndrome)
Initial decline in weight followed by decreased height velocity Malnutrition or systemic illness.
Dysmorphic features Chromosomal abnormality (Trisomy 21 or Turner s syndrome) or other specific syndrome
Disproportionate features or skeletal abnormalities Consistent with skeletal dysplasia or metabolic bone disease.
79
Eval of Attenuated Growth
Careful physical exam Free T4, TSH ESR Electrolytes, BUN creatinine, UA, LFT
Bone age of left hand and wrist
Markedly delayed bone age suggestive of endrocrinopathy Refer to endocrine
80
Accelerated Growth Differential Dx
* Upward crossing of percentiles of concern
* Over-nutrition most common cause – weight affected and more severely than height
* Differential diagnosis
* Precocious puberty (adrenal or gonadal)
* Hyperthyroidism
* Genetic (familial) or syndrome (Klinefelter or Marfan's)
* GH excess
* Development of pubic hair
81
Short Stature (5)
Normal Patterns of Growth
* Familial or genetic short stature
* Constitutional Growth delay
Primary growth disturbance
* Intrauterine growth retardation
Systemic illness
Genetic disorders
* Chromosomal defects: Turner syndrome, Down syndrome Syndromes: Noonan, Prader Willi, Russell Silver Syndrome
Disproportionate short stature
* Skeletal Dysplasia
* Spinal irradiation
Most commonly familial or due to constitutional growth delay or comb
May rarely be associated with serious underlying medical condition
82
WHEN TO WORRY ABOUT GROWTH
Abnormally slow growth rate
Downward crossing of percentile channels on the growth chart after age 18 mo.
Height below the 3rd percentile
Height significantly below genetic potential by 2 SD
83
SHORT stature EVAL (6)
Do a careful prenatal history with birthweight
* IUGR is birth weight less than 10th percentile for gestational age
Look at growth points
Look at growth velocity
Determine parental height, do mid-parental height
For constitutional growth delay, do bone age
* Slow growth during the first two to three years with normal or low normal annual growth after
* History is similar in family member
Look at weight to ht ratio : If decreased systemic illness
84
TURNER SYNDROME (8)
Multiple nevi
Low posterior hairline
webbed neck
Broad chest with wide spaced nipples
Short 4th metacarpals
Coarctation of the aorta with bicuspid aortic valve
Increased carrying angle of arms or CUBITUS VALGUS
50% have sleep apnea
85
Causes of short stature
Normal pattern of growth
Familial or genetic short stature
Constitutional growth delay
Primary growth disturbance
Intrauterine growth retardation
Genetic disorders
Disproportionate short stature
86
Systemic Illness associated with short stature
Systemic illness
* Hypocaloric Malnutrition
* GI
* Poorly controlled DM
Metabolic Renal Hepatic Cardiac Hematologic Respiratory (CF, severe asthma) Chronicinfection
Endocrine disorders
* Hypothyroidism
* Cushing's syndrome: Glucocorticoid excess (endogenous or exogenous)
Growth hormone deficiency
* Isolated, multiple
87
Abnormally rapid growth velocity
In general, a child whose height differs by more than 2 standard deviations (SD) from the population mean is considered too tall.
Although tall stature is as common as is short stature, few children or their families seek medical attention, presumably because tall stature is socially acceptable and often advantageous.
88
THE MAINSTAYS OF ASSESSMENT OF TALL OR RAPIDLY GROWING CHILDREN INCLUDE:
The child's pattern of growth
Medical History
Physical Exam
89
Stature overgrowth -- dysmorphic features found need to...
When dysmorphic features are found, special effort should be made to rule out syndromes that are associated with excessive growth.
Stature in overgrowth = infancy and adolescence
90
Overgrowth in infancy
Maternal DM
Cerebral Gigantism
Beckwith-Wiedemann Syndrome
91
Maternal Diabetes Mellitus
Maternal DM is the most common cause for LGA in infants
These infants usually are large, more so in weight than in length
92
Cerebral Gigantism (Soto's Syndrome) Assessment (7)
* Infants with cerebral gigantism tend to be large at birth and continue to grow rapidly during the early years of childhood.
* High forehead
* Frontal bossing
* Hypertelorism
* Prominent jaw
* High arched palate
* Mental retardation poor concentration
* Adult height is normal in many of these infants
93
Beckwith-Wiedemann Syndrome
Macrosomia
Visceromegaly
Macroglossia
Omphalocele
Prominent occiput Hypoglycemia with hyperinsulinism
The cause of this syndrome is unknown, but increased production of IGF-2 may explain the overgrowth.
94
Overgrowth in Childhood and adulthood Non-Endocrine Disorders
Non-Endocrine Disorders
Familial (Constitutional) Tall Stature
Exogenous Obesity
Precocious Puberty
Marfan Syndrome
Homocystinuria
Neurofibromatosis Type 1
95
Overgrowth in Childhood and adulthood Endocrine Disorders
Growth hormone excess
96
Non-endocrine disorders familial (Constitutional) Tall stature
Familial tall stature is a variant of the normal pattern of childhood growth.
Height is 2 SDs above the corresponding mean height for age and gender.
Genetic factors play the most important roles in the pathogenesis of familial tall stature.
Growth hormone secretion and serum IGF-1 and IGF binding protein-3 concentrations often are in the upper range of normal.
97
Exogenous obesity
OBESITY MAY BE ACCOMPANIED BY MODEST LINEAR OVERGROWTH AND EARLY ONSET OF PUBERTY
These children usually have diminished overall growth hormone production but high normal serum concentrations of growth hormone- binding proteins and IGF-1
Due to Leptin increase, may have upper limit TSH Bone age may be advanced and puberty starts early, causing premature epiphyseal fusion
98
Gigantism
Excessive linear growth that occurs with growth hormone (GH) excess when epiphyseal growth plates are open during childhood
99
Acromegaly
Disorder of GH excess in adulthood
100
Tall Stature Summary
Growth velocity is the best way to assess a child whose height \> 2 SD.
Dysmorphic features and developmental delay may suggest a non-endocrine cause of tall stature.
Although rare, growth hormone excess should be considered if the growth velocity is accelerated + a family history of MEN 1.
Transsphenoidal removal of the pituitary adenoma, when present, offers definitive treatment of growth hormone excess.
101
