Chapter 34 Growth Problems
ETIOLOGY
What Growth Problems Am I Likely to Encounter?
Growth problems can be discussed in four broad categories: stature, weight, neural, and maturation. Growth in each category generally reflects the family pattern and usually falls within the population-based ranges that are described in growth charts and tables of maturation. Growth outside of expected ranges may result from a primary, usually irreversible, process that has a genetic or congenital basis or from a secondary acquired disease or condition in which poor growth is often reversible. Parents and children express concerns about short stature (but not usually tall stature), excessive or inadequate weight gain, head size that is too large or too small, or pubertal maturation that is earlier or later than expected. Very rarely, a newborn will have ambiguous genitalia, an emergency that demands immediate referral.
What Causes Growth Problems?
Heredity, genetic syndromes, nutritional deficiencies or excesses, and endocrine disorders are among the more common causes of growth problems. Table 34-1 lists some of the conditions, diseases, and disorders that you might encounter in patients with abnormal growth patterns. Obesity is the most common growth problem in children and adolescents. It results most commonly from chronic calorie excess caused by an imbalance between intake and expenditure. A persistent daily excess of 100 calories will result in weight gain of > 10 lb per year above the expected age-appropriate gain.
Table 34-1 Causes of Growth Problems
Category | Problem | Cause |
---|---|---|
Stature | Short stature | Heredity* (including constitutional delay) |
Down and Turner syndromes Renal insufficiency and renal tubular acidosis | ||
Inflammatory bowel disease and celiac disease | ||
Hypothyroidism | ||
Cushing syndrome | ||
Growth hormone deficiency | ||
Tall stature | Heredity* | |
Exogenous obesity | ||
Marfan and Klinefelter syndromes | ||
Homocystinuria | ||
Weight | Obesity | Excessive calories* |
Hypothyroidism, hyperinsulinism, glucocorticoid excess (Cushing syndrome) | ||
Prader-Willi syndrome | ||
Poor weight gain | Inadequate calories* | |
Failure to thrive (“nonorganic”) | ||
Congestive heart failure | ||
Cystic fibrosis | ||
Hyperthyroidism | ||
Neural | Microcephaly | Heredity* |
In utero infections | ||
Syndromes (e.g., Down syndrome) | ||
Macrocephaly | Heredity* | |
Hydrocephalus | ||
Neurocutaneous diseases | ||
Maturation | Early puberty | Girls: Heredity,* excessive estrogen (exogenous or endogenous) |
Boys: Heredity,* excessive testosterone | ||
Delayed puberty | Girls: Heredity,* Turner syndrome, thyroid disease, calorie deficiency (eating disorder) | |
Boys: Heredity* (including constitutional delay) | ||
Ambiguous genitalia | Fetal developmental abnormalities | |
Congenital adrenal hyperplasia | ||
Partial androgen insensitivity syndrome |
EVALUATION
How Do I Determine the Cause of Stature Problems?
The growth chart helps identify concerning growth patterns if growth measurements have been plotted regularly and accurately. Statural growth typically “follows the curve” parallel to percentile lines and does not cross more than one line upward or downward. A truly “flat” curve crosses the percentile lines and is often a clue that a child has an underlying cause for poor statural growth. It is important to ask parents about their growth patterns during childhood (they may need to ask their own parents). If you include information about the stature of both parents in the medical record, you can calculate the predicted adult height using mid-parental stature (see Chapter 8).
How Should I Evaluate the Short Child?
Consider an evaluation if growth is flat, crosses percentile lines downward, or does not appear adequate to result in a final adult height close to that predicted from mid-parental stature. Review the family growth patterns for early or late development. Ask about signs and symptoms that suggest underlying gastrointestinal (GI) disease or hypothyroidism. Look carefully for physical findings of Turner syndrome in short girls (short, webbed neck; low-set, rotated ears; wide chest; nevi; nail dysplasia) and for the findings of Cushing syndrome or hypothyroidism. The child with Down syndrome or achondroplasia will be short, as may the child with cyanotic heart disease and chronic kidney disease. Laboratory testing should include screening for anemia, renal function, renal tubular acidosis, hypothyroidism, malabsorption, celiac disease, and growth hormone deficiency. Patients with inflammatory bowel disease usually have a positive stool test for blood.
When Should I Worry about Tall Stature?
Most tall stature is hereditary and is viewed positively in Western societies. Although few families express concern when a child is taller than peers, you should monitor growth to be certain that tall stature is consistent with the family growth patterns and does not reflect a pathologic process. Tall stature is associated with exogenous obesity, which should prompt a nutritional and behavioral history. A careful physical examination should discover findings consistent with Klinefelter or Marfan syndrome, homocystinuria, or pituitary gigantism. Look carefully for signs of early pubertal development in children with tall stature.
How Should I Evaluate the Obese Child?
Most obesity is exogenous and results from chronic excessive calorie intake and inadequate calorie expenditure. The most effective approach to evaluation and management of obesity involves the patient and family as active, willing participants. First ask for permission to discuss the topic, then encourage self-directed approaches to identify behaviors that contribute to the problem. A detailed history of the nutritional and exercise habits of the child and family is critical. It is important to establish whether obesity “runs in the family” and whether family members have the metabolic syndrome, type 2 diabetes mellitus, or early cardiovascular disease. The child with exogenous obesity almost always has tall stature. A waist circumference-to-height ratio (WC:Ht) of > 0.5 is associated with long-term adverse metabolic outcomes of obesity for children as well as for adults. Acanthosis nigricans may reflect insulin resistance and signal development of type 2 diabetes. Older children and adolescents with exogenous obesity should be evaluated for the metabolic syndrome (Table 34-2) and monitored closely for development of hypertension and type 2 diabetes. Cholesterol and lipid levels should be monitored.
Table 34-2 Criteria for the Metabolic Syndrome in Adolescence
Triglycerides (mg/dl) | ≥ 110 |
HDL-cholesterol (mg/dl) | |
Male | ≤ 40 |
Female | ≤ 40 |
Abdominal obesity (waist circumference) | |
Male | ≥ 90th percentile or WC:Ht > 0.5 |
Female | ≥ 90th percentile or WC:Ht > 0.5 |
Fasting glucose (mg/dl) | ≥ 110 |
Blood pressure | ≥ 90th percentile |
HDL, High-density lipoprotein; WC:Ht, waist circumference-to-height ratio.
Adapted from Cook S et al: Prevalence of a metabolic syndrome phenotype in adolescents, Arch Pediatr Adol Med 157:821, 2003.

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