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Abnormality of stature refers to deviation of a child’s height from the normal range for age and sex. It includes short stature (height below the 3rd percentile or < –2 SD) and tall stature (height above the 97th percentile or > +2 SD).

Short stature is defined as height less than the 3rd percentile or more than 2 standard deviations below the mean for age and sex, or when growth velocity is significantly reduced.

The most common cause of short stature worldwide is malnutrition, which leads to impaired linear growth due to inadequate caloric and protein intake.

Normal variants include familial short stature (genetic short parents, normal bone age) and constitutional delay of growth and puberty (delayed bone age, late puberty but normal final height).

Familial short stature has normal bone age equal to chronological age, while constitutional delay shows delayed bone age and delayed puberty with eventual catch-up growth.

Endocrine causes include growth hormone deficiency, hypothyroidism, Cushing syndrome, and poorly controlled diabetes mellitus.

Features include poor growth velocity, delayed bone age, increased truncal fat, immature facial appearance, and sometimes hypoglycemia in infancy.

Thyroid hormone is essential for growth plate maturation. Deficiency leads to reduced growth velocity, delayed skeletal maturation, and short stature.

Chronic diseases like renal failure, congenital heart disease, tuberculosis, and inflammatory bowel disease impair growth, typically with weight loss occurring before height impairment.

Turner syndrome, Down syndrome, Noonan syndrome, and skeletal dysplasias such as achondroplasia are important genetic causes.

Turner syndrome should be suspected when short stature is associated with webbed neck, shield chest, widely spaced nipples, delayed puberty, or primary amenorrhea.

Bone age is assessed by X-ray of the left hand and wrist. It helps differentiate normal variants (familial short stature) from endocrine disorders or constitutional delay.

Delayed bone age suggests constitutional delay of growth and puberty, growth hormone deficiency, hypothyroidism, or chronic systemic illness.

Advanced bone age is typically seen in precocious puberty, hyperthyroidism, congenital adrenal hyperplasia, or androgen excess states.

Baseline workup includes CBC, ESR/CRP, renal and liver function tests, thyroid function tests, celiac serology, and bone age assessment.

Tall stature is defined as height above the 97th percentile or more than +2 standard deviations above the mean for age and sex.

Causes include familial tall stature, growth hormone excess (gigantism), hyperthyroidism, precocious puberty, and genetic syndromes such as Marfan syndrome and Klinefelter syndrome.

Gigantism presents with excessive growth velocity, coarse facial features, enlarged hands and feet, elevated IGF-1, and often pituitary adenoma symptoms such as headache or visual defects.

Red flags include rapid crossing of growth percentiles, very low growth velocity, dysmorphic features, delayed or absent puberty, neurological symptoms, and suspicion of systemic disease.

Growth hormone therapy is indicated in GH deficiency, Turner syndrome, chronic renal failure, Prader-Willi syndrome, children born small for gestational age without catch-up growth, and selected idiopathic short stature cases.

Adverse effects include intracranial hypertension, slipped capital femoral epiphysis, worsening scoliosis, hyperglycemia, and edema, requiring careful monitoring.

Management depends on identifying the underlying cause, addressing nutrition and chronic illness, treating endocrine disorders, considering growth hormone therapy when appropriate, and monitoring growth velocity and pubertal development.