PE2.1-3 | Growth Problems — Practice Quiz

The vast majority (70–80%) of FTT cases are non-organic, predominantly due to inadequate caloric intake related to poverty, poor feeding practices, or psychosocial deprivation. The dietary history here is clearly inadequate.

Non-organic FTT from inadequate caloric intake is the most common cause in developing countries; always take a detailed dietary history and assess the psychosocial environment before ordering investigations.

Organic causes (malabsorption, metabolic, endocrine) account for only 20–30% of FTT and usually present with additional systemic features. With normal developmental history and isolated weight faltering, non-organic causes dominate.

SAM is defined as WHZ <−3 SD OR MUAC <11.5 cm (in children 6–59 months) OR bilateral pedal oedema. This child has all three — the oedema pattern (bilateral pedal) indicates kwashiorkor. ALL SAM children with oedema require inpatient management using the WHO 10-step protocol regardless of other illness.

SAM criteria: WHZ <−3 SD, MUAC <11.5 cm (6–59 months), or bilateral pedal oedema — any ONE criterion is sufficient; bilateral oedema = kwashiorkor = inpatient protocol.

Moderate acute malnutrition uses different cut-offs (WHZ −2 to −3 SD; MUAC 11.5–12.5 cm) and bilateral oedema is itself a criterion for SAM. Ambulatory management is not appropriate when oedema is present.

Weight-for-height (WHZ) and MUAC both reflect current nutritional status independently of height, making them the preferred indicators for acute wasting. Height-for-age reflects chronic stunting; weight-for-age is confounded by both.

WHZ (weight-for-height Z-score) and MUAC detect acute wasting and screen for SAM; HAZ detects chronic stunting; WAZ is non-specific. Use WHZ/MUAC to classify severity of acute malnutrition.

WAZ (weight-for-age) is a composite that does not distinguish wasting from stunting. HAZ reflects linear growth faltering (chronic malnutrition or stunting), not acute wasting.

Counselling for FTT involves empathetic acknowledgement of parental distress, education on responsive feeding (the child decides when to stop, parent decides what/when/where), regular structured meal and snack times, and age-appropriate food variety. Forced feeding aggravates food aversion and is counterproductive.

Counselling for FTT addresses the feeding relationship (responsive feeding, avoid force-feeding), meal structure, dietary variety, and psychosocial stressors — not just caloric prescriptions.

Forced feeding and coercive strategies worsen food aversion and the parent-child feeding relationship. Blanket formula exclusivity or exclusive breastfeeding at 18 months ignores complementary feeding needs.

Constitutional delay of growth and puberty (CDGP) features delayed bone age (≥2 years behind chronological age), normal height velocity for bone age, normal adult height potential (mid-parental height prediction), and family history of late puberty — though the parents may not explicitly report this. The key diagnostic clue is bone age significantly behind chronological age with predicted normal adult height.

In constitutional delay: bone age is delayed ≥2 years behind chronological age, height velocity is appropriate for bone age, and final adult height is normal — distinguish from familial short stature (normal bone age, normal velocity, short final height) and GH deficiency (very low velocity for bone age).

Familial short stature has a normal bone age (matching chronological age) with both parents short and a final height at the lower end of the target range. GH deficiency shows very low height velocity (<4 cm/year) AND delayed bone age but the IGF-1 would be low. Turner syndrome affects females only.

Short stature is defined as height below −2 SD (approximately the 3rd percentile) for age and sex on standardised growth charts (WHO or IAP). Children between −2 and −3 SD warrant monitoring; below −3 SD is severe short stature requiring investigation.

Short stature: height <−2 SD (3rd percentile) for age/sex; severe short stature: <−3 SD. Use WHO or IAP growth charts; plot height serially to assess velocity alongside single-point measurement.

The 10th and 5th percentiles are not the standard cut-offs for short stature. The internationally accepted threshold is −2 SD (3rd percentile); −3 SD indicates severe short stature.

Turner syndrome (45,XO) classically presents with webbed neck (pterygium colli), shield chest with wide-spaced nipples, cubitus valgus, low posterior hairline, lymphoedema, and primary amenorrhoea/absent puberty due to streak gonads. Short stature is universal in Turner syndrome.

Turner syndrome (45,XO): webbed neck, shield chest, wide-spaced nipples, primary amenorrhoea, streak gonads — all girls with unexplained short stature should be considered for karyotyping.

The features in options A, C, and D point to other chromosomal or endocrine conditions: A describes Klinefelter syndrome (47,XXY — affects males); C describes hypothyroidism or mucopolysaccharidosis; D describes Down syndrome (trisomy 21).

Isolated growth hormone deficiency (GH stimulation peak <10 ng/mL on two provocative tests, low IGF-1, low height velocity, and delayed bone age) is treated with daily subcutaneous recombinant human growth hormone (rhGH). This is the standard-of-care first-line treatment.

GH deficiency diagnosis requires low IGF-1 PLUS GH stimulation test peak <10 ng/mL on two tests; treatment is daily subcutaneous rhGH — start early for best final height outcomes.

Anabolic steroids cause rapid bone age advancement and premature epiphyseal fusion, reducing final adult height — they are contraindicated as primary GH deficiency treatment. Observation is inappropriate when GH deficiency is biochemically confirmed. Thyroid hormone is indicated only if hypothyroidism is co-existing.

Effective FTT counselling uses motivational interviewing principles: explore parental beliefs, acknowledge frustration, avoid blame, collaboratively set achievable dietary goals, and schedule close follow-up. Parental engagement and trust are essential for sustainable behavioural change.

FTT counselling requires empathy, exploration of feeding beliefs, avoidance of blame, collaborative dietary goals, and close follow-up — not just a nutritional prescription.

Blaming parents damages the therapeutic relationship and reduces adherence. Providing only a rigid caloric checklist ignores the relational and psychosocial context. FTT does not resolve spontaneously without addressing the underlying cause.

Proportionate short stature (height, weight, and head circumference all equally reduced) in a child born SGA, with average-height parents, and no dysmorphic features, is most consistent with SGA-related short stature. The first priority is careful clinical history, syndromic assessment, and serial growth charting (to assess velocity) — NOT immediate advanced hormonal testing, which has low yield without clinical red flags.

Short stature workup is stepwise: history → examination (proportionate/disproportionate, dysmorphic) → bone age → targeted investigations (TFT/IGF-1/karyotype) guided by clinical clues — not blanket hormonal screening.

GH stimulation tests, karyotype, and TFT/IGF-1 are indicated when there are specific clinical clues (low velocity, dysmorphic features, pubertal issues) or the initial clinical assessment is inconclusive — not as the first step in every short-stature workup.