Child with failure to gain weight or height Flashcards
Mild FTT
Fall across 3 centiles
Severe FTT
Fall across 3 centile lines
Organic causes of FTT
only 5% have underlying cause
Impaired suck/swallow - oro-motor dysfunction, neurological disorder e.g CP. cleft palate
Chronic illness leading to anorexia - Crohns disease, chronic renal failure, CF, liver disease
Non-organic causes of FTT
Psychosocial and environmental deprivation - abuse or neglect, parental mental health conditions (e.g maternal depression or ED), lack of education about needs of infant
Inadequate availability of food - feeding problems - insufficient breast milk, insufficient or unsuitable food offered, lack of regular feeding times
Other causes of FTT (not-organic or organic)
Inadequate retention - vomiting, severe GOR
Malabsorption - coeliac disease, CF, CMPA
Failure to utilise nutrients - syndromes, chromosomal disorders, prematurity, congenital infection, metabolic disorders
Increased requirements - thyrotoxicosis, CF, malignancy, chronic infection
Questions to ask in FTT history
Food diary over several days
Feeding, including details of what happens at meal times
Child well or does have other symptoms such as D+V, cough, lethargy
Child premature or have IUGR?
Any significant medical problems?
Growth or other family members and any illnesses in family?
Childs development normal?
Any psychosocial problems at home?
Signs of FTT on examination
dysmorphic features
signs suggestive of malabsorption: distended abdomen, thin buttocks, misery
Signs of chronic resp disease: chest deformity, clubbing, signs of HF, evidence of nutritional deficiencies
Investigations for FTT
FBC - anaemia, neutropenia, lymphopenia
U&Es - renal failure, renal tubular acidosis, metabolic disorders
LFTs - liver disease, malabsorption, metabolic disorders
TFTs - hypothyroidism or hyperthyroidism
Acute phase reactant - CRP
Igs - immune deficiency
Urine MCS - UTI
Stool MCS and elastase - intestinal infection, parasite
Mx of FTT
MDT and primary care
Health visitor - assess eating behaviour and provide support
Paediatric dietician
SALT
Input from clinical psychologist and social services may be helpful
Nursey placemement may alleviate stress at home and help with feeding
Hospital admission is usually only necessary in children under 6m with severe FTT who require active refeeding, may support mother in feeding
In extreme cases - hospital admission can be used to demonstrate child will gain weight when fed properly
Marasmus
Severe protein-energy malnutrition in children usually leads to marasmus
Weight for height more than -3SD below the median (<70% weight for height)
Wasted, wizened appearance
No oedema
Skinfold thickness and mid-arm circumference are markedly reduced
Affected children are often withdrawn and apathetic
Kwashiorkor
Another manifestation of severe protein malnutrition, generalised oedema and severe wasting, due to oedema weight may not be as severely reduced as in marasmus
Kwashiorkor
Oedema
“flaky-paint” rash with hyperkeratosis (thickened skin) and desquamination
Distended abdomen and enlarged liver
Angular stomatitis
Hair which is sparse and depigmentation
Diarrhoea
Hypothermia
Bradycardia
Hypotension
Low plasma albumin, potassium, glucose and Mg
Causes of kwashiorkor
Reared in traditional, polygamous societies where infants are not weaned from breast until 12m
Subsequent diet tends to be relatively high in starch
Often develops after acute intercurrent infection (measles or gastroenteritis)
Mx of Kwashiorkor
Acute:
Hypoglycaemia - correct urgently, particularly if coma or severely ill
Hypothermia - wrap child
Dehydration - correct but avoid being over-zelous with IV fluids can lead to HF
Electrolytes - correct deficiencies, esp. K+
Infection - give abx
Micronutrients - give vit A
Initiate feeding - small volumes and frequently, including at night - start low protein diet formula 75 then formula 100
Mechanism of vit D
Reduced intake
Defective metabolism of vit D
Causing a low serum calcium
Triggers release of PTH
Increased PTH normalises serum calcium but simultaneously demineralises all bone
PTH causes renal losses of phosphate and consequently low serum phosphate levels - further reduces potential for bone calcification
Presentation of vitamin D deficiency
Bone deformity
Rickets
Hypocalcaemia (seizures, neuromuscular irritability - tetany, apnoea and stridor) - high demand for calcium in rapidly growing bone results in hypocalcaemia before Rickets develops
What is rickets? RF, S+S
Failure in mineralisation of growing bone or osteoid tissue
Failure of mature bone to mineralise = osteomalacia
Rx: CF, Coeliac disease, pancreatic insufficiencies
S+S: earliest sign = ping-pong ball sensation of skull elicited by pressing firmly over occipital or posterior parietal bones
Costochondral junctions may be palpable (rachitic rosary)
Wrists (crawling infants) and ankles (walking infants) may be widened
Horizontal depression over lower chest attached to softened ribs and with diaphragm (Harrison sulcus)
Legs may be bowed
Causes of Rickets
Nutritional (primary) rickets:
northern altitudes
dark skin
decreased exposure to sunlight
maternal vi D deficiency
diets low in calcium, phosphorus and vit D
prolonged parenteral nutrition in infancy with inadequate calcium and phosphate
Intestinal malabsorption:
small bowel enteropathy (coeliac disease)
pancreatic insufficiency (e.g CF)
cholestatic liver disease
high phytic acids
Defective production of 25(OH)D2 - chronic liver disease
Increased metabolism of 25(OH)D3 - enzyme induction by anticonvulsants (e.g phenobarbitol)
Defective production of 1,25 (OH) D3 - Fanconi syndrome
Mx of Rickets disease
Nutritional rickets is managed by diet advice, correction of predisposing RF and daily cholecalciferol
If compliance is an issue, single high dose of oral vit D3, then daily maintenance dose
Healing occurs in 2-4w and can be monitored from lower ALP, increase vit D levels and healing on XR
Complete reversal my take years
Vitamin A deficiency
developed countries, vitamin A (retinol) seem as a complication of fat malabsorption when supplementation has been inadequate
S+S are rare, except for impaired adaptation to dark light
Commonest cause of blindness in developing countries
Causes eye damage (xenophthalmia) may progress from night blindness to corneal ulceration and scarring
Also result in increased susceptibility to infection, especially measles
Prevention in developing countries with high prevalence - give a dose of vit A
Supplementation with vit A is recommended for children with measles
Causes of short stature
Familial
IUGR and extreme prematurity
Constitutional delay of growth and puberty
Endocrine: hypothyroidism, GH deficiency, IGF-1 deficiency and steroid excess
Nutritional/chronic illness: inadequate nutrition, coeliac disease, crohn’s disease, CKD
Psychosocial deprivation
Chromosomal disorders and syndromes: Down’s syndrome, Turner, Noonan and Russel-silver syndrome
Disproportionate short stature: achondroplasia and short-limbed dysplasias
History to take for short stature
Birth length, weight, head circumference and GA
Pregnancy history: infection, IUGR, drug use, alcohol/smx
Feeding history
Developmental milestones
FHx of constitutional delay of growth and puberty or other diseases?
Features of chronic illness/endocrine
Meds - corticosteroids?
Investigations
Plot current and previous heights on growth charts
XR of hand and wrist for bone age - delayed in endocrine disorders
FBC - anaemia in coeliac or Crohn’s
Creatinine and electrolytes - chronic renal failure
Calcium, phopshate, ALP - renal and bone disorders
TSH - raised in primary hypothyroidism
Karyotype - turner syndrome shows as 45XO
IgA antibodies/anti-TTG - coeliac
CRP - Crohns
Growth hormone provocation tests (insulin, glucagon) - GH deficiency
Cortisol and dexamethasone suppression test - Cushings syndrome
Growth hormone deficiency treatment
GH deficiency is treated with biosynthetic GH is given subut daily
Recombinant IGF-1 has been used to treat children with GH resistance and IGF-1 deficiency who wouldn’t have previously responded to GH treatment
