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
