Deficiency anaemias
Commonest nutritional deficiency.
Occurs in 10–30% of those at high risk:
· Preterm, LBW infants, multiple
births;
· After exclusive breastfeeding
>6mths, delayed introduction of iron-containing solids, excessive cow’s milk
(protein enteropathy);
· Adolescent females (growth spurt
and menstruation);
· Low iron-containing diet due to
poverty, fad diets, or strict vegans.
· Dietary:
commonest cause, e.g. prolonged
and exclusive consumption of cow’s or
breast milk with late introduction of iron containing solids.
· Infancy
and early childhood: low
level of dietary iron, e.g. high milk intake
(low iron), GI blood loss, e.g. cow’s milk protein enteropathy.
· i Demand due to rapid growth: e.g. following prematurity or puberty.
· Malabsorption:
e.g. coeliac disease, IBD.
· Rarely
blood loss: e.g.
Meckel’s diverticulum, oesophagitis. Bleeding may be occult into cysts, tumours or s to drugs, e.g. NSAIDs.
· Intestinal
parasites: e.g.
hookworm (in less developed world).
· Most cases are subclinical. Onset
of symptoms of anaemia is usually insidious. Profoundly iron deficient toddlers
usually adapt to their anaemia and tolerate surprisingly low Hbs.
· Pallor, lethargy, poor feeding,
breathlessness (only in severe anaemia).
· May also develop symptoms
associated with iron deficiency, including neurological effects of listlessness
and irritability (infants), mood changes, reduced cognitive and psychomotor
performance (can occur at levels of mild/moderate deficiency before anaemia
develops), and rarely, pica (eating unusual items, e.g. soil, chewing on
pencils).
Iron deficiency anaemia is a sign
not a diagnosis—always look for underlying
cause (usually dietary or GI disease).
· FBC:
Hb d, MCV & MCH & MCHC
‘fall’ (below normal range for age), platelets
often raised.
· Blood
film: microcytic,
hypochromic anaemia.
· Serum
ferritin ‘fall’ (indicative of iron stores): it may be low before anaemia. Check C-reactive protein, as ferritin may be falsely raised due to
acute phase reaction (d serum iron and ‘rise’total iron binding capacity (TIBC)
confirms iron deficiency).
Give 5mg/kg elemental iron/day (as
oral ferrous salt) given in 2–3
divided doses (max dose of 200mg/day). Response in reticulocyte count is
usually within 5–10 days. Continue for 3mths after Hb normalizes to replenish
body stores. If indices don’t improve once Hb normalized, screen for
thalassaemia trait.
Iron supplementation in preterm
infants.
·Encourage iron-containing diet,
e.g. iron fortified formulas and breakfast cereals, meat, green vegetables,
beans, egg yolk, foods rich in vitamin C (i iron absorption).
·Avoid prolonged cow’s milk
consumption to detriment of solids intake.
Vitamin
B12 (cobalamin) usually
sourced from animal products. Vegan
or other diets lacking meat most at risk. Alternatively, can have defective
absorption due to intrinsic factor deficiency (congenital autosomal recessive
(AR) or juvenile autoimmune pernicious anaemia), defective B12
transport (transcobalamin II deficiency), intestinal disease causing
malabsorption (ileal resection, IBD, coeliac disease), or bacterial over-growth
in small bowel.
A common nutritional deficiency
worldwide. Causes include:
·Malnutrition (marasmus,
kwashiorkor), goat’s milk feeding.
·Malabsorption, e.g. coeliac
disease, IBD, other small intestinal disease;
·Increased requirements, e.g. rapid
growth, chronic haemolytic anaemias (give daily folic acid prophylactically),
hypermetabolic states (infection, hyperthyroidism), severe skin disease.
·Drugs, e.g. phenytoin, valproate,
trimethoprim, nitrofurantoin.
·Disorders
of folate metabolism: Lesch–Nyhan
syndrome; orotic aciduria.
·Insidious onset of pallor,
fatigue, anorexia, glossitis, developmental delay, and hypotonia.
·In severe cases, subacute combined
degeneration of cord (rare in children): paraesthesia of hands/feet, ataxic
gait, loss of vibration sense.
·Macrocytic
anaemia: Hb d, MCV ‘rise’(above the normal range for age, i.e. >82 aged 1yr, >90 aged 6–12yrs or >125fL as a newborn).
·WBC d, hypersegmented neutrophils,
platelets d, bilirubin i.
·d Serum B12 or ‘fall’ folate
level (red cell folate level is more reliable than serum folate, which reflects
recent intake).
·Bone marrow, if indicated, shows
megaloblastic appearance.
·Rarely, intrinsic factor
autoantibodies or test of B12 absorption, e.g. Schilling test.
Improve diet. Depending on whether
vitamin B12 or folic acid is deficient:
·B12
deficiency: IM
hydroxocobalamin (1mg)—usually response is within 1wk. Watch K+ level as it may drop. Treat 3 times/wk until
Hb normal; then give 2–3-monthly if the underlying problem persists (important
to identify cause).
·Folate
deficiency: daily
oral folic acid (500micrograms/kg). Response is prompt (within few days).
· look for underlying cause (usually
GI).
· never
treat with folic acid alone unless serum B12 level is known to be normal, as subacute combined degeneration of the cord can be precipitated.
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