Haematological disease in a child: Iron-deficiency anaemia (IDA) Flashcards

1
Q

Define IDA.

A

Reduced Hb with low mean cell volume (MCV <80 fl) and depleted iron stores.

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2
Q

Explain the aetiology/risk factors for IDA.

A

Three stages in the pathogenesis: Fe2 depletion -> Fe2-deficient erythropoiesis -> Fe2 deficiency anaemia.

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3
Q

What are the 4 categories of IDA.

A
  • Decreased Fe2+ store at birth
  • Nutritional (inadequate Fe2 supply)
  • Increased Fe2+ demand
  • Increased Fe2+ loss
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4
Q

What are some causes of decreased Fe2+ stores at birth?

A
  • Prematurity
  • Multiple pregnancy
  • Perinatal bleeding
  • Early umbilical cord clamping
  • Maternal Fe2 deficiency
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5
Q

What are some causes of inadequate Fe2+ supply?

A
  • Exclusive breastfeeding>6/12 (insufficient Fe2 in breast milk)
  • Early cow’s milk introduction (reduced bioavailability of iron than breast milk and formula milk is fortified with 6 mg iron/l)
  • Excessive reliance on milk in the second year of life
  • Increased infant fruit juice intake
  • Strict vegetarian diet
  • Behavioural (food refusal, grazing, dieting, eating disorders)
  • Crohn’s disease, coeliac disease (decreased absorption)
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6
Q

What are some causes of increased Fe2+ loss?

A
  • Acute haemorrhage (Meckel’s diverticulum, intestinal duplication cyst, peptic ulcer)
  • Chronic haemorrhage (cow’s milk protein intolerance, intestinal duplication, IBD, telangiectasia, intestinal polyp)
  • Parasites (hookworm – Ancylostoma duodenale in developing countries); menstruation.
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7
Q

What are some causes of increased Fe2+ demand?

A
  • Growth
  • Prematurity
  • IUGR
  • Post malnutrition
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8
Q

Summarise the epidemiology of IDA.

A

Inner city centres (UK) and Asian communities. Most common nutritional deficiency disorder worldwide.

Incidence: 5–40% depending on community.

Peak ages: 6 months to 3 years and adolescent girls. Uncommon in non-premature infants <6/12 (fetally acquired iron reserves).

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9
Q

What are the presenting symptoms of IDA?

A

General: Gradual onset; failure to thrive, poor exercise tolerance, global developmental delay, headaches, and irritability.

Behavioural: Anorexia, pica (ingestion of odd materials with increased Fe2.), irritability, impaired concentration, impaired progress at school.

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10
Q

What are the signs of IDA?

A

General: Signs of anaemia (pallor of skin and mucous membranes, tachycardia) and systolic flow murmurs.

Rarely: Brittle nails and hair (epithelial cell iron), spoon-shaped nails (koilonychia), glossitis (atrophy of tongue papillae), angular stomatitis, mild hepatosplenomegaly and lymphadenopathy.

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11
Q

What are some appropriate investigations for IDA?

A

Blood film: Microcytic, hypochromic (central pallor), anisocytosis (variable sizes), poikilocytosis (variable shapes).

Bloods: Low Hb, high serum ferritin, low serum Fe2, high TIBC, low haematocrit, low MCV.

Hb electrophoresis: Exclude b-thalassaemia trait or Sickle cell disease.

Bone marrow (only in complicated cases): Erythroid hyperplasia and decreased bone marrow Fe2+ or total absence of iron.

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12
Q

What is the management for IDA?

A

Preterm: Fortify breast milk with Fe2. Use Fe2-fortified milk formula.

Infants: Increase highly absorbable haem iron sources (meat, fish) and sources of non-haem iron (such as grains) in vegetarian families. Enhance non-haem iron absorption by eating vitamin C-rich foods at the same meal.

Oral FeSO4: Maximum rise of Hb 0.25–0.4 g/dl/day.

Blood transfusion: Indicated with severe anaemia leading to CHF and cardiovascular compromise. Packed RBCs should be given slowly or partial exchange transfusion.

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13
Q

What are some complications associated with IDA?

A

Possible impaired mental and psychomotor development. High output cardiac failure in severe cases.

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14
Q

What is the prognosis of IDA?

A

Good outcome if cause is nutritional or due to increased demand and prompt action is taken. If underlying GI cause, outcome dependent on underlying cause.

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