National guide to a preventive health assessment for Aboriginal and Torres Strait Islander people

Background

This chapter reviews the evidence for the prevention of iron deficiency anaemia (IDA).

IDA is very common in Aboriginal and Torres Strait Islander children, although data are lacking from many settings, particularly in urban areas. A prevalence of greater than 5% is considered by the World Health Organization (WHO) to be of public health significance; the data that are available indicates rates of IDA in Aboriginal and Torres Strait Islander children in remote Australia are significantly higher.^1–3 A recent retrospective cohort study in the Northern Territory found 52% of school-aged children had iron deficiency anaemia.⁴ IDA is associated with developmental delay of both cognitive and psychomotor functions, although it is not clear whether the relationship is causal or associative.^1,5–11 Morbidity from infectious disease is increased in iron deficient populations because of the adverse effect of iron deficiency on the immune system. IDA also increases the risk of heavy-metal poisoning in children because iron-deficient individuals have an increased absorption capacity for other heavy metals, including toxic metals such as lead and cadmium.¹²

Contributors to IDA in Aboriginal and Torres Strait Islander children are multifactorial and may include low birthweight, prematurity and maternal anaemia, twin birth, poor quality and late introduction of weaning foods, high rates of infection and tropical enteropathy syndrome associated with failure to thrive (FTT), and cow’s milk in the first year.^5,10,12–15 Moderate to severe infestations with hookworm, via intestinal blood loss, can also contribute to IDA.^1,13,15,16

In Aboriginal and Torres Strait Islander children, anaemia is most commonly diagnosed by capillary haemoglobin (Hb) with red cell indices, and further investigation is not usually required.^1,5,10,15 In Aboriginal and Torres Strait Islander children, anaemia is almost always caused by iron deficiency, and intercurrent rates of infection are high, making iron indices an unreliable indication of current iron stores. A common diagnostic approach in high prevalence areas is to measure the Hb response to iron therapy without measuring iron indices. If Hb does not improve, adherence should be confirmed and further investigation is warranted. The prevalence of haemoglobinopathies as a cause for microcytic anaemia is low, but should still be considered as a possible cause, particularly in those in whom treatment for IDA fails to show an improvement in Hb.^17,18

There is widespread agreement that Hb limits to define anaemia should differ according to age, gender and physiological status (eg pregnancy), and for babies whether they are breast or bottle fed. The Kimberley Aboriginal Medical Services and the Central Australian Rural Practitioners Association define anaemia in children aged 6–12 months as being Hb <105 g/L, children 1–4 years as Hb <110 g/L, and children 5–7 years as Hb <115 g/L.^1,15

Interventions

International guidelines state there is insufficient evidence to recommend either for or against universal screening for IDA in children.^19,20 However, these guidelines draw attention to groups of children at high risk of anaemia and the subsequent importance of clinical assessment as a means of informing decisions about whether to screen. Some Australian guidelines recommend screening all Aboriginal and Torres Strait Islander children.¹⁵ Screening can be done with venous blood, but this may not be acceptable to all carers of young children. If there is good training and quality control, point-of-care testing of capillary Hb can correlate well with laboratory testing.^1,15,21 Though Helicobacter pylori infection is associated with IDA in children, benefits of mass screening have not been demonstrated.^22–25 However, if an individual has a confirmed infection with
H. pylori, treatment generally improves IDA.²⁵

Evidence differs in regard to whether chemoprophylaxis using oral iron supplementation should be offered universally, without screening, to children who are at high risk of IDA and who are more than six months of age. This is iron supplementation aimed at preventing IDA,^{10,12,14,20,26,27} as opposed to using it only for therapeutic effect.^1,5,15,28 This approach may be considered in areas where childhood anaemia rates are high.⁹

There is good evidence to support widespread use of multicomponent interventions that do not involve medicinal iron supplementation in prevention of IDA. This includes delaying cord clamping beyond three minutes, which increases iron stores from birth.^29–33 Multicomponent interventions need to be both early and often, and may also involve food-based approaches, food and formula fortification, iron supplementation, treatment for hookworm, and integration of IDA prevention with other primary prevention programs such as immunisation and micronutrient supplementation for children with FTT. Interventions can be delivered through local healthcare providers, including GPs, nurses and Aboriginal health workers, and through government-funded nutritional supplementation programs.^{1,5,10,12,14,15,26,34} There are mixed data on whether there is improvement in cognition with oral iron supplementation, with outcomes dependent on the age that iron supplementation is provided.^35,36 In children under six years of age with IDA it is not clear whether oral iron supplementation confers benefits on cognitive or motor development. There is considerable variation in the populations studied, and there are no studies assessing this outcome in Aboriginal and Torres Strait Islander communities.^14,37

Iron supplementation provided as ‘sprinkles’ shows promise,^38–41 as it may have fewer side effects and improve adherence to daily iron supplementation. However, this has not been borne out in all studies.⁴² There is evidence that intermittent iron supplementation regimes comprising weekly, twice a week and three-week blocks of daily dosing improve Hb, although such approaches tend not to be as effective as daily dosing.^43–45
Exclusive breastfeeding until six months has many benefits and is currently recommended Australia-wide;^34,46 however, there are concerns that this may not provide enough iron to babies at increased risk of IDA.^5,10,13 Many guidelines recommend giving oral liquid iron supplements to premature and low birth-weight infants from one month of age.^1,15,47,48 While IDA is often associated with FTT in Aboriginal and Torres Strait Islander children, there are currently insufficient data demonstrating that treatment of iron deficiency improves growth.^36,48,49

In children with a history of IDA, recurrence of IDA may occur. This has major implications for long-term follow-up of children, highlighting the importance of IDA prevention programs being managed not just by individual clinicians, but at the health service level.^50–53
Guidelines make strong reference to the link between poverty and poor nutrition. In low-income households, nutrition counselling on its own is not recommended. However, it may be effective if combined with government-funded nutritional support programs that remove financial barriers to improved nutrition.^{10,19,26,34,54–56}