Is it enough?

Twenty two month old Bangladeshi baby B, who had a history of recurrent wheezing since the age of 6 months, presented with acute respiratory distress accompanied by nasal flaring, marked intercostal and subcostal recession, tracheal tug, and accessory muscle use. She also appeared very pale. Unusually, she had not responded to her bronchodilator inhaler and was progressively worsening. The attending doctor found it difficult to take a history as her mother could only speak in Bengali and no interpreter was present. Instead, he was forced to rely mostly on clinical signs.

Although the doctor started rigorous treatment for life threatening asthma, the baby’s signs and symptoms showed no noteworthy improvement. A reduction in her Glasgow coma scale score (from being alert on admission to occasional eye opening and being unresponsive to pain) and increasing exhaustion prompted the anaesthetic team to intubate and ventilate baby B.

On cannulation, her blood was dilute and free flowing. Initial blood results described evidence of uncompensated mixed acidosis and a profoundly severe apparent microcytic anaemia, haemoglobin concentrations were 2.9 g/dl (normal reference 12-18 g/dl) and serum ferritin 2.4 mg/l (20-330 mg/l). This necessitated an urgent blood transfusion with O Rh negative blood before cross matching results were obtained.

Baby B required ventilation for 2 days. A detailed history was taken through an interpreter. This showed a poor diet; her intake was mainly cow’s milk with a small quantity of rice. She had been previously identified as being iron deficient and had been started on iron supplements but had failed to attend a follow-up for assessment.

During this admission, dietary advice was given and treatment started with iron supplements. The dietitian informed the mother of the seriousness of her anaemia and reinforced the need to ensure an adequate diet and compliance with medication.

Baby B’s iron status improved in the following week. Unfortunately, she did not attend a follow-up appointment four weeks later. Her general practitioner and health visitor were contacted regarding these issues.

Questions

1. What other further investigations would you consider for anaemia, taking into account baby B’s ethnicity?
2. How do iron levels vary perinatally?
3. What are the differential diagnoses of an apparent microcytic anaemia?
4. What is the World Health Organization’s criteria in diagnosing iron deficiency anaemia in children 6 months to 6 years of age?
5. Describe the signs and symptoms of iron deficiency anaemia?
6. How is childhood iron deficiency anaemia treated?
7. What are the long term complications?

Answers

1. Haemoglobin electrophoresis should be done to exclude a thalassaemia trait as this is prevalent in relatively high rates in the Asian population and can exhibit itself as an apparent microcytic anaemia. In the case of baby B, no such trait was found.

A stool sample could show occult blood in cases of gastrointestinal blood loss or parasitic infestation, for example, hookworm, a common cause of anaemia in populations from hot and humid climates.

2. From 15.7 g/dl, fetal haemoglobin concentrations fall in the days after birth to concentrations as low as 11 g/dl, from increased removal and destruction of fetal red blood cells. During the next few weeks of growth and adjustment to a new environment, blood volume increases, and haemoglobin concentrations increase only slightly, resulting in an overall fall in haemoglobin concentrations. By 4 months, neonatal iron stores begin to deplete, necessitating exogenous iron to maintain normal haemoglobin concentrations (figure).
3. The differential diagnoses of hypochromic microcytic anaemia are:
• Iron deficiency
• Thalassaemia — commonly found in South East Asians and in the United States
• Anaemia of chronic disease (infection, inflammation, renal disease, cancer)
• Sideroblastic anaemia
• Lead poisoning (in children)
• Blood loss:
  - Meckel’s diverticulum
  - Oesophagitis
  - Peptic ulcer
  - Hookworm infestation — infects approximately 25% of the world’s mainly tropical and subtropical population, with the highest incidence found in India and China; in heavily infected children the parasite causes an eosinophilic enteritis, resulting in intestinal blood loss
  - Intestinal tumours — polyps, haemangioma
  - Unrecognised pulmonary haemosiderosis (rare)
• Gastrointestinal pathology leading to malabsorption of iron:
  - Coeliac’s disease
  - Inflammatory bowel disease
  - Hookworm infestation (enteritis)
  - Chronic diarrhoea — can also cause unrecognised blood loss.^{3 4}
  

4. WHO states that a child, from 6 months to 6 years of age, is anaemic when haemoglobin concentrations are below 11.0 g/dl.⁴ Baby B’s blood results are in the table.

Iron deficiency without anaemia is diagnosed based on the following¹: serum ferritin <10 mg/l, erythrocyte protoporphyrin >2.5 mg/g haemoglogbin, mean cell volume <72 fl, and a positive response to oral iron therapy.

5. The signs and symptoms of childhood iron deficiency anaemia include:
• Breathlessness
• Lethargy
• Malaise
• Reduced activity and impaired exercise tolerance
• Pica (mental changes — child has an increased appetite for non-foodstuffs, for example, paper, flecks of paint)
  
• Pallor
• Nail changes (koilonychias (spoon nails), longitudinal ridging)
• Angular cheilitis (scaling at the corners of the mouth), glossitis
• Peripheral oedema
• Modest splenomegaly
• Changes in hair or hair loss.

6. Simple ferrous salts (ferrous sulphate, gluconate, or fumarate) are taken in tablet or syrup form. The therapeutic dose in terms of elemental iron is calculated according to the age and weight of the child and the severity of the anaemia. Generally, infants and younger children are given 3-6 mg/kg of elemental iron daily (but not exceeding 60 mg/day) in three divided doses, aiming for a rise in haemoglobin concentrations of 1 g/dl a month. The reticulocyte count should be checked after two months to assess the response to the treatment. Iron therapy must be continued for a further two months, or six months in cases of severe iron deficiency anaemia, to replenish bodily iron stores. You must also treat the cause of the anaemia.²
   

In cases of malabsorptive disorders or where children are intolerant to oral iron therapy, a parenteral preparation (iron dextran or iron sucrose) is given, again calculated according to body weight and iron deficit. A test dose is necessary to screen for an anaphylactoid reaction, as this can occur. Cardiopulmonary resuscitation facilities must be to hand. It is important to note that parenteral iron therapy is no faster in producing a response than oral iron therapy.

7. The first eight months of life includes the vulnerable period of brain growth. Iron deficiency anaemia has been associated with developmental delay and psychomotor abnormalities, although it is unknown why. This is partially reversible with iron therapy.⁵
   

A double blind randomised interventional trial in inner city areas in Birmingham, England, supports this view, concluding that feeding infants until 18 months of age with iron supplemented milk as opposed to unmodified cows’ milk prevents iron deficiency anaemia and diminishes psychomotor delay and other abnormalities.⁶ Recent evidence indicates that iron deficiency anaemia may be associated with an increased susceptibility to infections.¹

Discussion

Iron deficiency anaemia is the most common nutritional disorder of childhood, occurring in 12% of children in the United Kingdom. The prevalence is higher in certain ethnic minorities, namely Chinese, African-Caribbean, and is almost double the national prevalence in the Pakistani, Bangladeshi and Indian populations living in Britain.^{4 7}  So why does childhood iron deficiency anaemia exist? There are three main reasons.

Poor socioeconomic circumstances
The costly nature of iron supplemented milk formulas and, more importantly, the lack of awareness of the importance of dietary iron may account for the high prevalence amongst this group.⁷

Consumption of milk
Unmodified cow’s milk is low in iron.¹ The introduction of cows’ milk as the main source of nutrition at 6 months results in a poor iron status between 1 and 2 years of age compared with children introduced to milk at 1 year of age. In such cases, iron status has been shown to decline with increasing volume of cow’s milk consumed: those at greatest risk tend to drink more than 600 ml per day; the use of feeding bottles is associated with larger volumes being consumed, in some cases a reported 1000 ml. For this reason, the Department of Health advises that cows’ milk should not be consumed as the main drink in infants less than 12 months of age.⁴

The mother’s place of birth
Various studies involving Asian communities in England have shown the extent of anaemia rates, with the common finding of anaemia being twice as prevalent in Asians, at 20-29% (mainly Bangladeshi and Pakistani) compared to non-Asian children.⁴

Diet (which is influenced by cultural health beliefs) is the main causative factor that predisposes Asians to a low iron status. Compared with white mothers, Asian mothers tend to introduce solid foods later, starting cows’ milk earlier as the main source of nutrition, often in large quantities of more than 600 ml per day—sometimes 60% of energy intake at the age of 18 months.

Asian infants tend to be partially or fully bottle fed for longer than in other populaces. Adding sugar to the milk, an Asian tendency, and bottle feeding in general may account for the large volumes consumed by infants.⁴

Preventing iron deficiency anaemia

Sufficient dietary iron from 4 months of age and during the weaning period is necessary to prevent the onset of iron deficiency anaemia. Primary prevention measures include the following.

Supplementary iron in food or milk formulas
Asians are less likely to be anaemic if they eat breakfast cereals, which, in the United Kingdom, tend to be fortified with vitamins and iron.⁴ Evidence suggests that iron supplements have no advantage over fortified formulas; it may even reduce growth rates, and its cost and unpleasant side effects make iron supplements an option to avoid.¹

Dietary education and feeding practices
Rigorous, culturally sensitive dietary educational programmes (including cookery demonstrations on home visits) for the mothers of children with iron deficiency anaemia have proved very beneficial. These provide advice on dietary habits, milk formulas, and weaning as well as encouraging compliance with iron therapy. With active reinforcement of advice, it has effectively improved maternal knowledge regarding the importance of a balanced diet, and has been successful in changing their child’s health.⁸ With limited resources, however, implementing a nationwide scheme has proved difficult.

Free formulas for at risk infants
In the United States, free bottled milk fortified with iron was shown to improve anaemia rates, and it is thought that introducing such a scheme in the United Kingdom may benefit our infants.⁷ In Birmingham, anaemia rates fell when people on income support received free iron supplemented milk until the age of 12 months. After 12 months, however, iron intake reduced, possibly due to socioeconomic circumstances.¹

Communication problems
Good understanding and communication between  patients and doctors are central to good medical practice. This case highlights the difficulty in communication between non-English speakers and the medical team, and emphasises the poor availability of interpreters during medical emergencies. It can add to an already stressful situation and impair the standard of care given. Evidence shows that non-English speakers are less likely to receive important preventative services.⁹

Conclusion

Are we doing enough to bring down the rates of childhood iron deficiency anaemia? In view of current research and evidence, the answer is no. Iron deficiency anaemia is a serious clinical problem because it can adversely affect the neurological and therefore global development of children at their most vulnerable stage of life.