Abstract

Severe childhood anaemia risks significant morbidity and mortality though may have different benign or malignant aetiologies. We set out to define the characteristics of this group of patients at our institution.

This study was performed in a large paediatric teaching hospital. We retrospectively identified children (<18y) presenting with Hb <5g/dL in the period 2006–9 by use of computerised laboratory records. Case notes were then reviewed and we recorded patient characteristics, final diagnosis and management with 2y of follow-up.

93 patients fitted study criteria. Patients were mean age 5y, (range 1d-17y). Diagnoses were: 33/93 leukaemia (25/33 acute lymphoblastic, 7/33 acute myeloid, 1/33 juvenile myelomonocytic leukaemia); 23/93 iron deficiency anaemia (IDA); 12/93 hereditary blood disorders (including 7/12 hereditary spherocytosis with 6/12 associated parvovirus); 25/93 “other” including 6/25 haemolytic-uraemic syndrome and 3/25 transient erythroblastopaenia. Of leukaemia 5/33 had presenting white cell count > 100x10⁹/L, and all received red-cell transfusion. Of IDA 19/23 had nutritional IDA (nIDA). 17/19 nIDA were aged <3y. 11/17 nIDA were of Pakistani origin (versus 3.5% of city population). Linking residential postcode with national index of multiple deprivation, 11/17 nIDA lived in the most (lowest 20%) deprived areas, rising to 9/11 in more severe nIDA (Hb <4g/dL). In IDA, all were prescribed iron supplementation, 21/23 feeding practises reviewed by dietician and 17/23 were transfused red-cells (all those with Hb <4g/dL). 9/23 IDA resolved within 1y though 3/23 had no repeat Hb recorded. Of all patients 11/93 died: 3/11 at initial presentation, 6/11 within 1y and 2/11 within 2y.

We show that severe anaemia is most commonly caused by acute leukaemia in this population. However nIDA due to poor infant feeding practise is an important preventable diagnosis and may merit particular health education. A disproportionate number of such patients are from deprived areas. A significant number of patients with nIDA had persistent anaemia >1y post presentation suggesting the need for structured follow-up and ongoing intervention.