With thanks to Dr Alexandra Briscoe and Professor Irene Roberts for their collaborative work.

The red cell count and haemoglobin (see February 2017 newsletter for normal ranges)

The red cell count is the actual number of red cells per mL of blood, and the haemoglobin (Hb) is the concentration of the Hb protein itself- the oxygen carrying protein.

A raised red cell count due to increased production of red cells is seen in children with chronic hypoxia, such as congenital heart disease and, in neonates, manifests as neonatal polycythaemia, usually due to chronic in utero hypoxia.

During the last 2 months of pregnancy erythropoiesis occurs at a rate of 3-5 x that of adults, consequentially the healthy newborn has a relative polycythaemia compared to infants and children-  manifest as a raised Hb, red cell count and haematocrit.

The Hb falls over the first 2-3 months of life in response to several factors- with the onset of respiration at birth- oxygenation increases, erythropoieitin production and erythropoiesis is decreased via negative feedback. Neonatal red blood cells have a shorter half-life of 90 days compared to 120 days for red cells in healthy children and adults. In addition over this time period, neonates undergo  rapid growth and weight increase with a subsequent increase in circulatory volume- leading to relative haemodilution. This physiological anaemia requires no intervention in otherwise healthy term infants and will rarely fall below 90g/L.

In contrast, infants born extremely prematurely at <28 weeks of completed gestation, will frequently require red cell transfusion. This is due to anaemia of prematurity. The cause is multifactorial, including low erythropoietin, shortened red cell lifespan, nutritional deficiency and iatrogenic blood letting, however the nadir in Hb occurs earlier (4-8 weeks compared to 8-12 weeks in term babies) and is more severe. Premature red blood cells have a life span of 35-50 days, and infants have a circulating blood volume of 90- 105 mls/kg, which could be as little as 45mls in a 24 week 500g infant. In addition, these infants do not receive maternal iron transfer via the placenta. Preterm infants also have a slow erythropoietin response to hypoxia and anaemia- this is because the site of production of erythropoietin is the liver rather than the kidney as per term infants. There is also evidence of increased metabolism of EPO in the preterm infant. (Strauss, 2010). Despite multiple studies into the use of exogenous erythropoietin for preterm infants, current guidelines recommend red cell transfusion for the management of anaemia of prematurity.

Reference:

Ronald G. Strauss, Anaemia of prematurity: Pathophysiology and treatment, Blood Reviews, Volume 24, Issue 6, November 2010, Pages 221-225, ISSN 0268-960X, http://dx.doi.org/10.1016/j.blre.2010.08.001.

(http://www.sciencedirect.com/science/article/pii/S0268960X10000408)