Critical haemoglobin thresholds in premature infants

Blood transfusion is an integral part of neonatal intensive care. Unfortunately, transfusion practice is often based on expert opinion1 2 and anecdote rather than scientific evidence. Historically, blood transfusions have been used as therapy for apnoea and bradycardia, poor feeding, poor weight gain, and pallor. Although many studies have examined these outcomes,3 few are methodologically sound, many lack sufficient power, and most contribute little to the discussion.

Theoretically, red blood cell transfusion is used to avoid the pathological state in which oxygen demand is greater than supply.4 5 As such, the principal outcome of any study of transfusion practice would need to incorporate measures of end organ hypoxia, specifically ischaemic brain injury, chronic lung disease, retinopathy of prematurity, and death. At the present time there are no methodologically sound prospective trials of transfusion practice that include long term neurodevelopmental outcome, the end result of brain hypoxia. This is in part because of the complexities of a randomised, non-blinded study but also because of the dynamic balance between systemic oxygen transport (SOT) and oxygen consumption (Vo ₂) (see fig 1).

In order to understand the concept of a critical haemoglobin threshold, if one exists, it is necessary to examine the balance between SOT and demand or VO₂.

Oxygen is used by the electron transport chain within the mitochondria for oxidative phosphorylation. Its supply depends on many factors, in particular the distance between the capillary and the cell, the diffusion characteristics, and the oxygen pressure gradient between the capillary and the cell.6 This pressure gradient depends on regional blood flow, oxygen transport, and the characteristics of the haemoglobin–oxygen dissociation curve (HODC).6