Correspondence (letter to the editor): The Causes and Prevention of Symptoms in Premature Babies

Follow-up examinations of premature infants show the substantial deficits in the subsequent development of these babies. The cause of such developmental disorders is the lack of oxygen in the first phase of life. This is caused by the fact that the oxygen transport system in premature infants differs from that in mature neonates. This is caused by high concentrations of fetal erythrocytes with fetal hemoglobin (HbF) in the first months of life. The oxygen affinity of these fetal erythroctytes is very much greater than that of adult platelets, and the result is chronic tissue hypoxia. This chronic undersupply of oxygen causes retinopathy of prematurity and the neurological deficits that Voss et al. observed in later follow-up investigations (1).

Avoiding this damage to premature infants is possible only by eliminating the cause and by avoiding oxygen deficiency (2). Measuring HbF in this risk group shows high concentrations. Exchanging fetal platelets with adult platelets in high-risk groups can avoid hypoxia in this phase of life. The exchange has to take place rapidly—that is, post-partum—and to a sufficient degree, in order for the prevention to be successful. The effect of this measure should be monitored by measuring HbF concentrations.

Neonatology will have to face this challenge in order to prevent cerebral deficits and retinopathy of prematurity. This necessity stems in particular from the fact that 0.6% of babies are born before the 28^th week of gestation. As the authors stated, 25.1% in this at-risk group die. Any option for prevention should therefore be sought out.