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[Pathophysiology and prevention of retinopathy of prematurity]
1Univ.-Augenklinik Düsseldorf.
Insights
Premature infants with high fetal hemoglobin (HbF) risk retinopathy due to chronic retinal hypoxemia. Replacing fetal erythrocytes can prevent this, offering secondary prevention for retinopathy of prematurity.
Area of Science:
- Neonatal Medicine
- Ophthalmology
- Hematology
Background:
- Retinopathy of prematurity (ROP) is a leading cause of blindness in premature infants.
- A link exists between erythropoiesis changes post-birth and ROP development.
- Fetal erythrocytes have a higher oxygen affinity than adult erythrocytes, potentially causing hypoxemia.
Purpose of the Study:
- To investigate the relationship between fetal hemoglobin levels and retinopathy in premature infants.
- To explore the potential for preventing ROP through erythrocyte management.
Main Methods:
- Analysis of fetal hemoglobin (HbF) levels in premature infants.
- Monitoring for signs of chronic retinal hypoxemia and neovascularization.
- Evaluating the effect of erythrocyte replacement in infants with high HbF.
Main Results:
- Premature infants with un-converted erythropoiesis experience a period of chronic retinal hypoxemia.
- High HbF levels are associated with increased risk of retinal hypoxemia and neovascularization.
- Erythrocyte replacement in infants with high HbF can mitigate retinal oxygen deficit.
Conclusions:
- Monitoring and managing fetal hemoglobin levels is crucial for preventing ROP.
- Erythrocyte management offers a viable strategy for secondary prevention of retinopathy in premature infants.
- Understanding erythropoiesis shifts post-birth is key to addressing ROP pathogenesis.
Abstract:
In premature infants there is a temporal and causal relation between the change in the erythropoiesis after birth and the manifestation of retinopathy. The physiological substitution of the fetal erythrocytes can be controlled by an analysis of the fetal hemoglobin. In premature infants in which the erythropoiesis has not yet been converted there is an interval of time where there is a chronic hypoxemia of the retina and in which neovascularisation occurs. The oxygen deficit arises because fetal blood - in comparison with adult blood - exhibits a higher affinity to oxygen. If high values of HbF are ascertained in premature infants the chronic hypoxemia of the retina can be avoided by replacing the erythrocytes. In this way, a secondary prevention of the illness is possible.