[Pathophysiology and prevention of retinopathy of prematurity].
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.
Hammerstein
W
W
Univ.-Augenklinik Düsseldorf.
D001724:Birth Weight / Q000502:physiology; D004920:Erythropoiesis / Q000502:physiology; D005319:Fetal Hemoglobin / Q000502:physiology; D006442:Glycated Hemoglobin / Q000502:physiology; D006443:Hemoglobin A2 / Q000502:physiology; D006801:Humans; D007223:Infant; D007231:Infant, Newborn; D010100:Oxygen / Q000097:blood; D015861:Retinal Neovascularization / Q000503:physiopathology / Q000517:prevention & control; D012178:Retinopathy of Prematurity / Q000503:physiopathology* / Q000517:prevention & control*; D012307:Risk Factors
D005319:Fetal Hemoglobin; D006442:Glycated Hemoglobin; D006443:Hemoglobin A2; D010100:Oxygen
Pathophysiologie und Prophylaxe der Frühgeborenenretinopathie.