Hyaloid Remnants in the Eyes of Premature Babies

Abstract

THE discovery that retrolental fibroplasia was a cause of blindness in premature infants (Terry, 1942) and of the role of oxygen in the causation of the disease (Ashton, Ward, and Serpell, 1953) has led to regular examination of the eyes of premature babies. In the search for evidence of this condition, the appearance of the immature fundus has become familiar. The pallor of the retina and disc, the thread-like vessels, and the vitreous haziness seen in the more immature are now well known. Careful examination of the eyes of the newborn is not a new idea, for Seissiger (1929) examined the eyes of 500 infants aged from 1 to 8 days and found, for instance, pupillary membrane remnants in 95 per cent. of them. Despite this, there has been little mention of the persistence of remnants of the hyaloid artery (Brit. med. J., 1960). Brown (1960) gives a good account of the eye of the premature infant, and states that the entire length of the hyaloid artery may be visible in a 28-week baby, while a remnant may be seen posteriorly at 32 weeks, which disappears by 38 weeks. Roper-Hall (1960) found complete hyaloid remnants in ten of eleven babies weighing between 2 and 3 lb. at birth; and remnants were seen in 58 per cent. of 55 weighing between 3 and 4 lb. and in 36-5 per cent. weighing between 4 and 5 lb. Forrester (1960) rarely failed to see remnants in babies of less than 3 lb. but found them uncommon in larger infants. Embryology The eye forms from a hollow protrusion from the anterior primary cerebral vesicle. The distal end of this protrusion enlarges to form the optic vesicle, the remainder becoming the optic stalk. The ectoderm of the side of the head overlying the optic vesicle becomes thickened and depressed to form the lens. The distal, swollen part of the optic vesicle is invaginated to form the optic cup, with the embryo lens lying in its mouth. While the cup is being formed the ventral wall of the stalk and vesicle is also invaginated to form a cleft, the choroidal fissure, in which the hyaloid artery is developed. This is enclosed, as the fissure closes in from behind forwards, to become the central retinal artery. Within the optic cup the vitreous body develops. This soon becomes very vascular, and is chiefly supplied by the hyaloid artery traversing the centre of the vitreous, lying in the canal of Cloquet. On reaching the back of the lens the artery divides into many branches to form the tunica vasculosa.

Retinal energy demands control vascular supply of the retina in development and disease: The role of neuronal lipid and glucose metabolism

“…Regression of the hyaloid vessels is controlled by retinal neurons, astrocytes, and macrophages via oxygensensing and Wnt pathways (Kurihara et al, 2010; Lobov et al, 2005; Rao et al, 2013). If hyaloid vessels do not entirely regress, the persistence of the hyaloid vasculature is associated with poor retinal development and poor vision in neonates (JONES, 1963; Liu and Nathans, 2008; Saint-Geniez and D’Amore, 2004). The regression of the hyaloid vessels normally occurs in humans around mid-gestation and mice after birth.…”

Persistent hyaloid artery with an aberrant peripheral retinal attachment: A unique presentation

“…[1] It may be present as Mittendorf’s dot located at the posterior lens capsule or as Bergmeister’s papilla located at the optic disc. [1] Persistent hyaloid artery extending from the disc upto the posterior lens capsule is uncommon.…”

“…[1] It may be present as Mittendorf’s dot located at the posterior lens capsule or as Bergmeister’s papilla located at the optic disc. [1] Persistent hyaloid artery extending from the disc upto the posterior lens capsule is uncommon. [1] We hereby present a patient with persistent hyaloid artery extending from the optic disc to the superior part of retina with no remnant at the posterior lens capsule.…”

“…[1] Persistent hyaloid artery extending from the disc upto the posterior lens capsule is uncommon. [1] We hereby present a patient with persistent hyaloid artery extending from the optic disc to the superior part of retina with no remnant at the posterior lens capsule.…”

“…It is most prominent around ninth week of gestation and slowly regresses by the seventh month. [12] Atrophy of the vessels begins in the posterior region (vasa hyloidea propria) and gradually progresses toward the anterior part (tunica vasculosa lentis). [2] Mitchell and colleagues proposed that the regression is facilitated by the lens development that separates the fetal vasculature from the vascular endothelial growth factor leading to a reduction in the level of this survival factor culminating in endothelial cell apoptosis.…”