It proceeds anteriorly and extends to the posterior pole of the lens. The hyaloid vascular system begins to form in the fourth to fifth week of gestation when the hyaloid artery enters the optic cup inferiorly from the primitive dorsal ophthalmic artery, a branch of the internal carotid. 2 Since the introduction of this broader and more inclusive definition, clinicians have been better able to stratify the disease entity and manage its various manifestations. PFV indicates that at least partial, and possibly total, persistence of this intraocular vasculature remains after birth. Goldberg, MD, in the 1997 Edward Jackson Memorial Lecture, introduced the term “persistent fetal vasculature” to replace “persistent hyperplastic primary vitreous,” which he felt was a misnomer because of its failure to include all of the fetal intraocular vasculature, rather than just the post-lental vessels. PFV typically presents as a unilateral, idiopathic congenital malformation. The posterior subtype has historically had very poor surgical outcomes and visual results. Within the differential diagnosis of congenital leukocoria, PFV must be distinguished from retinoblastoma and retinopathy of prematurity, along with other potentially serious conditions. These are typically categorized as anterior, posterior or combined. 1 Any abnormalities along the involutional pathway produce the various manifestations of PFV. This condition arises from failure of the hyaloid vasculature to undergo normal programmed involution.ĭuring development, this fetal vasculature nourishes the developing lens and vitreous. Persistent fetal vasculature, previously known as persistent hyperplastic primary vitreous, is a spectrum of disease and can present with no clinical effects or with severe morbidity.
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