Secondary Vitreus Essay

Persistent hyperplastic primary vitreous was first described by Reese in 1955 in his Jackson Memorial lecture.[5] In the embryo, the primary vitreous is formed during the first month of development and is supplied by the hyaloid blood system. Hyaloid artery generally begins to regress during the formation of the avascular secondary vitreous at around 9 weeks. Incomplete regression of the embryonic vitreous and the hyaloid vasculature leads to this entity.[4]
PHPV is usually found in otherwise healthy, full-term infants, however, systemic and neurological abnormalities are also described in the literature. Its severity can range from an isolated Mittendorf dot to more severe forms of retrolenticular membranes, retinal dysplasia, or detachment.[6] The most common presenting signs and symptoms are leukocoria, poor vision, and small eye and strabismus.[7] PHPV is classified into three types: Anterior, posterior, or combination of anterior and posterior. Complications of PHPV can be cataract, intraocular hemorrhage, secondary glaucoma, lens capsule rupture, traction retinal fold, and subsequent phthisis bulbi.[4]

Persistent hyperplastic primary vitreous has very characteristic radiological appearance, which helps in differentiating it from other differentials of white pupillary reflex with reliability. On 2 D ultrasonography an
Out of these retinoblastoma is most serious and closely resembles PHPV hence; must be excluded in all cases of leukocoria. ROP is a disease of prematurity but can occur in late preterm and term babies if they received an excess of oxygen/ mechanical ventilation in neonatal life. It is one of the preventable causes of visual morbidity and is of public health importance. Almost all of these entities can be differentiated by ocular examination along with ocular