Related Experiment Videos
Vitreoretinal reactions and persistent hyaloid vessels
Insights
Persistent primary vitreous in full-term infants can cause severe retinal changes. These findings may explain some cases of retrolental fibroplasia without typical risk factors.
Area of Science:
- Ophthalmology
- Neonatal Medicine
- Retinal Diseases
Background:
- Persistent primary vitreous (PPV) is a congenital condition.
- PPV can lead to various vitreoretinal abnormalities in infants.
Purpose of the Study:
- To investigate the vitreoretinal reactions associated with persistent primary vitreous in full-term infants.
- To explore the potential link between PPV and retrolental fibroplasia-like presentations.
Main Methods:
- Histological examination of eyes from full-term infants with persistent primary vitreous.
- Analysis of vitreoretinal changes, including vascular anomalies and retinal structural alterations.
Main Results:
- Observed vitreoretinal reactions included vascular anastomoses, retinal folds, avascular areas, and hypoplastic vessels.
- New vessel formation in avascular areas was supplied by persistent hyaloid vessels.
- Histological findings resembled classical retrolental fibroplasia.
Conclusions:
- Persistent primary vitreous can induce significant vitreoretinal changes mimicking retrolental fibroplasia.
- The persistent hyaloid vasculature plays a role in neovascularization in these cases.
- This provides a potential explanation for retrolental fibroplasia-like conditions in the absence of prematurity or oxygen exposure.
Abstract:
In cases with persistent primary vitreous in full-term infants there were vitreoretinal reactions including vitreoretinal anastomoses of blood vessels, vitreoretinal strands, traction folds of the retina, avascular retinal areas, hypoplasia of retinal blood vessels, rarefaction of retinal ganglion cells, and ischaemic structural changes of the retina. New vessel formation on the surface of avascular retinal areas was supplied from persistent hyaloid blood vessels. This finding may be of some importance in explaining those cases histologically resembling classical retrolental fibroplasia with no history of prematurity or oxygen treatment.