PVD, or Posterior vitreous detachment, is a result of changes to the macro-molecular structure of vitreous gels, resulting in liquefaction.
This is concurrent with some alteration of the extra-cellular matrix at the vitreoretinal interface, which allows the posterior vitreous cortex to separate from the limiting lamina within the retina.
Anomalous PVD, or APVD, is a result of gel liquefaction which exceeds the degree of vitreoretinal dehiscense.
The clinical variations of APVD depend on where within the fundus the vitreoretinal adhesion is the strongest.
Along the periphery, APVD can result in detachments and retinal tears.
Within the macula APVD causes vitreomacular traction syndrome, which results in vitreoschisis with macular holes - or this may contribute to diabetic macular edema.
At the retina and the optic disc, APVD can cause vitreopapillary traction, promoting neovasculation in the retina and optic disc.
By unifying vitreoretinal diseases and integrating them into the framework of APVD, an underscore is placed upon the need to more effectively treat and prevent these disorders by replicating two main components of a PVD: gel liquefaction, and vitreoretinal dehiscense.
Pharmacologic vitreolysis aims to mitigate APVD by breaking down vitreous macro-molecules while weakening vitreoretinal adhesion.
This helps to detach the posterior vitreous cortext more safely.
Not only would this facilitate surgery, but if performed during the initial, natural state of the disease, it should prevent progression of the disease.
In layman's terms, this unifying theory poses that the eye gel will naturally liquefy, thereby starting to weaken its retinal attachment.
As it retracts from the interface between the vitreous and retina, it is called a PVD.
APVD results from continued attachment of the gel even as it begins to naturally shrink away from the retina.
This theory promotes the use of chemicals, microfibrin, or fibrin, in order to facilitate the releasing of the vitreous from the traction which it is exerting on the retina.
I feel that this theory has greater value among young patients.
However, older patients may find that the vitreous has changed so much that this becomes unnecessary.
However, it is still a floater treatment which bears mention and discussion.
This is concurrent with some alteration of the extra-cellular matrix at the vitreoretinal interface, which allows the posterior vitreous cortex to separate from the limiting lamina within the retina.
Anomalous PVD, or APVD, is a result of gel liquefaction which exceeds the degree of vitreoretinal dehiscense.
The clinical variations of APVD depend on where within the fundus the vitreoretinal adhesion is the strongest.
Along the periphery, APVD can result in detachments and retinal tears.
Within the macula APVD causes vitreomacular traction syndrome, which results in vitreoschisis with macular holes - or this may contribute to diabetic macular edema.
At the retina and the optic disc, APVD can cause vitreopapillary traction, promoting neovasculation in the retina and optic disc.
By unifying vitreoretinal diseases and integrating them into the framework of APVD, an underscore is placed upon the need to more effectively treat and prevent these disorders by replicating two main components of a PVD: gel liquefaction, and vitreoretinal dehiscense.
Pharmacologic vitreolysis aims to mitigate APVD by breaking down vitreous macro-molecules while weakening vitreoretinal adhesion.
This helps to detach the posterior vitreous cortext more safely.
Not only would this facilitate surgery, but if performed during the initial, natural state of the disease, it should prevent progression of the disease.
In layman's terms, this unifying theory poses that the eye gel will naturally liquefy, thereby starting to weaken its retinal attachment.
As it retracts from the interface between the vitreous and retina, it is called a PVD.
APVD results from continued attachment of the gel even as it begins to naturally shrink away from the retina.
This theory promotes the use of chemicals, microfibrin, or fibrin, in order to facilitate the releasing of the vitreous from the traction which it is exerting on the retina.
I feel that this theory has greater value among young patients.
However, older patients may find that the vitreous has changed so much that this becomes unnecessary.
However, it is still a floater treatment which bears mention and discussion.
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