A patient is at a high risk for developing PVR if their PVR score is >6.33. Pathology
During rhegmatogenous retinal detachment, fluid from the vitreous humor enters a retinal hole. The mechanisms by which retinal holes or tears form are not fully understood yet. The accumulation of fluid in the subretinal space and the tractional force of the vitreous on the retina result in rhegmatogenous retinal detachment. During this process the retinal cell layers come in contact with vitreous cytokines. These cytokines trigger the ability of the retinal pigmented epithelium (RPE) to proliferate and migrate. The process involved resembles fibrotic wound healing by the RPE cells. The RPE cells undergo epithelial-mesenchymal transition (EMT) and develop the ability to migrate out into the vitreous. During this process the RPE cell layer-neural retinal adhesion and RPE-ECM (extracellular matrix) adhesions are lost. The RPE cells lay down fibrotic membranes while they migrate and these membranes contract and pull at the retina. All these finally lead to secondary retinal detachment after primary retinal detachment surgery. A number of studies have also shown that arachidonic acid metabolic cascade (one of the major inflammatory cascades) is important in the development of PVR. COX-2 expression was found in human idiopathic epiretinal membranes. Phospholipase A2 and cyclooxygenase blocking reduced structural abnormalities of the rat retina in concanavalin model of PVR and reduced the frequency of membrane formation by 43% in the dispase model of PVR and by 31% in the concanavalin one.
Fetal trimethadione syndrome (also known as paramethadione syndrome, German syndrome, tridione syndrome, among others) is a set of birth defects caused by the administration of the anticonvulsants trimethadione (also known as Tridione) or paramethadione to epileptic mothers during pregnancy.Fetal trimethadione syndrome is classified as a rare disease by the National Institute of Healths Office of Rare Diseases, meaning it affects less than 200,000 individuals in the United States.The fetal loss rate while using trimethadione has been reported to be as high as 87%. Presentation
Fetal trimethadione syndrome is characterized by the following major symptoms as a result of the teratogenic characteristics of trimethadione. Cranial and facial abnormalities which include; microcephaly, midfacial flattening, V-shaped eyebrows and a short nose
Cardiovascular abnormalities
Absent kidney and ureter
Meningocele, a birth defect of the spine
Omphalocele, a birth defect where portions of the abdominal contents project into the umbilical cord
A delay in mental and physical development

Diagnosis
Treatment
Surgery may help alleviate the effects of some physical defects, but prognosis is poor, especially for those with severe cardiovascular and cognitive problems. Speech and physical therapy, as well as special education is required for surviving children. References


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