Proliferative vitreoretinopathy (PVR) is a still incompletely defined term for a pathological process that occurs after retinal detachment and subsequent surgical treatment [1] [2]. Namely, PVR is predominantly described as the most common cause of surgical failure for rhegmatogenous retinal detachment (RRD) [1] [3], in which the detached retina creates a space for fluid to accumulate between the retinal pigment epithelium and the neurosensory component of this structure. The complete pathogenesis model is still not understood, but it is assumed that after retinal detachment (predominantly caused by trauma) and penetration of the blood-retina-barrier (RBB), local cells promote an inflammatory reaction by secreting various cytokines that aid in the process of healing [1] [4] [5]. More importantly, migration of various cell lineages is induced, including fibroblasts, polymorphonuclear leukocytes, lymphocytes, but also glial cells [1] [4]. These cells accumulate in the previous location of the retina, and in the attempt to repair retinal detachment, abnormal healing leads to the formation of scar tissue [1] [5]. Because no viable retinal tissue is formed, even after successful surgical treatment, patients suffer from reduced visual acuity that develops approximately a few months after the initial retinal detachment [1] [6] [7] [8]. Various intrinsic factors (severity of detachment, delay in diagnosis, the presence of vitreous hemorrhage, macular involvement, etc.) determine the extent of visual symptoms and the prognosis [1] [7] [9]. Furthermore, various studies have confirmed the recurrent nature of proliferative vitreoretinopathy, even after multiple surgeries [1] [9].

• Severe Clinical Course

  The early onset and the severe clinical course of proliferative vitreoretinopathy in these eyes showed parallels to traumatic proliferative vitreoretinopathy. The retina in all eyes could be reattached. [ncbi.nlm.nih.gov]

• Rubeosis Iridis

  No patients developed rubeosis iridis related to the total retinectomy. [ncbi.nlm.nih.gov]

• Ulcer

  Langenbach R, Morham SG, Tiano HF et al (1995) Prostaglandin synthase 1 gene disruption in mice reduces arachidonic acid-induced inflammation and indomethacin-induced gastric ulceration. Cell 83:483–492 CrossRef PubMed Google Scholar 21. [doi.org]

• Fear

  This feared complication has been reported to occur in up to 8% of patients after undergoing RD repair. [ncbi.nlm.nih.gov]

• Irritability

  It has been suggested that the posterior lens capsule may protect the anterior uvea, the site of active transport, from mechanical and physical irritation by the vitreous gel in phakic eyes [ 10 ]. [systematicreviewsjournal.biomedcentral.com]

  […] that the outward active transport of fluorescein from the vitreous was reduced in aphakic compared with phakic eyes. 27 They suggested that the posterior lens capsule may protect the anterior uvea (site of active transport) from mechanical and physical irritation [doi.org]

  02 Method of preventing NMDA receptor-mediated neuronal damage AT401615B ( en ) 1996-10-25 Use of special 5HT3 antagonists for the manufacture of medicines US5686100A ( en ) 1997-11-11 Prophylactic and therapeutic treatment of skin sensitization and irritation [google.la]

  […] with functional antagonists of the glycine/NMDA receptor complex AT401615B ( en ) 1996-10-25 Use of special 5HT3 antagonists for the manufacture of medicines US5686100A ( en ) 1997-11-11 Prophylactic and therapeutic treatment of skin sensitization and irritation [google.sr]

Despite the fact that the pathophysiological mechanisms that determine the course of recovery after retinal detachment, many studies have identified that some of the risk factors that facilitate a poorer prognosis (eg. delayed recognition and initiation of treatment) are highly preventable [9], primarily by conducting a proper ophthalmological examination and follow-up after retinal detachment. Physicians must consider proliferative vitreoretinopathy in the differential diagnosis of progressive visual acuity disturbances and loss of vision in patients who underwent surgical treatment for retinal detachment, meaning that a meticulously obtained patient history is vital in the diagnostic workup. Visual acuity testing is mandatory in all patients, and after clinical suspicion is raised, a dilated fundus examination is often sufficient to detect proliferative vitreoretinopathy [8]. Slit-lamp biomicroscopy can provide an insight into the retinal pathology [1], but ocular endoscopy has become a valuable tool (among many diagnostic and therapeutic approaches, including ultrasonography, optical coherence tomography, angiography, etc.) in the assessment of the retina, the ciliary body, and the vitreous body [10].

• Foam Cell

  A histological examination revealed that the epiretinal membrane consisted of collagen fibers, glial proliferation, foam cells and lymphocytes. The foam cell in the epiretinal membrane is a characteristic finding in an eye with Coats' disease. [ncbi.nlm.nih.gov]

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6. Mietz H, Heimann K. Onset and recurrence of proliferative vitreoretinopathy in various vitreoretinal disease. Br J Ophthalmol. 1995;79(10):874-877.
7. Sadeh AD, Dotan G, Bracha R, Lazar M, Loewenstein A. Characteristics and outcomes of paediatric rhegmatogenous retinal detachment treated by segmental scleral buckling plus an encircling element. Eye (Lond). 2001;15(Pt 1):31-33.
8. Schwartz SG, Flynn HW, Lee W-H, Ssemanda E, Ervin A-M. Tamponade in surgery for retinal detachment associated with proliferative vitreoretinopathy. Cochrane Database Syst Rev. 2009;(4): CD006126.
9. Tseng W, Cortez RT, Ramirez G, Stinnett S, Jaffe GJ. Prevalence and risk factors for proliferative vitreoretinopathy in eyes with rhegmatogenous retinal detachment but no previous vitreoretinal surgery. Am J Ophthalmol. 2004;137(6):1105-1115.
10. Boscher C, Kuhn F. An endoscopic overview of the anterior vitreous base in retinal detachment and anterior proliferative vitreoretinopathy. Acta Ophthalmol. 2014;92(4):e298-304.