Incidence Of, Risk Factors For, and Combined Mechanism of Late-Onset Open-Angle Glaucoma After Vitrectomy

Koreen, Larry; Yoshida, Norihiko; Escarião, Paulo; Niziol, Leslie M.; Koreen, Irina V.; Musch, David C.; Chang, Stanley

doi:10.1097/iae.0b013e318217fffb

Cited by 80 publications

(82 citation statements)

References 33 publications

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“…Remarkably, patients who had cataract surgery prior to vitrectomy developed glaucoma an average of 28 months earlier than those who were phakic at the time of vitrectomy and later had cataract surgery. More detailed follow-up studies supported the increased risk of glaucoma after vitrectomy and cataract surgery [18,19]. However, other studies conclude that the risk of glaucoma does not increase significantly after vitrectomy and cataract surgery.…”

Section: Vitrectomy Cataract and Glaucomamentioning

confidence: 94%

Preserve the (intraocular) environment: the importance of maintaining normal oxygen gradients in the eye

et al. 2014

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Oxygen levels in the eye are generally low and tightly regulated. Oxygen enters the eye largely by diffusion from retinal arterioles and through the cornea. In intact eyes, oxygen from the retinal arterioles diffuses into the vitreous body. There is a decreasing oxygen gradient from the retina to the lens, established by oxygen consumption by ascorbate in the vitreous fluid and lens metabolism. Age-related degeneration of the vitreous body or removal during vitrectomy exposes the posterior of the lens to increased oxygen, causing nuclear sclerotic cataracts. Lowering oxygen in the vitreous, as occurs in patients with ischemic diabetic retinopathy, protects against cataracts after vitrectomy. Vitrectomy and cataract surgery increase oxygen levels at the trabecular meshwork and with it the risk of open angle glaucoma. Two additional risk factors for glaucoma, African heritage and having a thinner cornea, are also associated with increased oxygen in the anterior chamber angle. Preservation of the vitreous body and the lens, two important oxygen consumers, would protect against nuclear sclerotic cataracts and open angle glaucoma. Delaying removal of the lens for as long as possible after vitrectomy would be an important step in delaying ocular hypertension and glaucoma progression.

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Section: Vitrectomy Cataract and Glaucomamentioning

confidence: 94%

Preserve the (intraocular) environment: the importance of maintaining normal oxygen gradients in the eye

et al. 2014

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“…Several groups have shown that vitrectomy and cataract surgery significantly increase IOP and the risk of developing POAG, 55,56 which is due to exposure of the TM and SC to a higher level of oxygen causing oxidative damage to these tissues. 57,58 We demonstrated in vitro in an aging model of hyperoxia that it altered eNOS and its phosphorylation status and resulted in reduced NO production.…”

Section: Discussionmentioning

confidence: 99%

Endothelial Nitric Oxide Synthase-Related Mechanotransduction Changes in Aged Porcine Angular Aqueous Plexus Cells

Lei

Stamer

et al. 2014

Investigative Ophthalmology & Visual Science

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Citation: Lei Y, Stamer WD, Wu J, Sun X. Endothelial nitric oxide synthaserelated mechanotransduction changes in aged porcine angular aqueous plexus cells. Invest Ophthalmol Vis Sci. 2014;55:8402-8408. DOI: 10.1167/iovs.14-14992 PURPOSE. To investigate effects of aging on endothelial nitric oxide synthase (eNOS) expression and signaling in angular aqueous plexus (AAP) (functional equivalent to human Schlemm's canal) cells subjected to shear stress. METHODS.The AAP cells were isolated differentially from porcine outflow tissues using puromycin selection. Cell aging was induced by culturing cells in hyperoxia condition (40% oxygen and 5% carbon dioxide) for 14 days. The AAP cells grown in chamber slides were exposed to a shear stress of 8 dynes/cm 2 for 24 hours. Expression of eNOS, eNOS-phospho Thr495, eNOS-phospho Ser1177, and Akt-phospho was tested by Western blot analysis and immunofluorescence staining. Nitric oxide (NO) levels were measured using the Griess assay. RESULTS.Compared with control, eNOS levels in aged cells were significantly reduced by 60% (P < 0.05; n ¼ 6). Phosphorylation of eNOS at Ser1177 and Akt at Ser473 was 63% and 80% lower in aged cells, respectively, whereas phosphorylation of the eNOS inhibition site (Thr495) increased by 6.1-fold (P < 0.05; n ¼ 6). Shear stress (8 dynes/cm 2 for 24 hours) increased eNOS abundance (total protein and at cell borders) and phosphorylation at Ser1177 by 1.7-fold and 1.8-fold, respectively (P < 0.05; n ¼ 6), whereas aged cells were unresponsive. In control cells exposed to shear stress, the NO concentration was 1.8-fold higher than in the static group (P < 0.05; n ¼ 4); however, aged cells were unresponsive to shear stress (mean 6 SD, 4.3 6 1.3 vs. 4.1 6 1.4 lM).CONCLUSIONS. Aged AAP cells appear compromised in their mechanotransduction machinery involving eNOS, the protein product of the gene, NOS3, polymorphisms of which impart a risk for the development of glaucoma.Keywords: aging, Schlemm's canal, eNOS G laucoma comprises a group of complex and heterogeneous blinding diseases, affecting almost 60 million people worldwide. 1 Clinically, glaucoma is characterized by cupping of the optic nerve head and visual field loss. Elevated IOP is the primary risk factor for glaucomatous optic nerve damage, and reducing pressure remains the only treatable end point that slows or stops disease progression. The risk of developing POAG also clearly increases with age. 2-8 Primarily, IOP is determined by changes in aqueous humor outflow resistance, which is thought to reside mainly in the juxtacanalicular region, where the trabecular meshwork (TM) and the inner wall of Schlemm's canal (SC) cells interact. 9,10 The endothelial cells of the inner wall of SC are important in regulating outflow resistance and thus IOP. 11,12Nitric oxide (NO) regulation appears to have a role in POAG. Family association studies [13][14][15] show a relationship between NOS3 gene polymorphisms, which encode for endothelial NO synthase (eNOS), and POAG. These recent findings are consistent wit...

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“…The incidence of glaucoma after pars plana vitrectomy has been reported between 11.6 and 20% [66, 87]. Acute post operative increase in IOP can be due to replacement with intra ocular tamponade (Gas/Silicone oil), use of intra operative endo-photocoagulation or post operative fibrinous inflammatory reaction.…”

Section: Glaucoma After Retinal Surgerymentioning

confidence: 99%

Retina and glaucoma: surgical complications

et al. 2018

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BackgroundThe close structural and microcirculatory co-relation between anterior and posterior segments of eye make them very vulnerable to complications when one of them is affected surgically. With the advent of anti-fibrotic agents in the management of glaucoma, the rates of vitreoretinal complications have become more frequent. Main bodyCommon retinal complications after glaucoma surgeries include choroidal detachment; ocular decompression retinopathy; haemorrhagic choroidal detachment; hypotony maculopathy; malignant glaucoma; vitreous haemorrhage; bleb endophthalmitis; retinal detachment. Similarly, intraocular pressure rise is often noted after scleral buckle; pars plana vitrectomy; intravitreal gas injection; silicone oil injection; intravitreal steroid injection.ConclusionThe article provides some insight into some of the complications after glaucoma and retina surgeries, including the pathogenetic mechanisms behind each complication and available management options.

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Incidence Of, Risk Factors For, and Combined Mechanism of Late-Onset Open-Angle Glaucoma After Vitrectomy

Cited by 80 publications

References 33 publications

Preserve the (intraocular) environment: the importance of maintaining normal oxygen gradients in the eye

Preserve the (intraocular) environment: the importance of maintaining normal oxygen gradients in the eye

Endothelial Nitric Oxide Synthase-Related Mechanotransduction Changes in Aged Porcine Angular Aqueous Plexus Cells

Retina and glaucoma: surgical complications

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