Elevated intraocular pressure causes cellular and molecular retinal injuries, advocating a more moderate intraocular pressure setting during phacoemulsification surgery

Zhao, Zhenni; Yu, Xiaowei; Yang, Xue; Zhang, Jiamin; Zhang, Dandan; Sun, Nannan; Fan, Zhipeng

doi:10.1007/s10792-020-01519-w

Cited by 9 publications

(4 citation statements)

References 54 publications

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“…Increases in retinal thickness after cataract surgery have been observed, and such changes are closely related to surgical injuries, IOP changes, and inflammatory reactions. 29–33 Our results agree with those reported in previous studies, with the increase in GCC thickness statistically significantly greater in group 2 ( P = .02).…”

Section: Discussionsupporting

confidence: 92%

Vitreous-lens interface changes after cataract surgery using active fluidics and active sentry with high and low infusion pressure settings

Scarfone,

Rodriguez,

Rufiner

et al. 2024

J Cataract Refract Surg

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Purpose: To determine if the infusion pressure used during phacoemulsification may have a detrimental effect on the Anterior Hyaloid Membrane Barrier (AHMB) in a pressure fluctuation-free environment via diagnostic SD-OCT post-operatively. Setting: Tandil Eye Clinic, Tandil, Buenos Aires, Argentina and Centro Oftalmológico Dr. Charles, CABA, Buenos Aires, Argentina. Design: Prospective randomized multicenter experimental and double-masked study. Methods: Phacoemulsification with intraocular lens implantation was done in all patients with the Centurion Vision System equipment with Active Fluidics and Active Sentry. Patients were randomly assigned to configuration 1 or 2. Configuration 1 intraocular pressure (IOP) 30 mmHg and configuration 2 intraocular pressure (IOP) 80 mmHg. Inclusion criteria: axial length > 22 mm < 25 mm, age > 50 < 70 years, complete adhesion of AHMB. Results: 80 eyes of 80 patients were included. Berger space was identified in 17 cases (42.5%) of group 2 and 3 cases (7.5%) of group 1 postoperatively via SD-OCT. A statistically significant relationship was established using Fisher's exact test (P = 0.0003). Postoperatively we observed PVD changes in only one patient (1.25%) during the three months of follow-up (p = 0.5). According to the Wong Baker faces scale, the patient's subjective perception was better for the low infusion pressure group (p = 0.0001 Fisher's exact test). Conclusions: Phacoemulsification with high infusion pressure can change the vitreous-lens interface. Positive Berger's space after phacoemulsification is a biomarker of this change and can occur in eyes without risk factors. Incidence is directly related to the infusion pressure used.

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Section: Discussionsupporting

confidence: 92%

Vitreous-lens interface changes after cataract surgery using active fluidics and active sentry with high and low infusion pressure settings

Scarfone,

Rodriguez,

Rufiner

et al. 2024

J Cataract Refract Surg

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“…This phenomenon has not been previously reported. Actually, loss or swelling of photoreceptors has been observed in various animal glaucoma models and in clinical glaucoma patients (Panda and Jonas, 1992;Nork et al, 2000;Choi et al, 2011;Zhao et al, 2020). Overall, our results demonstrated that repeated rapid IOP transients at 50 mmHg can cause injury to all three major retinal nuclear layers.…”

Section: Discussionsupporting

confidence: 65%

“…Eyes were fully dilated bilaterally using 1% (0.01 g/mL) tropicamide and topically anesthetized with 0.5% (5 g/L) tetracaine hydrochloride. Then a 32-gauge needle connected to a column of saline (0.9% (9 g/L) NaCl) was inserted into the anterior chamber of the right eye, as previously described (Zhao et al, 2020). The peak IOP value was set at 50 mmHg by positioning the column at the appropriate height.…”

Section: Establishment Of a Spike Iop Mouse Modelmentioning

confidence: 99%

Endoplasmic reticulum stress is involved in retinal injury induced by repeated transient spikes of intraocular pressure

Yang

Zhao

et al. 2021

J. Zhejiang Univ. Sci. B

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Clinically, a large proportion of glaucoma patients undergo repeated intraocular pressure (IOP) spike (Spike IOP) attacks during their sleep, which may facilitate retinopathy. In this study, we established a mouse model of repeated transient Spike IOP to investigate the direct damage to the retina following Spike IOP attacks, and elucidated the underlying molecular mechanism. We analyzed the changes in the number of retinal ganglion cells (RGCs) via immunofluorescence. Thereafter, we detected retinal cell apoptosis via terminal deoxynucleotidyl transferase deoxyuridine triphosphate (dUTP) nick-end labeling (TUNEL) staining, and performed RNA sequencing (RNA-seq) to reveal the underlying molecular mechanism. Finally, we validated the expression of key molecules in the endoplasmic reticulum (ER) stress pathway using quantitative real-time polymerase chain reaction (qRT-PCR) and western blot analysis. Results revealed a time-dependent RGC loss in Spike IOP, evidenced by a reduction in the number of Brn3a-positive RGCs in experimental eyes following a 7-d continuous treatment with Spike IOP. In addition, TUNEL staining indicated that apoptosis of retinal cells started in the outer nuclear layer (ONL), and then spread to the ganglion cell layer (GCL) with time. RNA-seq analysis revealed that ER stress might be involved in Spike IOP-induced retinal injury. This result was corroborated by western blot, which revealed upregulation of ER stress-related proteins including binding immunoglobulin protein/glucose-regulated protein 78 (BiP/GRP78), phosphorylated inositolrequiring enzyme 1 (p-IRE1), unspliced X-box-binding protein 1 (XBP1-u), spliced X-box-binding protein 1 (XBP1-s), phosphorylated c-Jun N-terminal kinase (p-JNK), C/EBP-homologous protein (CHOP), and B-cell lymphoma 2 (Bcl-2)associated X protein (Bax). These findings indicate that repeated IOP transients are detrimental to the retina, while ER stress plays an important role in retinal cell apoptosis in this situation. Notably, repeated Spike IOP among glaucoma patients is a crucial factor for progressive retinopathy.

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“…Such high pressures may induce impairment of perfusion of the optic nerve, retina, and choroid [ 11 ]. A recent study of acute ocular hypertension on a mouse model, that mimics a transient IOP elevation during phacoemulsification, concluded that operating at a higher intraocular pressure (90 mmHg setting vs. 45 mmHg setting) causes cellular and molecular retinal injuries [ 12 ]. All these previous studies suggest that operating on high bottle height/ target IOP settings can negatively affect the anatomy and physiology of the eye ( Fig.…”

Section: Discussionmentioning

confidence: 99%

Does low infusion pressure microincision cataract surgery (LIPMICS) reduce frequency of post-occlusion breaks?

Beres

Ortueta²,

Buehner³

et al. 2022

rjo

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Elevated intraocular pressure causes cellular and molecular retinal injuries, advocating a more moderate intraocular pressure setting during phacoemulsification surgery

Cited by 9 publications

References 54 publications

Vitreous-lens interface changes after cataract surgery using active fluidics and active sentry with high and low infusion pressure settings

Vitreous-lens interface changes after cataract surgery using active fluidics and active sentry with high and low infusion pressure settings

Endoplasmic reticulum stress is involved in retinal injury induced by repeated transient spikes of intraocular pressure

Does low infusion pressure microincision cataract surgery (LIPMICS) reduce frequency of post-occlusion breaks?

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