Has the EAGLE landed for the use of clear lens extraction in angle-closure glaucoma? And how should primary angle-closure suspects be treated?

Tanner, Luke; Gazzard, Gus; Nolan, Winifred; Foster, Paul J.

doi:10.1038/s41433-019-0634-5

Cited by 18 publications

(12 citation statements)

References 78 publications

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“…Table 2 presents the key preoperative, intraoperative, and postoperative factors requiring management in patients undergoing phaco with previous AAC [10][11][12][13][14][15][16].…”

Section: Discussionmentioning

confidence: 99%

Lessons From Management: Perioperative Phacoemulsification Planning Following Resolution of Acute Angle Closure

Lee¹,

Lau²,

Wong³

et al. 2021

Cureus

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Patients with loose zonular apparatus after acute angle closure may require phacoemulsification cataract surgery. The authors' experience from management of such patients provides excellent instruction on the surgical intervention for their cataracts. This is because patients who have recovered from acute angle closure glaucoma may not have evident zonular laxity preoperatively, as the iris may be taut secondary to the effects of associated ischaemia. If the surgeon's preoperative planning is directed to the possibility of loose zonular apparatus, then appropriate preoperative, intraoperative, and postoperative planning and management can be effected. This may permit preoperative patient counselling regarding the potentially increased complexity of the case. Intraoperatively, deliberately gentle capsulorrhexis, the use of iris hooks or a pupil expander to dilate the pupil, iris hooks to support the capsular bag, and the employment of a capsular tension ring may be helpful. Postoperatively, due to the previous ocular ischaemia, intraocular pressure elevation may ensue, and should be actively managed. The authors provide a summary of factors that require consideration in patients undergoing cataract surgery following acute angle closure.

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“…Table 2 presents the key preoperative, intraoperative, and postoperative factors requiring management in patients undergoing phaco with previous AAC [10][11][12][13][14][15][16].…”

Section: Discussionmentioning

confidence: 99%

Lessons From Management: Perioperative Phacoemulsification Planning Following Resolution of Acute Angle Closure

Lee¹,

Lau²,

Wong³

et al. 2021

Cureus

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“…Acute glaucoma, which remains the most common glaucoma type among Asians, is predicted to affect 20 million people worldwide and is characterized by a sudden and substantial increase in intraocular pressure (IOP), severe eye pain, and irreversible vision loss that can progress to permanent blindness [1][2][3]. The rapid elevation in IOP leads to retinal ischemia/ reperfusion (RIR) injury and retinal ganglion cells (RGCs) death [4].…”

Section: Introductionmentioning

confidence: 99%

NLRP12 collaborates with NLRP3 and NLRC4 to promote pyroptosis inducing ganglion cell death of acute glaucoma

Chen

Deng

Gan

et al. 2020

Mol Neurodegeneration

109

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Background: Acute glaucoma, characterized by a sudden elevation in intraocular pressure (IOP) and retinal ganglion cells (RGCs) death, is a major cause of irreversible blindness worldwide that lacks approved effective therapies, validated treatment targets and clear molecular mechanisms. We sought to explore the potential molecular mechanisms underlying the causal link between high IOP and glaucomatous RGCs death.Methods: A murine retinal ischemia/ reperfusion (RIR) model and an in vitro oxygen and glucose deprivation/ reoxygenation (OGDR) model were used to investigate the pathogenic mechanisms of acute glaucoma.Results: Our findings reveal a novel mechanism of microglia-induced pyroptosis-mediated RGCs death associated with glaucomatous vision loss. Genetic deletion of gasdermin D (GSDMD), the effector of pyroptosis, markedly ameliorated the RGCs death and retinal tissue damage in acute glaucoma. Moreover, GSDMD cleavage of microglial cells was dependent on caspase-8 (CASP8)-hypoxia-inducible factor-1α (HIF-1α) signaling. Mechanistically, the newly identified nucleotide-binding leucine-rich repeat-containing receptor (NLR) family pyrin domain-containing 12 (NLRP12) collaborated with NLR family pyrin domain-containing 3 (NLRP3) and NLR family CARD domain-containing protein 4 (NLRC4) downstream of the CASP8-HIF-1α axis, to elicit pyroptotic processes and interleukin-1β (IL-1β) maturation through caspase-1 activation, facilitating pyroptosis and neuroinflammation in acute glaucoma. Interestingly, processing of IL-1β in turn magnified the CASP8-HIF-1α-NLRP12/ NLRP3/NLRC4-pyroptosis circuit to accelerate inflammatory cascades.Conclusions: These data not only indicate that the collaborative effects of NLRP12, NLRP3 and NLRC4 on pyroptosis are responsible for RGCs death, but also shed novel mechanistic insights into microglial pyroptosis, paving novel therapeutic avenues for the treatment of glaucoma-induced irreversible vision loss through simultaneously targeting of pyroptosis.

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“…Initial treatment options include Laser Peripheral Iridotomy (LPI), surgical peripheral iridectomy, and Argon Laser Peripheral Iridoplasty (ALPI). [13] Iridotomy is necessary to relieve the pupillary block and reduce to lower the IOP. [14] Refractive surgery such as precise lens extraction may benefit high myopic eyes because the thick lens predisposes patients to angle-closure glaucoma.…”

Section: Discussionmentioning

confidence: 99%

A Rare Case of Chronic Primary Angle-Closure Glaucoma in a Young Woman with Coexisting Pathologic Myopia

Dhiyantari

Nurwasis

Komaratih

et al. 2021

VSEHJ

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Introduction: Primary Angle-Closure Glaucoma (PACG) is usually present in adults older than forty and is more common in hyperopic eyes. Angle-closure is usually related to structural or developmental ocular abnormalities in young individuals. Case presentation: We presented a rare case of PACG in a 32 years old woman with pathologic myopia of -23.0 RLE. The chief complaint was blurring of the right eye three months before the visit. Right eye Intraocular Pressure (IOP) was 30mmHg-38mmHg despite treatment with three intra-ocular pressure-lowering agents. Axial length was 32.36 mm and 31.19 mm RLE. Anterior chamber depth was 2.36 mm and 2.60 mm RLE. Lens thickness was 5.07 mm and 5.40 mm RLE. Signs of GON and pathologic myopia were found in both eyes. GON was present asymmetrically (0.9 and 0.6 RLE), with the myopic crescent as well as baring and peripapillary atrophy. The optic disc was slightly tilted with the myopic crescent. There was also a marked sign of retinal pigment epithelium thinning and attenuation along with myopic chorioretinal atrophy. Conclusions: PACG in a young myopic individual is challenging to diagnose because myopia and glaucoma share similar optic nerve head pathology. Comprehensive examinations including gonioscopy, biometry, and OCT may confirm the diagnosis. In the presented case, angle-closure was caused by thick lenses and a shallow anterior chamber, along with excessively long axial length. Primary angle-closure at a young individual with myopic eyes is highly uncommon. Nonetheless, clinicians should always consider glaucoma even in the presence of high axial length and myopic fundus.

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Has the EAGLE landed for the use of clear lens extraction in angle-closure glaucoma? And how should primary angle-closure suspects be treated?

Cited by 18 publications

References 78 publications

Lessons From Management: Perioperative Phacoemulsification Planning Following Resolution of Acute Angle Closure

Lessons From Management: Perioperative Phacoemulsification Planning Following Resolution of Acute Angle Closure

NLRP12 collaborates with NLRP3 and NLRC4 to promote pyroptosis inducing ganglion cell death of acute glaucoma

A Rare Case of Chronic Primary Angle-Closure Glaucoma in a Young Woman with Coexisting Pathologic Myopia

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