Temporary Filtering Bleb Failure Induced by Anterior Chamber Sulfur Hexafluoride Gas: A Complication after Descemet Membrane Endothelial Keratoplasty

Herein, we report two clinical cases with acute temporary filtering bleb obstruction by gas tamponade after Descemet membrane endothelial keratoplasty (DMEK) surgery and postoperative intraocular pressure (IOP) peaks. Both patients underwent uncomplicated DMEK surgery with 20% sulfur hexafluoride (SF6) anterior chamber tamponade and had previous trabeculectomy for glaucoma. Prior to surgery, both patients showed patent bleb function with low to normal IOP without antiglaucomatous medication. After uneventful DMEK surgery, both patients showed postoperative IOP peaks of up to 50 mm Hg despite patent inferior iridotomy and no sign of a pupillary block. In both cases, SF6 gas bubbles could be visualized obstructing the bleb. Both patients were treated with IOP-lowering agents topically as well as systemically. In addition, anterior chamber paracenteses were performed to reduce the SF6 volume within the anterior chamber. Under this treatment, IOP normalized within the first 18 h after surgery. We hypothesize that the SF6 gas tamponade from the anterior chamber migrates into the ostium and below the bleb, leading to an acute temporary insufficiency of bleb function and to a consecutive IOP peak after surgery. In contrast to a pupillary block, this mechanism cannot be antagonized by preoperative iridotomy and needs to be taken into account for every glaucoma patient with functional bleb undergoing DMEK surgery

Brittle Cornea Syndrome: Case Report with Novel Mutation in the PRDM5 Gene and Review of the Literature

A 3-year-old boy presented with acute corneal hydrops on the left eye and spontaneous corneal rupture on the right eye. A diagnosis of brittle cornea syndrome was confirmed by molecular analysis. A novel mutation, the homozygous variant c.17T>G, p.V6G, was found in the gene for PR-domain-containing protein 5 (PRDM5) in exon 1. Brittle cornea syndrome is a rare connective tissue disease with typical ocular, auditory, musculoskeletal, and cutaneous disorders. Almost all patients suffer from declined vision due to corneal scarring, thinning, and rupture. The most common ophthalmologic findings include keratoconus, progressive central corneal thinning, high myopia, irregular astigmatism, retinal detachment, and high risk for spontaneous corneal or scleral rupture. In addition to describing the case with a novel mutation here we review the current literature on brittle cornea syndrome pathogenesis, clinical findings, and therapy

Eyelid aging: pathophysiology and clinical management

Life expectancy is increasing in most countries. With increasing age, many individuals may develop involutional ophthalmic diseases, such as eyelid aging. Dermatochalasis, ptosis, ectropion, and entropion are common disorders in middle-aged and older adults. This review outlines the pathophysiology and clinical management of these involutional eyelid disorders. Recently, a decrease in elastic fibers with ultrastructural abnormalities and an overexpression of elastin-degrading enzymes have been demonstrated in involutional ectropion and entropion. This may be the consequence of local ischemia, inflammation, and/or chronic mechanical stress. Eyelid aging with progressive loss of tone and laxity may affect the ocular surface and adnexal tissues, resulting in different clinical symptoms and signs. Surgical management depends on the appropriate correction of the underlying anatomical defect