Unilateral Acute Angle-closure Glaucoma Research Articles

Unilateral acute angle-closure glaucoma as an unusual presentation of Vogt–Koyanagi–Harada disease: A diagnostic challenge

Vogt–Koyanagi–Harada syndrome is an inflammatory multisystem disorder with ocular, cutaneous and neurological manifestations occurring more commonly in certain dark-skinned ethnic groups such as Asians, patients of Middle-Eastern heritage, and hispanics. Only a few reports have described a masquerade presentation of acute angle closure as an initial manifestation for this uveitic entity, which is typically characterized by panuveitis with serous retinal detachments. This has almost always led to misdiagnosis, unwarranted surgical interventions, and a delay of appropriate timely therapy. In this report, we describe an unusual case of acute unilateral Harada disease presenting as acute angle-closure glaucoma that has remitted following institution of appropriate therapy.

Ciliochoroidal Effusion Syndrome Associated with Posterior Scleritis

To determine the cause of angle-closure glaucoma in a case of posterior scleritis. The patient was a 65-year-old woman with unilateral acute angle-closure glaucoma who did not respond to laser iridotomy. Slit-lamp examination demonstrated a shallow anterior chamber in the left eye. Intraocular pressure was 22 mmHg even after application of two antiglaucoma eye-drop preparations. B-scan ultrasonography demonstrated scleral thickening and choroidal detachment in the left eye. Ultrasound biomicroscopy showed a shallow anterior chamber with angle closure, annular ciliochoroidal effusion with ciliary body edema, and an anterior rotation of the ciliary body. After instillation of cycloplegics, the ciliary body and ciliary processes rotated posteriorly, resulting in the release of the pressure on the iris. These changes led to the opening of the angle and subsequent normalization of intraocular pressure. A diagnosis was made of ciliochoroidal effusion syndrome associated with posterior scleritis. Patients with posterior scleritis can develop ciliochoroidal effusion syndrome, which can lead to angle-closure glaucoma. The therapeutic strategy for acute angle-closure glaucoma induced by ciliochoroidal effusion syndrome differs completely from that for acute angle-closure glaucoma with pupillary block. In the case of ciliochoroidal effusion syndrome, it is important to relieve the compression of the angle by the iris by displacing the lens-iris diaphragm posteriorly by cycloplegics.

Akutes Winkelblockglaukom nach massiver intraokularer Blutung bei exsudativer altersbedingter Makuladegeneration unter gerinnungshemmender Therapie

Acute secondary angle closure glaucoma after massive vitreous and subretinal hemorrhage from exudative age related macular degeneration is a seldom, but devastating complication of an anticoagulative therapy. Four patients (age range 70-76 years) developed unilateral acute angle closure glaucoma after massive intraocular bleeding due to exudative age-related macular degeneration and anticoagulative therapy. Three patients received Phenprocomoun and one patient thrombolytic therapy with heparin. One eye had led to blindness at initial investigation. Pars plana vitrectomy was performed in the remaining three eyes. Within a few months, 2 of these 3 eyes were blind, one eye had light perception and all three eyes developed hypotonia. Acute angle closure glaucoma after intraocular bleeding may be the initial clinical manifestation of overtreatment with anticoagulants. Early pars plana vitrectomy probably will increase the surveillance rate of the eye but not the visual prognosis.

Corneal Endothelial Changes in Primary Acute Angle-closure Glaucoma

In 20 patients, corneal endothelium was examined by specular microscopy after acute angle-closure glaucoma, and before any surgical treatment in order to assess possible damage during pressure induced abnormal hydration of the cornea. The mean intraocular pressure was elevated to 55 mm Hg and had lasted, on an average, 47 (5–192) hours. The mean endothelial cell density in the affected eye was 1534 and in the nonaffected fellow eye 2243 cells/mm2 (mean decrease 33%, P = 0.002). The amount of cell loss correlates with the duration of the intraocular pressure increase. Thirty-five percent of these patients presented a bilateral cornea guttata. This high incidence of endothelial dystrophy was confirmed in a retrospective specular microscopic study in 20 patients with a history of unilateral acute angle-closure glaucoma. The decreased number of endothelial cells after acute angle-closure glaucoma frequently combined with bilateral cornea guttata, accounts for the corneal degeneration in these patients following a later cataract extraction.

Recurrent Orbital and Metastatic Melanoma in a Patient Undergoing Previous Glaucoma Surgery

A 61-year-old woman had unilateral acute angle-closure glaucoma and subsequently underwent a Scheie filtering operation. After a two-week interval, a large choroidal and ciliary body melanoma in the glaucomatous eye was found. No evidence of metastatic disease was found and the eye was enucleated. Histopathologic sections did not show extrascleral extension. Two and one-half years later the patient developed local orbital recurrence of the melanoma and fatal metastatic disease. We hypothesized a possible causal relationship between the filtering surgery and the local and systemic recurrence of the tumor.