Bilateral Acute Angle Closure Glaucoma Research Articles

Simultaneous Bilateral Acute Angle-closure Glaucoma in a Patient With Subarachnoid Hemorrhage

To present an unusual case of simultaneous bilateral acute angle-closure (AAC) glaucoma in a patient with subarachnoid hemorrhage due to an aneurysm involving the right middle cerebral artery. A 60-year-old woman with a clinically inexplicable bilateral nonreacting mydriasis after brain surgery underwent an ophthalmologic consultancy. The bilateral mydriasis was diagnosed as an unusual clinical presentation of simultaneous bilateral AAC glaucoma. One week after the AAC was bilaterally resolved, the patient underwent echographic examination because of the outbreak of a unilateral relapsed ocular hypertensive attack that required an ultrasound biomicroscopy (UBM) to be accurately diagnosed and treated. The bilateral AAC regressed completely after pharmacologic therapy. UBM evaluation of the eye with recurrence of the angle-closure glaucoma attack was necessary to confirm the diagnosis of unilateral relapsed angle-closure glaucoma due to an unresolved pupillary block. A viscoelastic-aided opening of the angle and peripheral surgical iridectomy were performed. UBM and tonometry were performed intraoperatively to confirm the success of the surgical treatment. The UBM allowed us to identify the pupillary block as the main mechanism involved in the pathogenesis of this unusual case of simultaneous bilateral AAC glaucoma. Despite the fact that drug-induced supraciliary uveal effusion and mydriasis due to surgical anesthesia have been frequently reported to contribute to this complication, we presumed that simultaneous intravenous administration of sedative drugs and adrenergic agonists, in a patient with individual biometric predisposing factors to the angle-closure, created the anatomic conditions which induced the pupillary block with obliteration of the trabeculum.

Measurement of anterior lens growth after acute primary angle-closure glaucoma

Case report: A 51-year-old woman presented with bilateral acute primary angle-closure glaucoma. Glaukomflecken were prominent. Anterior lens growth in front of the glaukomflecken was measured 12 years later.Comments: Lens thickness is important in the pathogenesis of acute primary angle closure, and lens growth can become significant with time in eyes already at risk.

Glaucoma agudo bilateral em paciente jovem secundário ao uso de topiramato: relato de caso

This paper reports a clinical case of uveal effusion in both eyes causing bilateral acute angle closure glaucoma in a young patient after oral administration of topiramate, a new anticonvulsant medication. Rarely, some drugs have produced uveal effusions, forward shift of the iris-lens diaphragm, transient myopia and secondary angle closure glaucoma. A 40-year old white woman was seen at the emergency department of the "Hospital Banco de Olhos de Porto Alegre (RS)"--Brazil, with severe headaches and blurry vision in both eyes. Her medications included topiramate, started 10 days before. Slit lamp examination revealed conjunctival injection, chemosis and shallow anterior chambers. Intraocular pressure measured 40 and 38 mmHg. Fundoscopic examination findings were normal. Ultrasound scan was performed and demonstrated separation between the choroidal layer and the sclera. A diagnosis of bilateral uveal effusion associated with the use of oral topiramate was made. Topiramate was then discontinued. The patient reported symptomatic improvement by the third day after initial examination. Symptoms were resolved and visual acuity returned to normal. Topiramate may cause ciliary body edema and relaxation of zonules, which induces a forward shift of the lens-iris diaphragm with acute myopia and angle closure. As the mechanism of angle closure does not involve pupillary block, peripheral iridectomy and topical miotics are not useful in the treatment of this type of secondary angle-closure glaucoma. Drug-induced uveal effusions occur rarely. The patient improved after topiramate discontinuation.

Bilateral acute angle closure glaucoma as a presentation of isolated microspherophakia in an adult: case report

BackgroundBilateral simultaneous angle closure glaucoma is a rare entity. To our knowledge this is the first reported case of bilateral acute angle-closure glaucoma secondary to isolated microspherophakia in an adult.Case presentationA 45-year-old woman presented with bilateral acute angle closure glaucoma, with a patent iridotomy in one eye. Prolonged miotic use prior to presentation had worsened the pupillary block. The diagnosis was not initially suspected, and the patient was subjected to pars-plana lensectomy and anterior vitrectomy for a presumed ciliary block glaucoma. The small spherical lens was detected intraoperatively, and spherophakia was diagnosed in retrospect. She had no systemic features of any of the known conditions associated with spherophakia. Pars-plana lensectomy both eyes controlled the intraocular pressure successfully.ConclusionThis case demonstrates the importance of considering the diagnosis of isolated microspherophakia in any case of bilateral acute angle closure glaucoma. Lensectomy appears to be an effective first-line strategy for managing these patients.

Escitalopram-Induced Uveal Effusions and Bilateral Angle Closure Glaucoma

To report the onset of bilateral angle closure glaucoma resulting from ciliochoroidal effusions noted after taking escitalopram. Case report. A 41-year-old woman with a medical history of depression was placed on escitalopram and presented with acute bilateral angle closure glaucoma. A medical history and ophthalmic examination (including slit-lamp photography and high-frequency ultrasonography) were performed at the time of diagnosis and at resolution of her symptoms. High-frequency ultrasonography revealed bilateral choroidal effusions with ciliary body detachments and angle closure. Attempts to reduce intraocular pressure with topical ocular antihypertensive drugs and subsequent laser peripheral iridotomy were unsuccessful. Over the course of four days, the use of topical cycloplegics, corticosteroids, and discontinuation of escitalopram resulted in normalization of intraocular pressures, deepening of anterior chamber depths, and resolution of her uveal effusions. The use of escitalopram resulted in uveal effusions, angle rotation, and acute bilateral angle closure glaucoma. Discontinuation of escitalopram and corticosteroid therapy resulted in normalization of the patient's eyes.

Topiramate-induced bilateral angle-closure glaucoma

Case report: We present an interventional case report of a rare occurrence of acute angle-closure glaucoma in a 35-year-old woman presenting 1 week after start of oral topiramate therapy for depression. Intraocular pressure measured 57 mm Hg OD and 56 mm Hg OS, and bilateral shallow anterior chamber and closed angles were observed. Ultrasound disclosed ciliochoroidal detachment, a closed angle with a forward shift of the lens, and swollen ciliary processes. Topiramate treatment was stopped. Antiglaucoma treatment was started and quickly tapered. After 5 days, examination showed deep anterior chambers and normal intraocular pressures with no medication. Comments: Topiramate use can result in acute bilateral angle-closure glaucoma, which is usually reversible if the drug is discontinued. Patients starting topiramate therapy need to be informed of this potential risk.

Bilateral angle‐closure glaucoma following oral topiramate therapy

Editor, T opiramate is a new antiepileptic drug that has been successfully used to treat migraines (Asconape 2002). It is a sulpha-derivative and acts by blocking glutamate receptors, enhancing the effect of the gamma amino butyric acid neurotransmitter (Sankar et al. 2001). We describe a case of bilateral acute angle-closure glaucoma (AACG) following the use of topiramate for migraine. A 51-year-old woman presented to the Eye Accident and Emergency Department with a 24-hour history of bilateral painful red eyes associatedwith amarked reduction of vision in both eyes. She also had photophobia and haloes. She had successfully undergone corneal laser surgery for hypermetropia (RE 0.25DS/þ 3.50@130; LE ?0.25DS/þ 2.75@73) 6months prior to this episode and did not wear any distance glasses. There was no other history of trauma, allergy, skin or joint problems. She suffered with migraines and had been prescribed topiramate 25mg once daily a week before by the neurologist. She had no family history of glaucoma. Examination revealed an unaided visual acuity of counting fingers in both eyes, without any improvement with pinhole. Both eyes had conjunctival congestion with ciliary flush and microcystic corneal epithelial oedema. Both anterior chambers were very shallow, with iridocorneal touch in the left eye. Flare and cells were present in both eyes. The pupils were mid-dilated and reacted only sluggishly to light. Both crystalline lenses exhibited glaucomflecken. The optic discs and maculae were healthy. Intraocular pressure (IOP) was found to be 38mmHg and 44mmHg in the right and left eyes, respectively. A diagnosis of bilateral acute angle-closure glaucoma was made and the patient was treated with intravenous acetazolamide 500mg along with topical steroids (prednisolone forte 1% q.i.d.) and topical beta-blockers (timolol 0.5% b.i.d.). Intraocular pressure dropped to 24mmHg and 28mmHg in the right and left eyes, respectively, within 2– 3 hours of the institution of therapy. Within 24 hours of presentation, bilateral peripheral iridotomy was performed successfully. The patient was advised to stop taking topiramate and was referred to the neurologist for alternative treatment. The patient became symptom-free and her vision returned to normal. Her IOP remained in the normal range and gonioscopy revealed open angles (Schaffer grade III). Her antiglaucoma treatment was tapered off. Many drugs have been reported to precipitate AACG, by either direct or indirect action. The most common cause is sympathomimetic activity caused by diagnostic mydriatics, tricyclic antidepressants, serotonin reuptake inhibitors, diuretics and other propriety medicines (Eke & Carr 1998; Barret & Jordan 2001). A few isolated case reports from the USA have described topiramate as causing AACG (Banta et al. 2001; Sankar et al. 2001; Asconape 2002). The possible mechanism is a swelling of the ciliary body that leads to forward displacement of the lens iris diaphragm, causing occlusion of the angle of the anterior chamber (Banta et al. 2001; Barret & Jordan 2001). To the best of our knowledge this is the first report from the UK of AACG secondary to topiramate use. We suggest that all patients should be warned of the possibility of AACG when topiramate is prescribed.

An uncommon presentation of acute angle closure glaucoma

Acute angle closure glaucoma is an ocular emergency that is treatable with prompt and appropriate intervention. Recognition of this disease entity is sometimes difficult. We report a case of bilateral acute angle closure glaucoma in a 55-year-old, otherwise healthy individual, and discuss the different ways the condition may present. The anatomic and pathophysiologic progression leading to an event of angle closure is discussed and treatment modalities available to the Emergency Physician are presented.

Presumed topiramate-induced bilateral acute angle-closure glaucoma

PURPOSE: We describe a case of bilateral angle-closure glaucoma associated with oral topiramate therapy. METHODS: Interventional case report. Case report with echographic illustration. RESULTS: A 51-year-old man developed bilateral acute angle-closure glaucoma 2 weeks after beginning topiramate therapy for bipolar affective disorder. Laser peripheral iridotomy was performed in the right eye without resolution of the acute attack. Echography revealed lens thickening and ciliochoroidal detachments in both eyes. Visual acuity, intraocular pressure, and anterior and posterior segment anatomy normalized 2 weeks after cessation of topiramate therapy. CONCLUSION: Topiramate, a new sulfa-derivative antiepileptic medication, may cause idiosyncratic ciliochoroidal detachments and ciliary body edema leading to anterior displacement of the lens-iris diaphragm, lens thickening, and acute angle-closure glaucoma.

Laser iridocystotomy for bilateral acute angle-closure glaucoma secondary to iris cysts

PURPOSE: To report laser iridocystotomy for bilateral acute angle-closure glaucoma secondary to peripheral iris cysts. METHOD: Case report. RESULTS: In a 55-year-old man with increased bilateral intraocular pressure, gonioscopy revealed varied angle narrowing. Bilateral angle-closure glaucoma secondary to peripheral iris cysts was diagnosed by ultrasound biomicroscopy. The peripheral iris cysts could not be seen in mydriasis by gonioscopy. Therefore, we decided to perform laser iridocystotomy with argon and Nd:YAG laser. Collapse of the cysts after laser treatment was demonstrated by ultrasound biomicroscopy. At follow-up, 9 months after laser treatment, intraocular pressure had dropped below 20 mm Hg in both eyes without further therapy. The iris cysts did not recur, which was demonstrated by ultrasound biomicroscopy. CONCLUSIONS: Peripheral iris cysts may produce angle closure and may cause secondary angle-closure glaucoma. If transpupillary laser cystotomy is not possible, laser iridocystotomy may produce collapse of the iris cysts and correction of secondary angle closure.

Acute Angle-Closure Glaucoma as a Complication of Combined β-Agonist and Ipratropium Bromide Therapy in the Emergency Department

Acute angle-closure glaucoma is an uncommon complication of inhaled ipratropium bromide therapy for asthma. All previously reported cases have occurred in hospitalized patients receiving continuing nebulized therapy. A 66-year-old woman with asthma returned to the emergency department with bilateral acute angle-closure glaucoma less than 48 hours after successful treatment with nebulized albuterol sulfate and ipratropium bromide given by metered-dose inhaler. Acute angle-closure glaucoma occurring after ipratropium bromide use is believed to result from local ophthalmic effects attributable to topical absorption instead of systemic action. Greater awareness of this complication and suggested preventive measures may lessen morbidity. [Hall SK: Acute angle-closure glaucoma as a complication of combined β-agonist and ipratropium bromide therapy in the emergency department. Ann Emerg Med April 1994;23:884-887.]

Anterior Lamellar Sclerectomy for Nanophthalmos

A 38-year-old woman with nanophthalmos suffered bilateral acute angle closure glaucoma. Peripheral iridotomies were unsuccessful in maintaining low intraocular pressure in either eye. The left eye had probable ciliary block glaucoma and was treated with subsequent pars plana vitrectomy and trabeculectomy. Further postoperative complications included a serous choroidal detachment treated by a lamellar sclerectomy in three quadrants with sclerotomies and drainage of suprachoroidal fluid. These procedures were successful in achieving a well-formed left globe with normal intraocular pressures. The right eye, however, continued to manifest elevated intraocular pressure despite peripheral iridoplasties. Before further intraocular surgery in the right eye, prophylactic lamellar sclerectomies in each quadrant, as well as sclerotomies in the inferior two quadrants, were performed in the hope that preplacement might reduce postoperative sequelae of anticipated filtering surgery and/ or vitrectomy. Surprisingly, the lamellar sclerectomies alone resulted in excellent intraocular pressure control. The pathogenesis of nanophthalmos is discussed in view of this finding.

Acute Angle-Closure Glaucoma in a Patient With Acquired Immunodeficiency Syndrome Successfully Treated With Argon Laser Peripheral Iridoplasty

Laser iridectomy relieves pupillary block and is the procedure of choice for angle-closure glaucoma. Since not all cases of angle closure glaucoma are due to this mechanism, iridectomy is not always curative. Argon laser peripheral iridoplasty causes a contraction of peripheral iris away from the trabecular meshwork, and is useful in these circumstances. We successfully treated bilateral acute angle-closure glaucoma in a patient with acquired immunodeficiency syndrome with this procedure.

Bilateral Angle-Closure Glaucoma in Association with the Acquired Immune Deficiency Syndrome

Two homosexual men, 35 and 42 years old, had bilateral acute angle-closure glaucoma in association with the acquired immune deficiency syndrome. In one patient, the angle-closure attack was the initial manifestation of AIDS. Choroidal effusion with secondary anterior rotation of the ciliary body at the scleral spur appeared to be the pathophysiologic mechanism. Pupillary block, angle crowding, and inflammatory synechial angle closure must be differentiated from anterior rotation of the ciliary body as the mechanism of the angle closure to provide optimal treatment. Whereas primary angle closures are treated with miotics and iridectomy, secondary angle closure may be worsened with this treatment. Cycloplegics and, if necessary, drainage of suprachoroidal fluid may be curative in AIDS-related angle closure associated with a choroidal detachment. Both patients died before the long-term efficacy of this treatment could be assessed.

Acute Angle Closure Glaucoma in a Young Negro Boy

A Negro boy who was also suffering from infectious mononucleosis and acute streptococcal sore throat had an attack of bilateral acute angle closure glaucoma. A bromopheniramine-phenylephrine-phenylpropanolamine mixture may have been a factor in precipitating angle closure.