CASE REPORT
Uveal Effusion as a Mechanism of Bilateral Angle-Closure Glaucoma Induced by Chlorthalidone James R. Singer, DO,*w Zachary D. Pearce, DO,*w Scott J. Westhouse, DO,*w and Karl J. Siebert, MD*w
Purpose: To report a novel case of acute bilateral uveal effusions, angle closure, and acute myopia induced by administration of chlorthalidone. Methods: Case report. Results: Bilateral shallow anterior chambers, high intraocular pressure, and a myopic shift were encountered in a patient 1 week after initiation of chlorthalidone. Ultrasound evaluation revealed bilateral ciliochoroidal effusions, appositional angle closure, and suspected ciliary body edema. Cessation of chlorthalidone, in addition to administration of cycloplegics and ocular antihypertensives, resulted in prompt resolution of this idiosyncratic reaction. Conclusions: The antihypertensive medication chlorthalidone may cause bilateral uveal effusions inducing acute angle-closure glaucoma and acute myopia. Key Words: uveal effusion, ciliary body edema, acute myopia, angle-closure glaucoma, medication reaction, sulfonamide, chlorthalidone, choroidal effusion, supraciliary effusion, ultrasound
(J Glaucoma 2015;24:84–86)
observed. Treatment was initiated with oral acetazolamide (250 mg) thrice daily, and timolol-brimonidine (Combigan; Allergan, Irvine, CA) drops twice daily OU. A monocular trial of pilocarpine 1% drops was started 3 times daily OS given the gonioscopic findings suggestive of plateau iris. The patient was advised to discontinue chlorthalidone. A day later, the patient’s uncorrected vision was 20/200 OD and 20/50 OS. IOP was 13 OD and 12 mm Hg OS, the angles remained closed, and anterior chambers remained shallow. A Bscan ultrasonogram was obtained which revealed shallow bilateral peripheral choroidal effusions (Fig. 1A). Concomitant bilateral ciliochoroidal effusions, anterior displacement of the lens-iris diaphragm, and suspected ciliary body edema were observed with ultrasound biomicroscopy (UBM) (Figs. 1B, C). Treatment with oral and topical aqueous suppressants was continued, pilocarpine discontinued, and cycloplegia initiated with cyclopentolate 1% 3 times daily OU. Three days later uncorrected vision improved to 20/20 OU, IOP remained normal, and deepening of the anterior chamber was noted. A follow-up UBM was performed 8 months after her initial presentation (Fig. 2). This revealed complete resolution of the ciliochoroidal effusions, return of the lens-iris diaphragm to a more posterior position, and subjectively observed improvement of the suspected ciliary body edema. The ultrasound images retrospectively collected for this manuscript precluded accurate measurement of the ciliary body thickness. As such, the definitive presence of ciliary body edema could not be determined.
CASE DESCRIPTION A 38-year-old Hispanic woman presented with acute bilateral vision loss, eye pain, and bifrontal cephalgia after initiation of oral chlorthalidone (12.5 mg daily) for treatment of systemic hypertension. Symptoms began approximately 7 days after the first dose and progressively worsened prompting her to seek emergent evaluation. Past medical history was significant for newly diagnosed hypertension. There was no prior history of ocular disease or refractive error. Examination revealed uncorrected vision of 20/80 OD (right eye) and 20/400 OS (left eye). Vision was correctable to 20/20 OD and 20/30 OS with 4.00 + 0.75 090 OD and 3.50 + 0.50 115 OS. Intraocular pressure (IOP) was 35 OD and 37 mm Hg OS. Pupillary reactions were sluggish but present. Slitlamp examination revealed shallow anterior chambers and minimal cataract formation in both eyes (OU). Gonioscopy revealed complete 360-degree appositional angle-closure OU with suspected plateau iris configuration. Nondilated funduscopic examination revealed optic nerves with moderate-sized cups and normalappearing fundi. Peripherally, no choroidal effusions were Received for publication September 13, 2013; accepted November 20, 2013. From the *Department of Ophthalmology Michigan State University, East Lansing; and wMetro Health Hospital, Wyoming, MI. Disclosure: The authors declare no conflict of interest. Reprints: James R. Singer, DO, Metro Health Hospital, 2221 Health Dr SW, Suite 1100, Wyoming, MI 49519 (e-mail: [email protected]). Copyright r 2014 by Lippincott Williams & Wilkins DOI: 10.1097/IJG.0000000000000037
84 | www.glaucomajournal.com
COMMENTS Antibiotics and hypertension/diuretic medications comprise the 2 main classes of sulfonamides.1 Shortly after the discovery of sulfonamides in the 1930s, the first report of associated acute transient myopia was reported in 1938.1,2 Subsequently, transient acute myopia and angle-closure glaucoma have been described after administration of multiple sulfonamide medications.1 More recently, multiple cases of topiramate-induced (Topamax; Ortho-McNeil-Jannsen Pharmaceuticals, Raritan, NJ) angle closure have been reported.1 Chlorthalidone, a sulfa-containing hypertension medication, has previously been reported to cause acute myopia.2–6 Chlorthalidone is also present in combination formulations. To the best of our knowledge, no cases of acute angle-closure glaucoma induced by chlorthalidone have been published to date. We report a novel case of acute bilateral angle-closure glaucoma, confirmed by ultrasound, and transient myopia induced by administration of chlorthalidone. The pathophysiology of acute myopia and angle-closure glaucoma in association with sulfonamides is controversial. Suggested etiologies include accommodative spasm, change in lens thickness, ciliary body edema, and supraciliary or suprachoroidal effusions.1 The biochemical etiology of the ciliary body swelling is unknown, but is postulated to be prostaglandin mediated.1 Ciliary body edema leads to anterior displacement of the lens-iris J Glaucoma
Volume 24, Number 1, January 2015
J Glaucoma
Volume 24, Number 1, January 2015
Angle-Closure Glaucoma Induced by Chlorthalidone
FIGURE 1. A, Longitudinal B-scan ultrasonogram demonstrating a shallow peripheral choroidal detachment (arrow). B, Ultrasound biomicroscopy (UBM) of the anterior segment showing appositional angle closure (arrow) due to anterior displacement of the lens-iris diaphragm complex. Possible ciliary body thickening due to presumed edema (double-headed arrow). C, UBM demonstrating the presence of a ciliochoroidal effusion (arrow).
diaphragm thereby precipitating acute myopia. Forward rotation of the lens-iris diaphragm predisposes the angle to appositional closure and elevated IOP. A high level of clinical suspicion for drug-induced reactions (especially to sulfonamides) must be maintained when bilateral angle-closure glaucoma in association with acute myopia is observed. This constellation of findings should prompt a thorough medication history. Furthermore, diagnostic testing including B-scan ultrasonography, UBM, and/or anterior segment optical coherence tomography should be considered to evaluate for uveal effusions, ciliary body edema, and anterior movement of the lens-iris diaphragm. In cases of isolated acute myopia, the mainstay of treatment includes initiation of cycloplegia and cessation of precipitating medications. Cases associated with acute angle-closure glaucoma may be amenable to oral and/or topical ocular aqueous suppressants. Symptoms typically resolve within days of stopping the medication. Use of corticosteroids may also be considered to stabilize the blood/aqueous and blood/retina barrier, thereby promoting resolution of the edema and effusions, although this was not required in our case. Miotics should be avoided as they may further stimulate anterior movement of the lensiris diaphragm effectively worsening the condition. In our patient, a monocular trial of pilocarpine was initiated due to suspected plateau iris configuration causing secondary angle closure. However, upon discovery of the bilateral uveal effusions the next day it became apparent the patient was instead experiencing an idiosyncratic medicationassociated reaction. The pilocarpine was discontinued and appropriate treatment was then promptly initiated. Timely evaluation and treatment of this rare reaction generally results in resolution of symptoms and good outcomes. ACKNOWLEDGEMENT
FIGURE 2. Ultrasound biomicroscopy (UBM) of the anterior segment during follow-up examination 8 months after the initial reaction. A, The anterior chamber has deepened and the angle opened (arrow) after return of the lens-iris diaphragm to a more posterior position. B, Complete resolution of the supraciliary uveal effusion is noted (arrow) and the suspected ciliary body thickening has improved (double-headed arrow). r
2014 Lippincott Williams & Wilkins
The authors thank Dr Thomas Aaberg, Jr, MD, for his assistance in obtaining and reviewing several of the ultrasound images in this manuscript. REFERENCES 1. Panday VA, Rhee DJ. Review of sulfonamide-induced acute myopia and acute bilateral angle-closure glaucoma. Compr Ophthalmol Update. 2007;8:271–276.
www.glaucomajournal.com |
85
Singer et al
2. Ericson LA. Hygroton-induced myopia and retinal edema. Acta Ophthalmol. 1963;41:538–543. 3. Michaelson JJ. Transient myopia due to hygroton. Am J Ophthalmol. 1962;54:1146–1147. 4. Weinstock FJ. Transient severe myopia. JAMA. 1971;217: 1245–1246.
86 | www.glaucomajournal.com
J Glaucoma
Volume 24, Number 1, January 2015
5. D’Alenda P, Robinson M. Hygroton-induced myopia. Calif Med. 1969;110:134–135. 6. Mahesh G, Giridhar A, Saikumar S, et al. Drug-induced acute myopia following chlorthalidone treatment. Indian J Ophthalmol. 2007;55:386–388.
r
2014 Lippincott Williams & Wilkins
Uveal Effusion as a Mechanism of Bilateral Angle-Closure Glaucoma Induced by Chlorthalidone James R. Singer, DO,*w Zachary D. Pearce, DO,*w Scott J. Westhouse, DO,*w and Karl J. Siebert, MD*w
Purpose: To report a novel case of acute bilateral uveal effusions, angle closure, and acute myopia induced by administration of chlorthalidone. Methods: Case report. Results: Bilateral shallow anterior chambers, high intraocular pressure, and a myopic shift were encountered in a patient 1 week after initiation of chlorthalidone. Ultrasound evaluation revealed bilateral ciliochoroidal effusions, appositional angle closure, and suspected ciliary body edema. Cessation of chlorthalidone, in addition to administration of cycloplegics and ocular antihypertensives, resulted in prompt resolution of this idiosyncratic reaction. Conclusions: The antihypertensive medication chlorthalidone may cause bilateral uveal effusions inducing acute angle-closure glaucoma and acute myopia. Key Words: uveal effusion, ciliary body edema, acute myopia, angle-closure glaucoma, medication reaction, sulfonamide, chlorthalidone, choroidal effusion, supraciliary effusion, ultrasound
(J Glaucoma 2015;24:84–86)
observed. Treatment was initiated with oral acetazolamide (250 mg) thrice daily, and timolol-brimonidine (Combigan; Allergan, Irvine, CA) drops twice daily OU. A monocular trial of pilocarpine 1% drops was started 3 times daily OS given the gonioscopic findings suggestive of plateau iris. The patient was advised to discontinue chlorthalidone. A day later, the patient’s uncorrected vision was 20/200 OD and 20/50 OS. IOP was 13 OD and 12 mm Hg OS, the angles remained closed, and anterior chambers remained shallow. A Bscan ultrasonogram was obtained which revealed shallow bilateral peripheral choroidal effusions (Fig. 1A). Concomitant bilateral ciliochoroidal effusions, anterior displacement of the lens-iris diaphragm, and suspected ciliary body edema were observed with ultrasound biomicroscopy (UBM) (Figs. 1B, C). Treatment with oral and topical aqueous suppressants was continued, pilocarpine discontinued, and cycloplegia initiated with cyclopentolate 1% 3 times daily OU. Three days later uncorrected vision improved to 20/20 OU, IOP remained normal, and deepening of the anterior chamber was noted. A follow-up UBM was performed 8 months after her initial presentation (Fig. 2). This revealed complete resolution of the ciliochoroidal effusions, return of the lens-iris diaphragm to a more posterior position, and subjectively observed improvement of the suspected ciliary body edema. The ultrasound images retrospectively collected for this manuscript precluded accurate measurement of the ciliary body thickness. As such, the definitive presence of ciliary body edema could not be determined.
CASE DESCRIPTION A 38-year-old Hispanic woman presented with acute bilateral vision loss, eye pain, and bifrontal cephalgia after initiation of oral chlorthalidone (12.5 mg daily) for treatment of systemic hypertension. Symptoms began approximately 7 days after the first dose and progressively worsened prompting her to seek emergent evaluation. Past medical history was significant for newly diagnosed hypertension. There was no prior history of ocular disease or refractive error. Examination revealed uncorrected vision of 20/80 OD (right eye) and 20/400 OS (left eye). Vision was correctable to 20/20 OD and 20/30 OS with 4.00 + 0.75 090 OD and 3.50 + 0.50 115 OS. Intraocular pressure (IOP) was 35 OD and 37 mm Hg OS. Pupillary reactions were sluggish but present. Slitlamp examination revealed shallow anterior chambers and minimal cataract formation in both eyes (OU). Gonioscopy revealed complete 360-degree appositional angle-closure OU with suspected plateau iris configuration. Nondilated funduscopic examination revealed optic nerves with moderate-sized cups and normalappearing fundi. Peripherally, no choroidal effusions were Received for publication September 13, 2013; accepted November 20, 2013. From the *Department of Ophthalmology Michigan State University, East Lansing; and wMetro Health Hospital, Wyoming, MI. Disclosure: The authors declare no conflict of interest. Reprints: James R. Singer, DO, Metro Health Hospital, 2221 Health Dr SW, Suite 1100, Wyoming, MI 49519 (e-mail: [email protected]). Copyright r 2014 by Lippincott Williams & Wilkins DOI: 10.1097/IJG.0000000000000037
84 | www.glaucomajournal.com
COMMENTS Antibiotics and hypertension/diuretic medications comprise the 2 main classes of sulfonamides.1 Shortly after the discovery of sulfonamides in the 1930s, the first report of associated acute transient myopia was reported in 1938.1,2 Subsequently, transient acute myopia and angle-closure glaucoma have been described after administration of multiple sulfonamide medications.1 More recently, multiple cases of topiramate-induced (Topamax; Ortho-McNeil-Jannsen Pharmaceuticals, Raritan, NJ) angle closure have been reported.1 Chlorthalidone, a sulfa-containing hypertension medication, has previously been reported to cause acute myopia.2–6 Chlorthalidone is also present in combination formulations. To the best of our knowledge, no cases of acute angle-closure glaucoma induced by chlorthalidone have been published to date. We report a novel case of acute bilateral angle-closure glaucoma, confirmed by ultrasound, and transient myopia induced by administration of chlorthalidone. The pathophysiology of acute myopia and angle-closure glaucoma in association with sulfonamides is controversial. Suggested etiologies include accommodative spasm, change in lens thickness, ciliary body edema, and supraciliary or suprachoroidal effusions.1 The biochemical etiology of the ciliary body swelling is unknown, but is postulated to be prostaglandin mediated.1 Ciliary body edema leads to anterior displacement of the lens-iris J Glaucoma
Volume 24, Number 1, January 2015
J Glaucoma
Volume 24, Number 1, January 2015
Angle-Closure Glaucoma Induced by Chlorthalidone
FIGURE 1. A, Longitudinal B-scan ultrasonogram demonstrating a shallow peripheral choroidal detachment (arrow). B, Ultrasound biomicroscopy (UBM) of the anterior segment showing appositional angle closure (arrow) due to anterior displacement of the lens-iris diaphragm complex. Possible ciliary body thickening due to presumed edema (double-headed arrow). C, UBM demonstrating the presence of a ciliochoroidal effusion (arrow).
diaphragm thereby precipitating acute myopia. Forward rotation of the lens-iris diaphragm predisposes the angle to appositional closure and elevated IOP. A high level of clinical suspicion for drug-induced reactions (especially to sulfonamides) must be maintained when bilateral angle-closure glaucoma in association with acute myopia is observed. This constellation of findings should prompt a thorough medication history. Furthermore, diagnostic testing including B-scan ultrasonography, UBM, and/or anterior segment optical coherence tomography should be considered to evaluate for uveal effusions, ciliary body edema, and anterior movement of the lens-iris diaphragm. In cases of isolated acute myopia, the mainstay of treatment includes initiation of cycloplegia and cessation of precipitating medications. Cases associated with acute angle-closure glaucoma may be amenable to oral and/or topical ocular aqueous suppressants. Symptoms typically resolve within days of stopping the medication. Use of corticosteroids may also be considered to stabilize the blood/aqueous and blood/retina barrier, thereby promoting resolution of the edema and effusions, although this was not required in our case. Miotics should be avoided as they may further stimulate anterior movement of the lensiris diaphragm effectively worsening the condition. In our patient, a monocular trial of pilocarpine was initiated due to suspected plateau iris configuration causing secondary angle closure. However, upon discovery of the bilateral uveal effusions the next day it became apparent the patient was instead experiencing an idiosyncratic medicationassociated reaction. The pilocarpine was discontinued and appropriate treatment was then promptly initiated. Timely evaluation and treatment of this rare reaction generally results in resolution of symptoms and good outcomes. ACKNOWLEDGEMENT
FIGURE 2. Ultrasound biomicroscopy (UBM) of the anterior segment during follow-up examination 8 months after the initial reaction. A, The anterior chamber has deepened and the angle opened (arrow) after return of the lens-iris diaphragm to a more posterior position. B, Complete resolution of the supraciliary uveal effusion is noted (arrow) and the suspected ciliary body thickening has improved (double-headed arrow). r
2014 Lippincott Williams & Wilkins
The authors thank Dr Thomas Aaberg, Jr, MD, for his assistance in obtaining and reviewing several of the ultrasound images in this manuscript. REFERENCES 1. Panday VA, Rhee DJ. Review of sulfonamide-induced acute myopia and acute bilateral angle-closure glaucoma. Compr Ophthalmol Update. 2007;8:271–276.
www.glaucomajournal.com |
85
Singer et al
2. Ericson LA. Hygroton-induced myopia and retinal edema. Acta Ophthalmol. 1963;41:538–543. 3. Michaelson JJ. Transient myopia due to hygroton. Am J Ophthalmol. 1962;54:1146–1147. 4. Weinstock FJ. Transient severe myopia. JAMA. 1971;217: 1245–1246.
86 | www.glaucomajournal.com
J Glaucoma
Volume 24, Number 1, January 2015
5. D’Alenda P, Robinson M. Hygroton-induced myopia. Calif Med. 1969;110:134–135. 6. Mahesh G, Giridhar A, Saikumar S, et al. Drug-induced acute myopia following chlorthalidone treatment. Indian J Ophthalmol. 2007;55:386–388.
r
2014 Lippincott Williams & Wilkins
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