SURVEY OF OPHTHALMOLOGY
VOLUME 36. NUMBER 4. JANUARY-FEBRUARY 1992
AFTERIMAGES , JONATHAN
WIRTSCHAFTER, EDITOR
Bilateral Angle-Closure Glaucoma Associated with Uveal Effusion: Presenting Sign of HIV Infection ROBERT
W. NASH,
M.D., AND THOMAS
D. LINDQUIST,
M.D., PH.D.
Departmentof Ophthalmology,Universityof Washington, Seattle, Washington
Abstract. A 40-year-old homosexual man presented with acute myopia and bilateral angleclosure glaucoma. Recognition of an anterior chamber configuration of a modestly shallowed central chamber with marked peripheral shallowing clinically suggested uveal effusion. B-scan echography provided definitive, confirmatory evidence of diffuse choroidal thickening with ciliochoroidal effusion. Treatment with aqueous suppressants, cycloplegics, and topical steroids resulted in complete resolution of the angle closure and reversal of induced myopia. The patient, who was systemically well without signs of AIDS or AIDS-related complex, was later tested and found to be serologically-positive for the human immunodeficiency virus. (Surv Ophthalmol 36:255-258, 1992)
Key words. AIDS . angle-closure glaucoma echography human immunodeficiency virus (HIV) uveal effision l
l
glaucoma
l
l
eyes. Past medical and ocular history was unremarkable. Review of systems revealed recent night sweats. Physical examination was remarkable only for the eye findings showing a robust male without regional adenopathy. Eye examination revealed uncorrected visual acuities of 20/200 in the right eye and 201400 in the left eye. External and ocular motility examination was normal. The pupils were equal in size and normally reactive without afferent pupillary defect. Manifest refraction revealed moderate myopia (right eye - 3.25 20/20; left eye - 2.‘75 20/20‘*) with normal corrected acuities. The ocular surface was unremarkable to biomicroscopy. The anterior chamber was quiet; the central chamber was modestly shallowed with marked shallowing of the peripheral chamber for 360”. Gonioscopy revealed appositional closure for 360” without evidence of peripheral anterior synechiae. The iris had no bomb6 or plateau configuration. Intraocular pressure by applanation was 32 mm Hg in each eye.
Bilateral angle-closure glaucoma associated with uveal effusion has been reported in several patients with the acquired immunodeficiency syndrome (AIDS).2s5 Ciliary body swelling leads to forward rotation of the lens-iris diaphragm, causing peripheral anterior chamber shallowing and appositional angle closure without iris bomb& Recognition of a non-pupillary block mechanism of angle closure allows appropriate medical and surgical therapy. Other reported cases have been in patients with diagnosed AIDS or signs of AIDS-related complex (ARC).‘,” We report a case of bilateral uveal effusion with closed-angle glaucoma as the presenting sign of human immunodeficiency virus (HIV) infection.
Case Report A 40-year-old homosexual male presented with complaints of generalized fatigue, bilateral retrobulbar headaches of two weeks’ duration, and decreased distance vision for one day. The patient indicated that he previously had good and equal uncorrected vision reported to be 20120 in both 255
256
Surv Ophthalmol
36 (4) January-February
1992
NASH, LINDQUIST
Fig. 1. B-scan ultrasonography confirmed choroidal thickening with ciliochoroidal effusion bilaterally (arrows). Chatter lines anteriorly are artifactual. A: Right eye scanned equatorially. B: Left eye scanned superiorly.
Fig. 2.
Post-dilation ciliary processes could be readily visualized. Left: Direct illumination. Right: Indirect illumination.
Fig. 3.
Post-n -eatment, the cilia-choroidal
ef fusions resorbed bilaterally. A: Right eye. B: Left eye.
BILATERAL ANGLE-CLOSURE
Uveal effusion with induced myopia and angle closure was suspected and B-scan echography confirmed diffuse, mild choroidal thickening (Fig. 1). The pupils were dilated with 1% cyclopentolate, and prominent ciliary processes could easily be seen by direct (Fig. 2A) and indirect illumination (Fig. 2B). The lens and vitreous were clear, and the fundus was remarkable for loss of visualization of choroidal detail. There were no choroidal folds or detachment. A laboratory work-up consisting of complete blood count, syphilis serology, chest radiography, and tuberculin skin test was undertaken and proved to be negative. HIV serology was suggested, but the patient refused testing. Outpatient treatment consisted of topical scopolamine hydrochloride i/4% twice daily in each eye, topical timolol maleate 0.5% twice daily in each eye, and acetazolamide 250 mg by mouth 4 times daily. The following day intraocular pressure was 26 mm Hg right eye and 32 mm Hg left eye and the remainder of the examination was unchanged except that internal limiting membrane folding was now evident. Contrast-enhanced computerized tomography of the orbits to rule out posterior scleritis was negative. Topical prednisolone acetate 4 times daily in each eye was added to the regimen. The patient returned three days later. Visual acuity remained normal with a moderate myopic refraction. The pupils were 5 mm in both eyes and fixed; the peripheral chamber remained shallow; gonioscopy revealed slit-like to near-appositional angles; intraocular pressure was 14 mm Hg right eye, 12 mm Hg left eye, and the fundus showed 360” of lowlying choroidal effusion to the equator. A single
TABLE Etiologies
Pupillary block mechanism
Chronic angle closure Acute angle closure Subacute angle closure Miotic-induced angle closure
257
GLAUCOMA AND HIV
cotton wool spot was noted in the posterior pole of the left eye. Acetazolamide was discontinued. Over the ensuing week, intraocular pressure remained low, and the induced myopia reversed with a final refraction, two weeks after the onset of symptoms, of + 0.75 right eye, + 1.00 left eye with 20/15 acuity in both eyes. The anterior chamber had deepened and gonioscopy revealed angles open to the scleral spur for 360” without peripheral anterior synechiae. The fundus appeared normal and B-scan ultrasonography showed resolution of the cilia-choroidal effusion bilaterally (Fig. 3). All medications were discontinued. The patient remains well systemically and his ocular examination three months later was remarkable only for an asymptomatic retinal cotton wool spot in the left eye. He did reveal that he had been tested and found to be HIV-positive, and was under the care of an internist.
Discussion Angle-closure glaucoma is a heterogenous disorder with many diverse etiologies. These are logically divided into those associated with a pupillary block mechanism and those associated with mechanically-induced anterior rotation of the lens-iris diaphragm (Table 1).4 This differentiation provides a framework for specific diagnosis and is important therapeutically, as only those forms having pupillary block as a primary mechanism will respond to laser or surgical peripheral iridectomy. Uveal effusion should be suspected in cases of angle closure which lack an iris bomb6 configuration. A central chamber of moderate depth with peripheral shallowing is suggestive and the diagno-
1
qf Angle-closure
Glaucoma 4
Anterior rotation lens-iris diaphragm Carotid-cavernous fistula Cyclocryotherapy Panretinal photocoagulation Post-scleral buckling procedure Central retinal vein occlusion Nanophthalmos Inflammatory uveal effusion Posterior scleritis Phakomorphic glaucoma Retrolental mass Ectopia lentis Persistent hyperplastic primary vitreous Coats’ disease Familial exudative vitreoretinopathy Panophthalmitis Hypertension
Other Ciliary block Synechial Neovascular glaucoma Aniridia Plateau iris
258
Surv Ophthalmol
36 (4) January-February
1992
sis may be confirmed by echography (Fig. 1) that demonstrates choroidal thickening with or without ciliochoroidal detachment.’ Miotics, the conventional treatment for angle closure, may cause further anterior rotation at the scleral spur and are contraindicated.6 Initial treatment involves cycloplegics, topical corticosteroids, and aqueous suppressants, as needed. Computerized tomography may help rule out posterior scleritis, and laboratory evaluation should include complete blood count, chest radiograph, tuberculin skin test, and serologic tests for syphilis and HIV. If medical treatment is ineffective, argon laser iridoplasty may open the angle.5 Should this fail, posterior sclerostomies with drainage of suprachoroidal fluid should be considered.’ Uveal effusion with induced myopia and angle closure may be a presenting sign of HIV infection although the etiologic and pathophysiologic mechanisms are unknown. This case report demonstrates that medical therapy alone may be efficaceous.
NASH, LINDQUIST
References 1. Atta HR, Frazier Byrine S: The findings ofstandardized echography for choroidal folds. Arch Ophthulnd 106:1234-1241, 1988 2. Koster HR, Liebman JM, Ritch R, Hudack S: Acute angleclosure glaucoma in a patient with acquired immunodeficiency syndrome successfully treated with argon laser peripheral iridoplasty. Ophthalmic Surg 21:500-501, 1990 3. Johnson MW, Gass JDM: Surgical management of idiopathic uveal effusion syndrome. Ophthalmology 97:778-785, 1990 4. Ritch R, Krupin T, Shields MB (eds): Th Cla2lcmntr. St Louis, CV Mosby, 1989 5. Ullman S, Wilson RP, Schwartz L: Bilateral angle-closure glaucoma in association with the acquired immune deficiency syndrome. Am J Ophthulmol101:419-424, 1986 6. Wilkie J. Drance SN, Schulzer M: The effects of miotics on anterior-chamber depth. AmJ Ophthulmol 68:78-83, 1969
Sunnorted in Dart bv NIH Grant EY01730; the Chatlos Foundatio; the Was6ingtdn and Northern Idahd Lions’ Sight Conservation Foundation; and by a departmental award from Research to Prevent Blindness, Inc. Reprint requests should be addressed to Thomas D. Lindquist, M.D., Ph.D., Department of Ophthalmology, RJ-IO, University of Washington, Seattle, WA 98195.
VOLUME 36. NUMBER 4. JANUARY-FEBRUARY 1992
AFTERIMAGES , JONATHAN
WIRTSCHAFTER, EDITOR
Bilateral Angle-Closure Glaucoma Associated with Uveal Effusion: Presenting Sign of HIV Infection ROBERT
W. NASH,
M.D., AND THOMAS
D. LINDQUIST,
M.D., PH.D.
Departmentof Ophthalmology,Universityof Washington, Seattle, Washington
Abstract. A 40-year-old homosexual man presented with acute myopia and bilateral angleclosure glaucoma. Recognition of an anterior chamber configuration of a modestly shallowed central chamber with marked peripheral shallowing clinically suggested uveal effusion. B-scan echography provided definitive, confirmatory evidence of diffuse choroidal thickening with ciliochoroidal effusion. Treatment with aqueous suppressants, cycloplegics, and topical steroids resulted in complete resolution of the angle closure and reversal of induced myopia. The patient, who was systemically well without signs of AIDS or AIDS-related complex, was later tested and found to be serologically-positive for the human immunodeficiency virus. (Surv Ophthalmol 36:255-258, 1992)
Key words. AIDS . angle-closure glaucoma echography human immunodeficiency virus (HIV) uveal effision l
l
glaucoma
l
l
eyes. Past medical and ocular history was unremarkable. Review of systems revealed recent night sweats. Physical examination was remarkable only for the eye findings showing a robust male without regional adenopathy. Eye examination revealed uncorrected visual acuities of 20/200 in the right eye and 201400 in the left eye. External and ocular motility examination was normal. The pupils were equal in size and normally reactive without afferent pupillary defect. Manifest refraction revealed moderate myopia (right eye - 3.25 20/20; left eye - 2.‘75 20/20‘*) with normal corrected acuities. The ocular surface was unremarkable to biomicroscopy. The anterior chamber was quiet; the central chamber was modestly shallowed with marked shallowing of the peripheral chamber for 360”. Gonioscopy revealed appositional closure for 360” without evidence of peripheral anterior synechiae. The iris had no bomb6 or plateau configuration. Intraocular pressure by applanation was 32 mm Hg in each eye.
Bilateral angle-closure glaucoma associated with uveal effusion has been reported in several patients with the acquired immunodeficiency syndrome (AIDS).2s5 Ciliary body swelling leads to forward rotation of the lens-iris diaphragm, causing peripheral anterior chamber shallowing and appositional angle closure without iris bomb& Recognition of a non-pupillary block mechanism of angle closure allows appropriate medical and surgical therapy. Other reported cases have been in patients with diagnosed AIDS or signs of AIDS-related complex (ARC).‘,” We report a case of bilateral uveal effusion with closed-angle glaucoma as the presenting sign of human immunodeficiency virus (HIV) infection.
Case Report A 40-year-old homosexual male presented with complaints of generalized fatigue, bilateral retrobulbar headaches of two weeks’ duration, and decreased distance vision for one day. The patient indicated that he previously had good and equal uncorrected vision reported to be 20120 in both 255
256
Surv Ophthalmol
36 (4) January-February
1992
NASH, LINDQUIST
Fig. 1. B-scan ultrasonography confirmed choroidal thickening with ciliochoroidal effusion bilaterally (arrows). Chatter lines anteriorly are artifactual. A: Right eye scanned equatorially. B: Left eye scanned superiorly.
Fig. 2.
Post-dilation ciliary processes could be readily visualized. Left: Direct illumination. Right: Indirect illumination.
Fig. 3.
Post-n -eatment, the cilia-choroidal
ef fusions resorbed bilaterally. A: Right eye. B: Left eye.
BILATERAL ANGLE-CLOSURE
Uveal effusion with induced myopia and angle closure was suspected and B-scan echography confirmed diffuse, mild choroidal thickening (Fig. 1). The pupils were dilated with 1% cyclopentolate, and prominent ciliary processes could easily be seen by direct (Fig. 2A) and indirect illumination (Fig. 2B). The lens and vitreous were clear, and the fundus was remarkable for loss of visualization of choroidal detail. There were no choroidal folds or detachment. A laboratory work-up consisting of complete blood count, syphilis serology, chest radiography, and tuberculin skin test was undertaken and proved to be negative. HIV serology was suggested, but the patient refused testing. Outpatient treatment consisted of topical scopolamine hydrochloride i/4% twice daily in each eye, topical timolol maleate 0.5% twice daily in each eye, and acetazolamide 250 mg by mouth 4 times daily. The following day intraocular pressure was 26 mm Hg right eye and 32 mm Hg left eye and the remainder of the examination was unchanged except that internal limiting membrane folding was now evident. Contrast-enhanced computerized tomography of the orbits to rule out posterior scleritis was negative. Topical prednisolone acetate 4 times daily in each eye was added to the regimen. The patient returned three days later. Visual acuity remained normal with a moderate myopic refraction. The pupils were 5 mm in both eyes and fixed; the peripheral chamber remained shallow; gonioscopy revealed slit-like to near-appositional angles; intraocular pressure was 14 mm Hg right eye, 12 mm Hg left eye, and the fundus showed 360” of lowlying choroidal effusion to the equator. A single
TABLE Etiologies
Pupillary block mechanism
Chronic angle closure Acute angle closure Subacute angle closure Miotic-induced angle closure
257
GLAUCOMA AND HIV
cotton wool spot was noted in the posterior pole of the left eye. Acetazolamide was discontinued. Over the ensuing week, intraocular pressure remained low, and the induced myopia reversed with a final refraction, two weeks after the onset of symptoms, of + 0.75 right eye, + 1.00 left eye with 20/15 acuity in both eyes. The anterior chamber had deepened and gonioscopy revealed angles open to the scleral spur for 360” without peripheral anterior synechiae. The fundus appeared normal and B-scan ultrasonography showed resolution of the cilia-choroidal effusion bilaterally (Fig. 3). All medications were discontinued. The patient remains well systemically and his ocular examination three months later was remarkable only for an asymptomatic retinal cotton wool spot in the left eye. He did reveal that he had been tested and found to be HIV-positive, and was under the care of an internist.
Discussion Angle-closure glaucoma is a heterogenous disorder with many diverse etiologies. These are logically divided into those associated with a pupillary block mechanism and those associated with mechanically-induced anterior rotation of the lens-iris diaphragm (Table 1).4 This differentiation provides a framework for specific diagnosis and is important therapeutically, as only those forms having pupillary block as a primary mechanism will respond to laser or surgical peripheral iridectomy. Uveal effusion should be suspected in cases of angle closure which lack an iris bomb6 configuration. A central chamber of moderate depth with peripheral shallowing is suggestive and the diagno-
1
qf Angle-closure
Glaucoma 4
Anterior rotation lens-iris diaphragm Carotid-cavernous fistula Cyclocryotherapy Panretinal photocoagulation Post-scleral buckling procedure Central retinal vein occlusion Nanophthalmos Inflammatory uveal effusion Posterior scleritis Phakomorphic glaucoma Retrolental mass Ectopia lentis Persistent hyperplastic primary vitreous Coats’ disease Familial exudative vitreoretinopathy Panophthalmitis Hypertension
Other Ciliary block Synechial Neovascular glaucoma Aniridia Plateau iris
258
Surv Ophthalmol
36 (4) January-February
1992
sis may be confirmed by echography (Fig. 1) that demonstrates choroidal thickening with or without ciliochoroidal detachment.’ Miotics, the conventional treatment for angle closure, may cause further anterior rotation at the scleral spur and are contraindicated.6 Initial treatment involves cycloplegics, topical corticosteroids, and aqueous suppressants, as needed. Computerized tomography may help rule out posterior scleritis, and laboratory evaluation should include complete blood count, chest radiograph, tuberculin skin test, and serologic tests for syphilis and HIV. If medical treatment is ineffective, argon laser iridoplasty may open the angle.5 Should this fail, posterior sclerostomies with drainage of suprachoroidal fluid should be considered.’ Uveal effusion with induced myopia and angle closure may be a presenting sign of HIV infection although the etiologic and pathophysiologic mechanisms are unknown. This case report demonstrates that medical therapy alone may be efficaceous.
NASH, LINDQUIST
References 1. Atta HR, Frazier Byrine S: The findings ofstandardized echography for choroidal folds. Arch Ophthulnd 106:1234-1241, 1988 2. Koster HR, Liebman JM, Ritch R, Hudack S: Acute angleclosure glaucoma in a patient with acquired immunodeficiency syndrome successfully treated with argon laser peripheral iridoplasty. Ophthalmic Surg 21:500-501, 1990 3. Johnson MW, Gass JDM: Surgical management of idiopathic uveal effusion syndrome. Ophthalmology 97:778-785, 1990 4. Ritch R, Krupin T, Shields MB (eds): Th Cla2lcmntr. St Louis, CV Mosby, 1989 5. Ullman S, Wilson RP, Schwartz L: Bilateral angle-closure glaucoma in association with the acquired immune deficiency syndrome. Am J Ophthulmol101:419-424, 1986 6. Wilkie J. Drance SN, Schulzer M: The effects of miotics on anterior-chamber depth. AmJ Ophthulmol 68:78-83, 1969
Sunnorted in Dart bv NIH Grant EY01730; the Chatlos Foundatio; the Was6ingtdn and Northern Idahd Lions’ Sight Conservation Foundation; and by a departmental award from Research to Prevent Blindness, Inc. Reprint requests should be addressed to Thomas D. Lindquist, M.D., Ph.D., Department of Ophthalmology, RJ-IO, University of Washington, Seattle, WA 98195.
