Elderly man experiences transient blurred vision
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A 79-year-old Caucasian man presented with a chief complaint of transient blurred vision in the right eye for the past several years.
His ocular history was remarkable for ocular hypertension (OHTN) in the right eye and cataract extraction in both eyes. Additionally, the patient stated he underwent surgery in the late 1990s to repair a retinal detachment in his right eye.
His systemic history was positive for hypertension, hyperlipidemia and type 2 diabetes. Current medications included metformin, glipizide and insulin to manage the patient’s long-standing diabetes and timolol 0.5% every morning in the right eye for his OHTN. The patient had no known drug allergies.
Entering visual acuity for the right eye was 20/60 and for the left eye was 20/20 through habitual glasses; +0.75 D -1.50 D x 090 OD, +0.25 D -2.50 D x 080. There was no improvement with pinhole testing in the right eye. The left pupil was equal, round and reactive to light, with accommodation with mild irregularity to the right eye pupil secondary to surgical trauma. Extraocular muscle testing exhibited a full range of motion in both eyes.
Confrontational visual field testing was full to finger count in both eyes. Anterior segment evaluation showed normal adnexa, trace blepharitis and thickened lid margins in both eyes. Corneal findings included trace diffuse endothelial pigmentation in the right eye with a small corneal scar inferior to the visual axis and 1+ endothelial pigmentation in the left eye. Posterior chamber IOLs were clear and centered in both eyes with trace posterior capsular opacification in the left eye. IOPs by Goldmann applanation measured 20 mm Hg OD and 15 mm Hg OS.
Dilated fundus examination showed cup-to-disc ratios of 0.70 horizontal/0.60 vertical in the right eye with laminar reconfiguration and thin superior temporal rim; and 0.40 round in the left eye with thick nonexcavated rim tissue 360 degrees. A diffuse epiretinal membrane was seen in the right eye and an inferior retinal nerve fiber layer (RNFL) wedge defect was seen emanating from the optic nerve.
Ultrasound pachymetry was 532 um OD and 548 um OS. The left eye was open to the ciliary body 360 degrees. The Ocular Response Analyzer (Reichert) revealed in the right eye: corneal compensated IOP (IOPCC) of 19.9 mm Hg and corneal hysteresis (CH) of 9.7, and in the left eye: IOPCC 15.5 mm Hg, CH 11.0. Humphrey visual field in the right eye was reliable; the glaucoma hemifield test was borderline: FN 0%, FP 2%, visual field index 98%. There was a repeatable dense inferior temporal paracentral defect.
What’s your diagnosis?
See answer on the next page.
After a comprehensive work-up, the patient was diagnosed with secondary open angle glaucoma due to migration of silicone oil tamponade used in the repair of his retinal detachment. Presumably the patient’s history of elevated IOP was secondary to restriction of trabecular outflow by silicone blockade.
A common side effect of the use of silicone oil in ocular surgeries is secondary glaucoma. The prevalence of emulsified oil discovered in the anterior chamber postoperatively ranges from 22% to 58% in the literature (Valone et al., Suic et al.) New postoperative glaucomatous optic neuropathy has been noted in upwards of 10% of patients after intravitreal instillation of silicone oil and has been best explained by angle oil emulsification (Valone et al.).
Secondary glaucoma induced by silicone oil is believed to be multifactorial in origin. Four different mechanisms have been proposed for the pathogenesis of glaucoma that require different therapeutic strategies: Overfill of the posterior chamber leading to total anterior chamber fill causing mechanical obstruction of outflow; pupillary block with silicone oil incites angle closure glaucoma; denaturation of silicone oil into micro droplets may sweep into the trabecular meshwork with the development of secondary open angle glaucoma; or inflammation or exacerbation of pre-existing glaucoma.
In most eyes, medical therapy is successful in controlling IOP; however, silicone oil removal with or without concurrent glaucoma surgery may also be required. This case emphasizes the importance of timely and accurate gonioscopy. Reviewing differential diagnosis for unilateral elevated IOP will help improve prompt diagnosis and promote proper interpretation for treatment.
Anterior uveitis
Uveitis is described as a group of conditions characterized by intraocular inflammation. Anterior uveitis can be unilateral or bilateral. Acute anterior uveitis is a rapid onset inflammation, obstruction of inter-trabecular spaces and increased IOP. Chronic anterior uveitis is a classified by repeated bouts of inflammation leading to fibroblastic infiltration and formation of scar tissue that obstructs the anterior chamber angle.
The inflammatory cells produced during an anterior uveitis attack can limit aqueous outflow by two mechanisms: physically obstructing the outflow of the trabecular meshwork (TM) or producing cytotoxic agents that can lead to permanent scarring of the TM lamellae and endothelial cells. This seemed to be a weak differential considering that the patient noted no history of symptoms consistent with having suffered any uveitis, and there were no ocular signs consistent with prior inflammatory events with the exception of the corneal endothelial pigmentation.
Fuchs heterochromic iridocyclitis
Fuchs heterochromic iridocyclitis (FHI) generally presents as a mild unilateral inflammation of the anterior chamber with stellate keratic precipitates and iris heterochromia with prominent iris and angle vessels secondary to iris atrophy. FHI is a breakdown of the blood-aqueous barrier resulting in leakage of cells.
The expected sequelae of chronic uveitis (posterior synechiae, persistent cystoid macular edema) are usually not seen in FHI. No iris atrophy or heterochromia was noted on examination within this case, making FHI an unlikely diagnosis.
Traumatic glaucoma (angle recession)
Angle recession typically occurs after an ocular trauma. This trauma can result in a tear between the longitudinal and circular muscles of the ciliary body. The initial damage to the trabecular meshwork and Schlemm’s canal can result in long-term fibrosis of these effected structures, with the resulting dysfunction giving way to elevated IOP and ultimately glaucomatous optic nerve head damage.
The patient’s history indicated no such trauma occurring or any sign of angle recession on gonioscopy, effectively eliminating angle recession as a potential differential diagnosis.
Glaucomatocyclitic crisis (Posner-Schlossman syndrome)
Posner-Schlossman syndrome (PSS), or glaucomatocyclitic crisis, is a unilateral ocular condition characterized by recurrent attacks of intraocular inflammation and raised IOP that can result in chronic secondary glaucoma. Three main theories have been proposed to explain why elevation in IOP occurs: a thick and edematous trabecular band (trabeculitis), trabecular blockage by pigments and chronic inflammatory cells, and peripheral anterior synechiae with secondary angle-closure glaucoma. There was no inflammatory reaction detected on examination, limiting the strength of PSS as a differential.
Pseudoexfoliation glaucoma
Pseudoexfoliation syndrome (PES) is an age-related systemic microfibrillopathy caused by progressive accumulation and gradual deposition of extracellular grey and white material over various tissues. Accumulation of these extracellular material can cause obstruction of the trabecular meshwork, leading to an increase in IOP. If IOP elevation is noted with optic nerve damage, reclassification to pseudoexfoliation glaucoma (PEG) is made. Pseudoexfoliation type material typically deposits on the lens, iris, ciliary epithelium or trabecular meshwork.
No such material was present with slit lamp examination or gonioscopy.
Pigmentary glaucoma
Pigment dispersion occurs due to rubbing of the iris pigment epithelium against the lens zonules, typically because of a back-bowed or concave iris insertion. The loss of pigment results in midperipheral iris transillumination defects. This syndrome is more common in myopes.
Secondary open-angle pigmentary glaucoma (PG) can result from a reduction of the outflow of aqueous humor and consequent increase in IOP, leading to glaucomatous optic neuropathy.
A diagnosis of PG is common between 40 and 50 years of age, occurring more frequently in men. On this patient’s examination findings, endothelial pigment does help strengthen PG as a differential; however, no iris transillumination defects were present, eliminating it as a possibility.
Treatment, management
Now having a better understanding of the mechanism of the patient’s glaucoma, as a result of the initial gonioscopic evaluation, we know how to better treat and manage the patient’s condition. The aqueous production suppressant, timolol 0.5 every morning in the right eye was discontinued, and Cosopt (dorzolamide HCl, timolol maleate, Akorn) twice daily in both eyes was begun. More aggressive IOP control and frequent monitoring of this patient is imperative to ensure slowing progression of glaucomatous optic neuropathy. If additional lowering of IOP is not obtained via pharmacologic means, surgical intervention may be warranted to remove the obstructing silicone oil.
This case highlights silicone oil tamponade treatment for retinal detachments and its correlating complication with resulting secondary glaucoma. Assessing and understanding the underlying etiology of the glaucomatous optic neuropathy can allow appropriate treatment. Gonioscopy is a significant tool in every optometrist’s toolbox and should be used regularly to help identify and manage all forms of glaucoma.
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- For more information:
- Logan Brunner, OD, is a resident at the Memphis VAMC in Memphis, Tenn. He can be reached at lbrunner@sco.edu.
- Cameron Clinard, OD, FAAO, is a former resident at Memphis VAMC and currently practices at Triangle Vision Optometry in Chapel Hill, N.C. She may be reached at cwclinard@gmail.com.
- Edited by Leo P. Semes, OD, FAAO, Professor Emeritus in the Department of Optometry and Vision Science at the University of Alabama at Birmingham and a member of the Primary Care Optometry News Editorial Board. He may be reached at lsemes@uab.edu.
Disclosures: The authors report no relevant financial disclosures.