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• Case report
• Open access
• Published: 23 December 2014

Visual improvement following glaucoma surgery: a case report

• William S Foulsham 1 ,
• Lanxing Fu 2 &
• Andrew J Tatham 2  

BMC Ophthalmology volume  14 , Article number:  162 ( 2014 ) Cite this article

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Glaucoma is a progressive optic neuropathy and a leading cause of blindness. Neural losses from glaucoma are irreversible, and so the aim of glaucoma treatment is to slow progression and minimize the risk of further damage. Functional improvement with treatment is not expected. We report the case of a patient who experienced a significant improvement in vision following glaucoma surgery and review the literature regarding this phenomenon.

Case presentation

A 64-year old male presented with a 13-month history of gradual vision loss in the right eye to the extent that he could only perceive hand movements. His intraocular pressure (IOP) measured 50 mmHg and he was found to have advanced primary open angle glaucoma. Medical treatment was commenced and he underwent a successful right Mitomycin C-augmented trabeculectomy. Unexpectedly he experienced marked improvement in vision post-operatively, with improvements maintained through six months of follow-up. At his most recent visit visual acuity was 6/18 in the affected eye. Although the mechanism of improved vision cannot be proven it is likely that successful lowering of IOP resulted in some reversal of retinal ganglion cell dysfunction. Important factors may have included his relatively young age, high IOP and short duration of symptoms.

Although rare, functional improvements may occur following trabeculectomy. Glaucoma surgery should be offered early to those with advanced disease, and considered even in those with reduced visual acuity.

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Glaucoma is characterized by progressive optic nerve degeneration, evident clinically as structural changes to the optic nerve head and corresponding loss of visual field [ 1 ]. The pathogenesis is not fully understood but it is thought to involve a heterogeneous group of pathological processes that share the final common pathway of progressive death of retinal ganglion cells and their axons [ 2 ]. Glaucomatous damage is deemed irreversible; therefore the optimal management currently depends on early detection and treatment to minimize the risk of progression and development of visual loss.

The first line treatment for glaucoma has traditionally consisted of medical management with topical intraocular pressure lowering agents. However, recent guidance, such as that from the United Kingdom National Institute of Clinical Excellence (NICE) stipulate that, for patients with advanced disease at presentation, surgery may be an appropriate first line therapy [ 3 ]. The aim of early surgery is to reduce the risk of further deterioration in visual function, as improvement in vision following glaucoma surgery is not expected. There is however, some evidence that retinal ganglion cells damaged by glaucoma might undergo a period of reversible dysfunction preceding cell death [ 4 , 5 ]. Furthermore, reversible changes in optic nerve head morphology have been reported following reductions of intraocular pressure [ 6 – 9 ]. These observations suggest that certain structural and functional improvements may in fact be possible in some patients.

The aim of the current article is to 1) report the case of a patient with advanced glaucoma at initial presentation that demonstrated marked improvement in visual acuity following reduction in intraocular pressure with trabeculectomy, and 2) to critically appraise the published literature as to whether functional improvement is possible following glaucoma surgery.

A 64-year-old university professor presented to our facility complaining of a 13-month history of progressive visual loss in his right eye. There was no associated headache or ocular pain and he had no other symptoms of note. He had no previous history of ocular problems, although he had not attended for an eye examination for more than ten years. The patient’s past medical history was significant for bladder cancer managed with surgery and chemotherapy twelve years ago. He had no history of previous ocular surgery or trauma and was not using any systemic medications, including corticosteroids. There was a positive family history of glaucoma, with the patient’s older sister being diagnosed at age 52, although she had not required surgery or developed significant visual impairment.On examination, best-corrected visual acuity was hand movements in the right eye, and 6/6 in the left. There was no injection of the conjunctivae; corneas were clear and anterior chambers deep and quiet. Both pupils were round and symmetrical in size, however there was a right relative afferent pupillary defect. Goldman applanation tonometry revealed a very high intraocular pressure (IOP) in both eyes, measuring 50 mmHg in the right and 48 mmHg in the left. Central corneal thickness was 596 μm in the right eye and 597 μm in the left. Refractive error measured only +0.50 diopter sphere in both eyes. Gonioscopy demonstrated wide-open angles bilaterally, the trabecular meshwork was heavily pigmented but there were no iris transillumination defects. On dilated fundal examination there was evidence of advanced glaucomatous excavation of both optic nerve heads, particularly severe in the right eye, where there was almost complete loss of the neuroretinal rim (Figure  1 A). Optical coherence tomography (OCT) showed significant thinning of the retinal nerve fiber layer (RNFL) in both eyes, again worse in the right, with average RNFL thicknesses of 41.28 μm in the right eye and 75.11 μm in the left (Figure  1 B). Standard automated perimetry was not possible in the right eye due to the poor visual acuity, but in the left eye was reliable with a superonasal defect and mean deviation of -6.54 dB (Figure  1 C).

Investigations conducted at presentation. (A) Fundoscopic examination showing advanced glaucomatous excavation bilaterally. (B) Optical coherence tomography report demonstrating asymmetric RNFL thinning more pronounced in the right eye. (C) Left eye pattern deviation plot from standard automated perimetry.

A diagnosis of advanced primary open angle glaucoma was made and the patient was commenced on topical latanoprost and brinzolamide to both eyes. After 24 hours IOPs had decreased to 28 mmHg (right eye) and 21 mmHg (left eye). Visual acuity had improved to 6/60 in the right eye, and 6/5 in the left eye. Although there had been a good percentage reduction in IOP with medication, due to the advanced glaucomatous damage a lower target pressure was required and the decision was made to proceed with Mitomycin C-augmented trabeculectomy to the right eye. Surgery was performed four weeks after presentation. During surgery the eye was treated with 0.2 mg/ml Mitomycin C (Kyowa Hakko Kirin Co, Ltd., Tokyo, Japan) for 3 minutes, and 3 10-0 nylon releasable sutures were used to secure the scleral flap. There were no complications noted and at day one post-operative review, IOP in the right eye was 30 mmHg, decreasing to 10 mmHg with gentle ocular massage. The patient was prescribed topical dexamethasone 0.1% 2 hourly during daytime hours and chloramphenicol four times per day to the right eye.Over the next 2 to 3 weeks IOP was gradually lowered through loosening of the releasable sutures and at the 4 week postoperative review was 9 mmHg. Surprisingly, the patient reported a gradual improvement in vision in the right eye since surgery, and at the 4 week visit the best-corrected visual acuity had improved to 6/18. The reduction in IOP and improvement in visual acuity has subsequently been maintained over six months of follow-up. During this period, the patient also reported a subjective amelioration of vision. Fundal photographs, OCT and standard automated perimetry were repeated six months following surgery and are shown in Figure  2 . Although there was an improvement in vision, structural parameters in the right eye appeared unchanged with no change in neuroretinal rim appearance and average RNFL thickness in the right eye measuring 39.18 μm at most recent follow up.

Investigations conducted at 6 months follow-up (post-trabeculectomy). (A) Fundoscopic examination. (B) Optical coherence tomography. (C) Right eye grey scale and left eye pattern deviation plots from standard automated perimetry.

The patient described in this case had severe glaucomatous damage at presentation, evident from the marked loss of neural tissue seen on optic disc examination, the presence of extreme thinning of RNFL on OCT, and the severe functional deficit, with a visual acuity of only hand movements and a relative afferent pupillary defect. Such severe disease at presentation conveys a poor prognosis and requires a low target pressure to minimize the risk of visual loss. Surgery was offered with the sole aim of preventing loss of remaining vision and with no expectation for visual recovery. Surprisingly, lowering of IOP resulted in a dramatic improvement in visual function.

Improvements in structural measurements are widely appreciated to occur following successful reduction in intraocular pressure with glaucoma surgery. For example, Kotecha and colleagues have shown using confocal scanning laser ophthalmoscopy that reversal in disc cupping can occur following trabeculectomy [ 10 ]. In a series of 22 eyes from 20 patients evaluated using spectral domain OCT, Russo and colleagues have demonstrated significant decreases in cup depth following trabeculectomy at both 1 week and 1 month postoperatively [ 11 ]. Increases in RNFL thickness measurements are less widely reported. However, in a small series of 38 eyes of 31 patients with glaucoma, Aydin and colleagues found a significant increase in circumpapillary RNFL thickness following glaucoma surgery. 31 of 38 eyes had an increase in RNFL thickness at 6 to 12 months following surgery, with a mean increase of 12.6 μm [ 12 ]. In fact there is a considerable body of evidence demonstrating reversal of structural glaucomatous damage following pressure-lowering surgical interventions, with apparent reversal of structural changes especially common in younger patients with congenital, infantile and juvenile-onset glaucoma [ 13 – 17 ].

In contrast to the improvements observed in structural measurements, evidence for functional improvement following glaucoma surgery is scarce. Leung and colleagues described a single case of a patient with juvenile open-angle glaucoma who recovered from an inferotemporal visual field defect following trabeculectomy [ 18 ]. However, due to the variability inherent in visual field testing detecting genuine improvement may be challenging.

Clinical interventions in glaucoma are generally judged on their capacity to reduce the incidence of progression of visual field endpoints, however, few studies have investigated whether improvements in visual function might occur. One exception was the Otago Glaucoma Surgery Outcome Study, which was a prospective case series including 841 eyes of 607 patients with primary open or closed angle glaucoma. Patients were treated with trabeculectomy and followed for an average of 7.5 years. Visual acuity was tested at each visit and categorised as ≥6/9, <6/9 but >6/120, or ≥6/120, with improvement in visual acuity defined by an improvement in class. The results demonstrated 151 of 841 eyes (18%) had an improvement in vision following trabeculectomy [ 19 ]. However, a limitation of this study was that 23% of eyes with improvement in vision underwent concurrent cataract extraction. In future surgical glaucoma studies it would be interesting to determine the true incidence of visual improvement.

It is important to consider the possible mechanism of visual improvement in our patient. Although the defining histological feature of glaucoma is loss of retinal ganglion cells and their axons, the exact mechanism of retinal ganglion cell death is not known. Retinal ganglion cell death is believed to be biphasic; with a primary insult initiating damage that provokes a cascade of events, in turn creating a noxious environment that envelops retinal ganglion cells, resulting in secondary cell degeneration [ 20 ]. Increased IOP and vascular deregulation may contribute to the primary insult, obstructing axoplasmic flow and altering microcirculation in the optic nerve. The secondary cascade is likely to involve excitotoxic damage from the accumulation of glutamate, increased intracellular calcium and resultant retinal ganglion cell apoptosis [ 21 ].

Once apoptosis has occurred it is difficult to conceive how visual function might improve, however, Swanson and colleagues have proposed that retinal ganglion cells might undergo a period of reversible dysfunction preceding apoptosis [ 22 ]. Evidence for this theory largely comes from primate studies of experimental glaucoma. In one study involving rhesus monkeys with unilateral laser-induced experimental glaucoma, Harwerth and colleagues found reductions in visual field sensitivity could be present without apparent retinal ganglion cell loss on histology [ 23 , 24 ]. Marx and colleagues examined flash and pattern electroretinograms (PERG) in experimental glaucoma [ 25 , 26 ]. The results showed that 50% reductions in PERG amplitude could occur in the absence of observable glaucomatous optic disc changes. A limitation of these studies is that they utilized animal models of experimental glaucoma, in which glaucoma was rapidly induced. However, similar findings have been reported in humans. For example, Ventura and colleagues conducted a study of 84 patients with suspected glaucoma and found a disproportionate reduction in PERG amplitude compared to RNFL thickness, supporting the concept that retinal ganglion cell dysfunction might precede permanent structural and functional changes [ 27 ].

The possibility of reversible RGC dysfunction has driven interest in the concepts of neuroprotection, neuroregeneration and neuroenhancement. Neuroprotection may allow preservation of retinal ganglion cells by halting the secondary cascade of glaucoma pathogenesis [ 28 – 30 ]. Neuroregeneration is the process of promoting the rebuilding of optic nerve axons and neuroenhancement is treatment to provide short-term improvements in function of surviving retinal ganglion cells.

The patient described in the present case presented with a visual acuity of hand movements, yet recovered 6/18 vision following trabeculectomy. In this case surgical reduction in IOP is likely to have had a neuroprotective effect, increasing the chance of preserving remaining retinal ganglion cells. However, the improvement in visual function is likely to have been due to a neuroenhancing effect of IOP reduction. Although the mechanism of improved vision cannot be proved, it is probable the reduction in IOP from the very high preoperative levels may have improved retinal ganglion cells function through restoration of axoplasmic flow and improved microcirculation to the optic nerve. Contributing factors may have included the patient’s relatively young age, high IOP and short duration of symptoms.

It is also important to acknowledge that the patient may have had an improvement in vision without surgery, and had already experienced some improvement in vision with IOP reduction with medical treatment. Unfortunately, due to the severe glaucomatous in the right eye, the visual prognosis remains poor.

In conclusion, although glaucomatous damage is deemed irreversible, our patient experienced a significant improvement in vision following successful reduction in IOP. This patient’s experience is a single case, yet it contributes to the evidence that filtration surgery may lead to functional as well as structural improvement in some patients. This may be an important consideration for future clinical studies, which tend not examine possible improvements in vision with glaucoma surgery. For example, although the Advanced Glaucoma Intervention Study (AGIS) provided evidence that trabeculectomy is an effective procedure for lowering IOP and reducing the risk of visual field progression in advanced glaucoma, the study did not report whether there was improvement in vision in any patients following surgery [ 31 ]. This case also supports the recommendation that early surgery should be considered in patients presenting with advanced glaucomatous damage.

Written informed consent was obtained from the patient for publication of this case report and any accompanying images. A copy of the written consent is available for review by the Editor-in-Chief of this journal.

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Supported in part by NHS Research Scotland Career Research Fellowship (A.J.T).

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William S Foulsham

Princess Alexandra Eye Pavilion and Department of Ophthalmology, University of Edinburgh, Edinburgh, UK

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Financial Disclosure(s): Dr. Tatham – Research support – Heidelberg Engineering. Drs. Foulsham and Fu have no financial disclosures.

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WSF drafted the manuscript and performed a literature review. LF participated in information gathering and editing. AJT conceived the idea, managed the patient’s ophthalmologic problems and co-wrote the case report. All authors have read and approved the final manuscript.

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Foulsham, W.S., Fu, L. & Tatham, A.J. Visual improvement following glaucoma surgery: a case report. BMC Ophthalmol 14 , 162 (2014). https://doi.org/10.1186/1471-2415-14-162

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Received : 31 July 2014

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DOI : https://doi.org/10.1186/1471-2415-14-162

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Patient Case #1: 58-year-old patient with open angle glaucoma utilizing minimally invasive glaucoma surgery procedure

Ehsan Sadri, MD, FACS, reviews the case of a 58-year-old male with open angle glaucoma utilizing minimally invasive glaucoma surgery procedure.

EP: 1 . Patient Case #1: 58-year-old patient with open angle glaucoma utilizing minimally invasive glaucoma surgery procedure

Ep: 2 . impressions and take away points from patient case #1, ep: 3 . patient case #2: 67-year-old white female with open angle glaucoma benefits from minimally invasive glaucoma surgery, ep: 4 . impressions and take away points from patient case #2.

Ehsan Sadri, MD, FACS: Hi everybody, my name is Dr Ehsan Sadri. I’m a board-certified ophthalmologist, fellowship trained in glaucoma, practicing in lovely Newport Beach, California. I am the founder and medical director of Visionary Eye Institute. I’m also the co-founder of Visionary Ventures, also located in Southern California. It’s absolutely my delight to be here with you, and an honor and a pleasure.

Our first case is a 58-year-old practicing vascular surgeon who had LASIK surgery in 1995. He was referred in for a glaucoma and cataract evaluation. He’s on maximal medical therapies, intolerant to other medications, as you can see, he’s on latanoprost and Combigan. His best-corrected visual acuity is 20/50; he does have dense arcus, which we’ll show in the next couple of slides. He presents with intraocular pressure of 16 mm Hg. We don’t know his range in the past, but presumably, it was higher. The corneal thickness test is 490 μm, and you can see the cup/disc ratio is 0.85 in the right eye and 0.9 in the left eye.

This is a startling example of his right optic nerve, and he is obviously, again, status post-LASIK. We don’t know his pre-LASIK, preoperative measurements and refractive error, but you can see from a physical examination that he obviously has high myopia, and it’s very tough to delineate where the disc vs the rest of the tissue is. But there’s a circle that I put there for us to be able to delineate where the cup-to-disc is.

This is visual field progressive loss; you can see it’s pretty remarkable and disconcerting that he’s presenting this way because he has loss of visual field functionality in both eyes. And he’s obviously a very reliable patient on examination. For this patient, you can see he underwent cataract extraction surgery with monofocal lens implants. We did an OMNI trabeculotomy, goniotomy, and eye stents in both eyes. His intraocular pressures now are pretty steady, between 10 and 12 mm Hg, which is actually the target for this patient, and his best-corrected visual acuity is 20/20. He’s still practicing.

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Case presentation: bilateral angle-closure glaucoma, a thorough workup detects congenital changes in a patient's crystalline lenses., tania paul, md , and nathan m. radcliffe, md.

A 35-year-old woman presented to the ER with complaints of ocular pain that had persisted for 1 day. She reported a sensation of pressure and blurry vision in her left eye with no apparent exacerbating factors. In the ER, her UCVA measured 20/30 OD and 20/100 OS. A slit-lamp examination of her left eye revealed moderate conjunctival injection, corneal edema, and pigmentary deposits on the corneal endothelium. The anterior chambers of both eyes were shallow centrally and flat peripherally (Figure 1), but these findings were more pronounced in her left eye. The crystalline lenses were clear, and the IOP measured 46 mm Hg OD and 52 mm Hg OS. Both pupils were nonreactive and dilated midway, and they demonstrated posterior synechiae presumed to be from chronic iridolenticular contact. Fundoscopy revealed pink optic nerves with sharp margins, bilateral vertical cup-to-disc ratios of 0.25, intact neuroretinal rims, and retinal nerve fiber layers without parapapillary atrophy. Darkroom gonioscopy revealed a convex iris approach and intermittent peripheral anterior synechiae in both eyes for 360°. The patient was diagnosed with bilateral acute angle-closure glaucoma (ACG) and was started on topical ocular hypotensive treatment. No systemic medications or cyclopeglic agents were prescribed. When we evaluated the patient 2 days after her initial presentation to the ER, the eye drops had adequately reduced and stabilized her IOP, and the corneal edema in her left eye had resolved. The patient subsequently underwent bilateral peripheral iridotomies.

Postoperatively, the patient's UCVA returned to 20/15 OU, and her IOP was initially controlled with topical therapy in both eyes. Her anterior chambers remained shallow however, and she continued to demonstrate appositional closure on gonioscopy that was not relieved with compression. A subsequent fundoscopic and stereophotographic evaluation of the optic nerves showed cup-to-disc ratios of 0.4 OD and 0.7 OS. We also noted pathological changes in the retinal nerve fiber layer bilaterally (Figure 2) and an inferior notch in the left optic nerve that correlated with superior visual field defects (Figure 3) (mean deviation, -10.99 dB OD and -17.75 dB OS) on Humphrey visual field testing (Carl Zeiss Meditec, Inc., Dublin, CA).

Two months after the patient initially presented to the ER, she was re-evaluated in our office, at which time her IOPs were elevated despite self-reported adherence to a regimen of three topical ocular hypotensive medications. She did not report experiencing ocular pain, headache, blurred vision, or erythema despite IOPs of 48 mm Hg OS and 50 mm Hg OD. The examination did not reveal any corneal edema or intraocular inflammation in either eye.

How would you proceed?

• What further testing would you order to identify the underlying cause of this patient's ACG? Is her presentation characteristic of a syndrome?
• If the patient requires surgery, would you perform cataract extraction, a trabeculectomy, or a combined procedure?
• Would you perform goniosynechiolysis? What are the indications for this procedure in this setting?
• If you performed a lensectomy, what refractive end-point would you target for this 35-year-old emmetrope who has never experienced asthenopia?

SURGICAL COURSE Ultrasound biometry and biomicroscopy showed axial lengths of 21.6 mm OD and 21.7 mm OS and bilateral lens thicknesses of 4.75 mm. An evaluation with an Artemis 2 very high-frequency ultrasound (Arcscan, Inc., Golden, CO; not available in the United States) confirmed persistent iridotrabecular apposition with lens-induced angle closure (Figure 4). We noted that the ciliary body was somewhat hypoplastic and anteriorly rotated in both eyes. We did not observe any uveal effusions.

These pathological changes were suggestive of spherophakia. A review of systems showed that the patient was of short stature but did not have brachydactyly or abnormal dentition. Because she had been adopted, she could not provide a family history.

When we discussed her options for treatment, the patient, who was an executive in the fashion industry, stated that she preferred to avoid spectacle correction for near and distance vision postoperatively. Specifically, she desired the ability to read and use her handheld personal digital assistant without eyeglasses.

Unfortunately, the patient was not a good candidate for pseudoaccommodating or accommodating IOLs, because her pupils were irregular and she had advanced visual field loss. We were also concerned that she could have zonular instability secondary to spherophakia and that her short axial length would make it difficult to predict her refractive outcome. We instead implanted a monofocal IOL and targeted a mildly myopic refraction (-1.50 D) in the patient's left eye only. This refraction was chosen to help the patient obtain spectacle independence, with or without monovision, depending on the targeted refraction in her second eye. We decided to extract the lens from her left eye, because the angle closure had a phacomorphic component and the patient had more visual field defects in this eye than in her right eye. In addition, we performed goniosynechiolysis to resolve the extensive peripheral anterior synechiae (presumed to be of less than 1 year's duration) and to re-establish the left eye's anatomic angle.

OUTCOME Postoperatively, the patient achieved an acuity of 20/20 OD with mild myopic correction. Unlike her right eye, which still required three topical medications to maintain a stable IOP, her left eye had excellent IOPs, ranging between 7 and 10 mm Hg without hypotensive drugs. We also noted significant postoperative deepening of the anterior chamber (Figure 5), and gonioscopy revealed an essentially open angle with some residual peripheral anterior synechiae nasally. Despite these positive results, the patient is bothered by asthenopia in her left eye and has deferred surgical intervention in her right eye. We continue to monitor her closely.

DISCUSSION Bilateral ACG is an unusual and uncommon occurrence. The differential diagnoses for bilateral ACG are limited and include uveal effusion related to medication, general anesthesia, snake venom, and lenticular/zonular abnormalities. 1-5 In this case, we ruled out uveal effusions. Based on the size and shape of the patient's crystalline lenses, we instead considered a diagnosis of spherophakia.

Spherophakia is a rare congenital abnormality in which the crystalline lens' unusually large anteroposterior diameter causes it to take on a spherical formation. Clues to the diagnosis of spherophakia include a shallow anterior chamber, ACG, and high lenticular myopia (diameters of 4.5 to 4.9 mm). 6 Increased curvature of the lens is associated with weak, elongated zonules that can lead to ACG with pupillary block and the formation of peripheral anterior synechiae, subluxation of the lens into the anterior chamber, inflammation of the ciliary body, or progressive narrowing of the angle by the lens' anterior movement. 7,8

Microspherophakia (the presence of a spherical lens with a reduced equatorial diameter) is associated with systemic diseases such as Weill-Marchesani syndrome, Marfan syndrome, homocysteinuria, Klinefelter syndrome, Alport syndrome, and Meyer-Schwickerath-Weyers syndrome. 8-12

Investigators have hypothesized that spherophakia occurs when an incompletely developed ciliary body and its loose elongated zonules do not exert sufficient pressure to flatten the developing lens. The lenses of patients with spherophakia therefore retain a fetal spherical conformation. 13

Pupillary block in spherophakia is exacerbated by treatment with miotic drugs, because the relaxation of the ciliary body allows the lens to move forward and obstruct the pupillary aperture. On the other hand, mydriatic agents can sometimes relieve pupillary block by increasing tension on the zonules and pulling the lens complex posteriorly. 14

Surgeons can attempt to break an attack of ACG with laser peripheral iridotomy or lensectomy. The latter option may not be effective for eyes that have peripheral anterior synechiae or a damaged trabecular meshwork. Surgeons have advocated that patients who have peripheral anterior synechiae over more than 270° of their angle undergo goniosynechiolysis to help open the angle. 15-17

If damage to the trabecular meshwork is advanced, the previously described surgical interventions may not prevent glaucomatous progression. In these cases, patients may require filtering surgery or the implantation of a tube to lower their IOP. These options present their own problems, however, because filtering surgery tends to flatten the chambers of eyes with ACG and may contribute to the development of malignant glaucoma. 15

Tania Paul, MD, is a resident at Weill Cornell Medical College Department of Ophthalmology, New York-Presbyterian Hospital, New York. She acknowledged no financial interest in the products or companies mentioned herein. Dr. Paul may be reached at (646) 962-2020; [email protected] .

Nathan M. Radcliffe, MD, is an assistant professor of ophthalmology at Weill Cornell Medical College, New York-Presbyterian Hospital, New York. He acknowledged no financial interest in the products or companies mentioned herein. Dr. Radcliffe may be reached at (646) 962-0603; [email protected] .

• Banta JT, Hoffman K, Budenz DL, et al. Presumed topiramate induced bilateral acute angle closure glaucoma. Am J Ophthalmol. 2001;132:112-114.
• Craig JE, Ong TJ, Louis DL, Wells JM. Mechanism of topiramate-induced acute onset myopia and angle closure glaucoma. Am J Ophthalmol. 2004;137(1):193-195.
• de Guzman MH, Thiagalingam S, Ong PY, Goldberg I. Bilateral acute angle closure caused by supraciliary effusions associated with venlafaxine intake. Med J Aust. 2005;182(3):121-123.
• Ates H, Kayikcioglu O, Andac K. Bilateral angle closure glaucoma following general anesthesia. Int Ophthalmol. 1999;23:129-130.
• Srinivasan R, Kaliaperumal S, Dutta TK. Bilateral angle closure glaucoma following snake bite. J Assoc Physicians India. 2005;53:46-48.
• Willoughby CE, Wishart PK. Lensectomy in the management of glaucoma in spherophakia. J Cataract Refract Surg. 2002;28:1061-1064.
• Kaushik S, Sachdev N, Singh S, et al. Bilateral acute angle closure glaucoma as a presentation of isolated microspherophakia in an adult: case report. BMC Ophthalmol. 2006;6:29-35.
• Johnson GJ, Bosanquet RC. Spherophakia in a Newfoundland family: 8 years' experience. Can J Ophthalmol. 1983;18:159-164.
• Macken PL, Pavlin CJ, Tuli R, Trope GE. Ultrasound biomicroscopic features of spherophakia. Aust N Z J Ophthalmol. 1995;23(3):217-220.
• Nelson LB, Maumenee IH. Ectopia lentis. Surv Ophthalmol. 1982;27:143-160.
• Johnson VP, Grayson M, Christian JC. Dominant microspherophakia. Arch Ophthalmol. 1971;85:534-542.
• Widder RA, Engels, B, Severin M, et al. A case of angle-closure glaucoma, cataract, nanophthalmos, and spherophakia in oculo-dento-digital syndrome. Graefes Arch Clin Exp Ophthalmol. 2003;241(2):161-163.
• Dietlein TS, Mietz H, Jacobi PC, Krieglstein GK. Spherophakia, nanophthalmia, hypoplastic ciliary body, and glaucoma in brachydactyly-associated syndromes. Graefes Arch Clin Exp Ophthalmol. 1996;234:187-192.
• Ritch R, Wand M. Treatment of the Weill-Marchesani syndrome. Ann Ophthalmol. 1981;13:665-667.
• Kanamori A, Nakamura M, Matsui N, et al. Goniosynechialysis with lens aspiration and posterior chamber intraocular lens implantation for glaucoma in spherophakia. J Cataract Refract Surg. 2004;30:513-551.
• Campbell DG, Vela A. Modern goniosynechialysis for the treatment of synechial angle-closure glaucoma. Ophthalmology. 1984;91:1052-1060.
• Teekhasaenee C, Ritch R. Combined phacoemulsification and goniosynechialysis for uncontrolled chronic angle-closure glaucoma after acute angle-closure glaucoma. Ophthalmology. 1999;106:669-674

Diagnostic Tools for Primary Angle Closure

Jason A. Goldsmith, MD, MS

Elevated IOP After the Implantation of a Valved Drainage Device

Mark Werner, MD

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Steven D. Vold, MD

Drug Delivery Systems in Ophthalmology

Gary D. Novack, PhD

How to Approach Patients With OHT

Allison Angelilli, MD; Jeffrey M. Liebmann, MD; Arthur J. Sit, SM, MD; and Anjali M. Bhorade, MD, MS

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Diagnosing & Managing Glaucoma: A Case Study

The importance of imaging the macula in glaucoma and its effects on patient education

T his case study is an example of how meticulously and elegantly we can identify structural and functional defects by incorporating more than one imaging modality when diagnosing glaucoma patients. Although nerve fiber layer OCT imaging is often 
the most useful to detect early glaucoma, in some instances, the defect can be so localized that it is easy to miss when surrounded by healthy nerve fiber layer (NFL).

In this case study, however, the lesson is two-fold. Not only are images of the macula useful for clinical knowledge and decision making for individual patient management, but there is also considerable value in imaging the NFL and macula connected to patient 
education. A large part of the challenge associated with managing glaucoma patients is convincing them to comply with their treatment regimens. This case study also serves as an example of how imaging allows me to educate patients about their condition and progression. These visuals are easily understood by patients and encourage them to adhere to their treatment and, ultimately, improve their disease.

A 66-year-old female presented to my clinic for glaucoma consultation. The highest IOP that had been recorded throughout her prior history was 22 mmHg. Her risk factors were minimal. She had normal central corneal thickness, no significant familial risk factors, an angle open, and an unremarkable slit-lamp examination with OCT (Cirrus HD-OCT, Carl Zeiss Meditec) showed that she had a robust nerve fiber layer, which is typically reassuring ( Figure 1 ).

However, upon completing visual field testing (Humphrey Visual Field Analyzer, Carl Zeiss Meditec), I was surprised that the patient had a definite localized paracentral scotoma ( Figure 2 ).When I compared the visual field results with the OCT result, there was a disconnect. On OCT, the NFL appeared to be quite healthy, thus, the definite and reproducible visual field defect was unexpected.

Next, I administered a macular cube scan, which showed that the right eye was normal, but the left was quite abnormal and consistent with the visual field imaging. The very pronounced defect inferiorly on the macular cube correlated perfectly with the visual field images. I then reviewed the nerve fiber layer again on the OCT images, and I could see the defect on the left NFL at the 4 o’clock position on the optic nerve ( Figure 3 ). If I had only relied on OCT imaging, it would have been very easy to overlook the abnormality in the left eye. I used the images and the visual fields to demonstrate the well-defined structural and functional defects to the patient. The study results had a clear impact on the patient, so her resolve to follow the suggested treatment regimen was enhanced significantly.

An Important Lesson

This case confirms that we should not rely only on just one parameter. It would have been easy to analyze the OCT NFL image and deem it to be a normal scan, but, by also taking a macular scan, in addition to a visual field, the abnormality was clearly apparent. This is a rare example in which the NFL OCT misses glaucoma and the visual field picks it up. It was only when I imaged the macula that it became obvious that there was an abnormality in the NFL as well.

In many similar cases, I might only take images of the NFL and not request a visual field if the images of the NFL looked normal, because in such cases, the likelihood of finding a field defect is small, but we also know from the Ocular Hypertension Treatment Study (OHTS) trial 1 and others that abnormalities don’t always show up on the first attempt at diagnostic testing. In the OHTS trial, 
2,304 patients underwent at least two visual field examinations in both eyes to determine whether they were at risk for developing open-angle glaucoma to be deemed eligible for the trial. The study was designed to evaluate the safety and efficacy of a topical ocular hypotensive medication. On patients whose prior test was abnormal, questionable, or unreliable, researchers performed a third test.

Seventy-nine percent of the patients were eligible based on their initial visual field tests. The third eligibility test was required for 11% of the patients. Researchers reported that by repeating the test one time after an initial unreliable test, they could identify an additional 560 patients as being at risk for developing primary open-angle glaucoma. The practical implications of the OHTS trial’s findings are that there are many instances in our clinics every day where we may be missing an opportunity to properly diagnose a patient by failing to incorporate additional testing.

As a result, many patients benefit from imaging of the macula and NFL in my practice. I perform both types of imaging routinely for patients who have early-to-moderate glaucoma. In some instances, I also image patients with more advanced glaucoma because they’re often far advanced in one eye and only moderate or mild in their fellow eye.

In addition to diagnosis, I use macula and NFL imaging in glaucoma patients to determine if they’re stable or progressing. When progression is identified, it presets an opportunity to review compliance to be certain that patients comprehend the potential severity of their disease. I’ve found that many poorly compliant patients become more compliant when their imaging studies are shared with them and they can clearly see the structural changes.

Furthermore, I’ve found that imaging of the NFL and macula as an educational tool is useful for patients who are at a crossroads in their treatment. When I have patients who need surgery, have had a change in their treatment regimen, or are not complying, I show them their imaging results, because glaucoma is relatively asymptomatic — until it isn’t. Once it’s symptomatic and the patient becomes aware of his visual deficit, he can never turn back the clock.

When I show images, I can point out the structural defect and how it correlates to the visual field to show patients their defects in terrific detail. I also find it useful for family members caring for loved ones who have glaucoma. Imaging helps them better understand the physiology and the seriousness of the disease.

IT TAKES TWO

In this example, the macular scan in conjunction with the visual field and NFL was more useful than the visual field or NFL alone. As a bonus, demonstrating the patient’s abnormality to them, visually and graphically, improves disease education and compliance, especially in patients who need to improve their compliance with recommended therapies.

• Kass MA, Heuer DK, Higginbotham EJ, et al. The Ocular Hypertension Treatment Study: a randomized trial determines that topical ocular hypotensive medication delays or prevents the onset of primary open-angle glaucoma. Arch Ophthalmol. 2002;120(6):701-713;discussion 829-830.

Dr. Samuelson is an attending surgeon at Minnesota Eye Consultants in Minneapolis and an adjunct professor at the University of Minnesota in Minneapolis. Dr. Samuelson may be reached at (612) 813-3628; [email protected] . He is a consultant to Carl Zeiss Meditec, Inc.

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When is glaucoma &#8220;controlled&#8221;, outliers &amp; moving targets, iop at-home monitoring.

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Glaucoma Case Studies

Case One: Low-tension glaucoma: diagnosis and management; Case Two: Reversal of cupping following trabeculectomy

Glaucoma Case Studies Case One: Low-tension glaucoma: diagnosis and management

• Best-corrected visual acuity (BCVA) was 20/40 in both eyes
• No afferent pupillary defect was present
• Tonometry showed intraocular pressure (IOP) of 12 mmHg OU
• Anterior-segment exam was normal
• Gonioscopy reveled open angles bilaterally
• Dilated-fundoscopic exam revealed advanced cupping of both optic nerves, with cup to disc ratios of 0.95 OU. Peripapillary atrophy was also recorded on the exam.

Case Two: Reversal of cupping following trabeculectomy

Case history presentation: A 75-year-old female was referred for evaluation and treatment of open-angle glaucoma. She had uncontrolled IOP and glaucomatous progression of optic-nerve heads and visual fields on maximal tolerated medical therapy with dorzolamide hydrochloride-timolol maleate (Cosopt), brimonidine tartrate (Alphagan), and latanoprost. She had been treated medically for open-angle glaucoma for approximately 5 years.

• Best-corrected visual acuity was 20/30 OD, and 20/25+ OS
• Humphrey visual fields revealed paracentral losses in both eyes, right greater than left
• Anterior segment was remarkable for pseudophakia OD and mild, nuclear sclerotic cataract OS
• Applanation tonometry was measured at 32 mm Hg OD and 31 mm Hg OS
• Fundoscopic examination showed optic-nerve heads with advanced glaucomatous cupping in both eyes. (See images below.)

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Ophthalmic Case Study 1

Case study 1 - cc: acute r eye pain.

HPI: The patient is a 51 year-old stay-at-home mother who presented to the ED with severe R brow, R cheek and R eye pain/pressure that started 2-3 hrs prior. She also noticed blurry vision from that eye and rainbow-colored halos around lights around the same time. Accompanying symptoms include acute nausea. She has vomited twice since feeling the eye pain. Denies prior episodes. Denies flashes, floaters or diplopia. There is mild redness in the R eye.

Past Ocular History: Started wearing reading glasses at age 42; now wears progressive bifocals with hyperopic correction for distance No prior eye surgeries, trauma, amblyopia or strabismus

Ocular Medications: None

Past Medical History: Degenerative disc disease – lower back

Surgical History: None

Past Family Ocular History: Father: chronic angle closure glaucoma No FHx of macular degeneration or other blinding diseases.

Social History: 30 pack year smoking history Drinks alcohol on occasion No illicit drug use

Medications: Multivitamins Vicodin prn (uses few days/month for back pain)

Allergies: None

ROS: Denies recent illnesses, new medications, CNS, lungs, GI, skin, joint problems except for above.

Ocular Exam

Visual Acuity (cc): OD: 20/70 OS: 20/20

IOP (tonoapplantation): OD: 62 mmHg OS: 11 mmHg

Pupils: OD pupil mid dilated, sluggish to respond to light. OS pupil round and reactive to light No obvious APD

Extraocular Movements: Full OU No nystagmus

Confrontational Visual Fields: Full to finger counting OU

External: Normal, both sides

Diagnosis Suspected acute angle closure glaucoma R eye Narrow angle L eye

Definition: Acute angle closure glaucoma occurs when there is a relatively sudden blockage of the trabecular meshwork causing elevation of the intraocular pressure. One possible mechanism is the anterior bulging of the peripheral iris, occluding the trabecular meshwork and trapping aqueous humor inside the eye. The reason for the sudden anterior bulging of the peripheral iris may be due to pupillary block (where the lens presses up against the iris trapping all the aqueous humor behind it). This results in increased fluid in the posterior chamber, creating a pressure gradient that subsequently pushes the iris anteriorly and causes it to block the angle. The intraocular fluid accumulates and rises significantly (normal intraocular pressure is between 8 and 21 mmHg). Pupillary block is greatest when the iris is in a mid-dilated state. Individuals with a naturally occurring narrow angle are at a higher risk for acute angle closure.

Examination: Acute angle closure typically presents with severe ocular pain, headache, blurred vision, halos around lights, nausea, and vomiting. Some of the apparent non-ocular manifestations (nausea/vomiting) could be misleading to the inexperienced physician. However, the prompt recognition and subsequent treatment of an acute angle closure crisis is paramount in the preservation of the patient’s vision. Typical eye exam findings, as in this patient, include mild conjunctival injection, hazy cornea, mid dilated pupil, shallow angle and elevated intraocular pressure.

Angle closure is best observed using a gonioscopic contact lens that allows the viewer to see into the angle of the eye. Even if the acute episode is diagnosed and treated quickly and appropriately, there can still be optic nerve damage and resultant visual loss. Another possible change includes iris ischemia which can cause sloughing of iris pigment. Pigment can be noted in the anterior chamber and on the corneal endothelium. Iris damage may cause the pupil to remain in a dilated position. The intraocular pressure may also rise enough to cause retinal vascular occlusion and retinal ischemia. Anterior subcapsular lens opacities may also occur as a result of ischemia (this is termed glaukomflecken).  

Treatment: Treatment of acute angle closure glaucoma is either laser or surgical peripheral iridectomy (placing a hole in the peripheral iris). This procedure restores aqueous flow from the posterior to anterior chamber by creating an extra opening in the iris, relieving the pathologic pressure gradient. This ultimately allows the iris to regress and pull away from the trabecular meshwork and then normal aqueous humor drainage is restored. This procedure is often curative of the affected eye. A prophylactic peripheral iridectomy of the non-affected eye is necessary to prevent an episode from occurring in the fellow eye. Individuals with one episode of acute angle closure glaucoma have a high likelihood of an attack in the fellow eye over the next 5-10 years. Even when the intraocular pressure has decreased, subsequent follow up is necessary to be sure that the angle remains open. IOP may decrease soon after the attack due to ciliary body ischemia and decreased aqueous humor production and not because the angle has reopened.

• Nausea/vomiting
• Ocular pain
• Halos around lights
• The apposition of the pupil border against the lens obstructs aqueous humor flow through the pupil and creates a pressure gradient with increased pressure behind the iris. This moves the iris forward with subsequent apposition of the peripheral iris with the trabecular meshwork.
• Decreased drainage by the trabecular meshwork causes increased pressure in the anterior chamber and pushes the iris against the lens.
• A portion of vitreous humor moves anteriorly and around the lens, blocking the trabecular meshwork.
• Increased aqueous humor drainage through the trabecular meshwork causes a decreased pressure in the anterior chamber, causing a pressure gradient that presses the iris forward and blocks the angle.

References/Resources: Glaucoma BCSC, American Academy of Ophthalmology, 2009.

1. A patient presents with a sudden increase of intraocular pressure to 55 mmHg in the L eye. Gonioscopic examination demonstrates a closed angle with trabecular meshwork obstruction. Which of the following is not a likely presenting symptom in this patient:

b. Diplopia

Most patients would have some ocular pain, periorbital headache, and maybe nausea with an acute increase in intraocular pressure to that degree. Corneal swelling would cause halos around light. Diplopia is a binocular condition and would not necessarily affect the patient in this case. 

2. What is the mechanism of angle closure in an episode of acute angle closure glaucoma resulting from a pupillary block?

a. The apposition of the pupil border against the lens obstructs aqueous humor flow through the pupil and creates a pressure gradient with increased pressure behind the iris. This moves the iris forward with subsequent apposition of the peripheral iris with the trabecular meshwork.

Medical College of Wisconsin Ophthalmology and Visual Sciences Case Studies

Ophthalmic case study 10, ophthalmic case study 2, ophthalmic case study 11, ophthalmic case study 3, ophthalmic case study 12, ophthalmic case study 4, ophthalmic case study 13, ophthalmic case study 5, ophthalmic case study 14, ophthalmic case study 6, ophthalmic case study 15, ophthalmic case study 7, ophthalmic case study 16, ophthalmic case study 8, ophthalmic case study 17, ophthalmic case study 9, ophthalmic case study 18, contact ophthalmology.

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• Open-angle glaucoma

Usually, fluid (aqueous humor) in the eye flows freely through the anterior chamber and exits through the drainage system (trabecular meshwork). If that system is blocked or isn't functioning well, the pressure inside the eye (intraocular pressure) builds, which in turn damages the optic nerve. With the most common type of glaucoma, this results in gradual vision loss.

Glaucoma is a group of eye conditions that damage the optic nerve. The optic nerve sends visual information from your eye to your brain and is vital for good vision. Damage to the optic nerve is often related to high pressure in your eye. But glaucoma can happen even with normal eye pressure.

Glaucoma can occur at any age but is more common in older adults. It is one of the leading causes of blindness for people over the age of 60.

Many forms of glaucoma have no warning signs. The effect is so gradual that you may not notice a change in vision until the condition is in its later stages.

It's important to have regular eye exams that include measurements of your eye pressure. If glaucoma is recognized early, vision loss can be slowed or prevented. If you have glaucoma, you'll need treatment or monitoring for the rest of your life.

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The symptoms of glaucoma depend on the type and stage of your condition.

• No symptoms in early stages
• Gradually, patchy blind spots in your side vision. Side vision also is known as peripheral vision
• In later stages, difficulty seeing things in your central vision

Acute angle-closure glaucoma

• Severe headache
• Severe eye pain
• Nausea or vomiting
• Blurred vision
• Halos or colored rings around lights
• Eye redness

Normal-tension glaucoma

• Gradually, blurred vision
• In later stages, loss of side vision

Glaucoma in children

• A dull or cloudy eye (infants)
• Increased blinking (infants)
• Tears without crying (infants)
• Nearsightedness that gets worse

Pigmentary glaucoma

• Halos around lights
• Blurred vision with exercise
• Gradual loss of side vision

When to see a doctor

If you experience symptoms that come on suddenly, you may have acute angle-closure glaucoma. Symptoms include severe headache and severe eye pain. You need treatment as soon as possible. Go to an emergency room or call an eye doctor's (ophthalmologist's) office immediately.

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Glaucoma develops when the optic nerve becomes damaged. As this nerve gradually deteriorates, blind spots develop in your vision. For reasons that doctors don't fully understand, this nerve damage is usually related to increased pressure in the eye.

Elevated eye pressure happens as the result of a buildup of fluid that flows throughout the inside of the eye. This fluid also is known as the aqueous humor. It usually drains through a tissue located at the angle where the iris and cornea meet. This tissue also is called the trabecular meshwork. The cornea is important to vision because it lets light into the eye. When the eye makes too much fluid or the drainage system doesn't work properly, eye pressure may increase.

This is the most common form of glaucoma. The drainage angle formed by the iris and cornea remains open. But other parts of the drainage system don't drain properly. This may lead to a slow, gradual increase in eye pressure.

Angle-closure glaucoma

This form of glaucoma occurs when the iris bulges. The bulging iris partially or completely blocks the drainage angle. As a result, fluid can't circulate through the eye and pressure increases. Angle-closure glaucoma may occur suddenly or gradually.

No one knows the exact reason why the optic nerve becomes damaged when eye pressure is normal. The optic nerve may be sensitive or experience less blood flow. This limited blood flow may be caused by the buildup of fatty deposits in the arteries or other conditions that damage circulation. The buildup of fatty deposits in the arteries also is known as atherosclerosis.

A child may be born with glaucoma or develop it in the first few years of life. Blocked drainage, injury or an underlying medical condition may cause optic nerve damage.

In pigmentary glaucoma, small pigment granules flake off from the iris and block or slow fluid drainage from the eye. Activities such as jogging sometimes stir up the pigment granules. That leads to a deposit of pigment granules on tissue located at the angle where the iris and cornea meet. The granule deposits cause an increase in pressure.

Glaucoma tends to run in families. In some people, scientists have identified genes related to high eye pressure and optic nerve damage.

Risk factors

Glaucoma can damage vision before you notice any symptoms. So be aware of these risk factors:

• High internal eye pressure, also known as intraocular pressure
• Age over 55
• Black, Asian or Hispanic heritage
• Family history of glaucoma
• Certain medical conditions, such as diabetes, migraines, high blood pressure and sickle cell anemia
• Corneas that are thin in the center
• Extreme nearsightedness or farsightedness
• Eye injury or certain types of eye surgery
• Taking corticosteroid medicines, especially eye drops, for a long time

Some people have narrow drainage angles, putting them at increased risk of angle-closure glaucoma.

These steps may help detect and manage glaucoma in its early stages. That may help to prevent vision loss or slow its progress.

Get regular eye examinations. Regular comprehensive eye exams can help detect glaucoma in its early stages, before significant damage occurs. As a general rule, the American Academy of Ophthalmology recommends a comprehensive eye exam every 5 to 10 years if you're under 40 years old; every 2 to 4 years if you're 40 to 54 years old; every 1 to 3 years if you're 55 to 64 years old; and every 1 to 2 years if you're older than 65.

If you're at risk of glaucoma, you'll need more frequent screening. Ask your health care provider to recommend the right screening schedule for you.

• Know your family's eye health history. Glaucoma tends to run in families. If you're at increased risk, you may need more frequent screening.
• Wear eye protection. Serious eye injuries can lead to glaucoma. Wear eye protection when using power tools or playing sports.
• Take prescribed eye drops regularly. Glaucoma eye drops can significantly reduce the risk that high eye pressure will progress to glaucoma. Use eye drops as prescribed by your health care provider even if you have no symptoms.

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Staying the course through follow-up care and therapeutic drug monitoring

For most of his adult life, Billy Dowell Jr. has lived with a serious immune-mediated disease process that has threatened not only his dream of playing professional golf, but his very existence. His illness caused painful pelvic joint inflammation, resulted in a perforated bowel, and led to glaucoma. It’s been ongoing, unrelenting, and extremely unpleasant. “I’ve been through the roughest of the rough,” says Billy, a resident of Jacksonville, Florida, who moved there in May…

• What is glaucoma? American Academy of Ophthalmology. https://www.aao.org/eye-health/diseases/what-is-glaucoma. Accessed Aug. 21, 2022.
• At a glance: Glaucoma. National Eye Institute. https://www.nei.nih.gov/learn-about-eye-health/eye-conditions-and-diseases/glaucoma. Accessed Aug. 21, 2022.
• AskMayoExpert. Glaucoma (adult). Mayo Clinic; 2021.
• What is glaucoma? Glaucoma Research Foundation. https://www.glaucoma.org/glaucoma/. Accessed Aug. 22, 2022.
• Glaucoma. American Optometric Association. https://www.aoa.org/healthy-eyes/eye-and-vision-conditions/glaucoma?sso=y. Accessed Aug. 22, 2022.
• Childhood glaucoma: Diagnosis, treatment, and hope. Glaucoma Research Foundation. https://glaucoma.org/childhood-glaucoma-diagnosis-treatment-and-hope/. Accessed Aug. 24, 2022.
• Jacobs D, et al. Open-angle glaucoma: Epidemiology, clinical presentation, and diagnosis. https://www.uptodate.com/contents/search. Accessed Aug. 22, 2022.
• Overview of glaucoma. Merck Manual Professional Version. https://www.merckmanuals.com/professional/eye-disorders/glaucoma/overview-of-glaucoma. Accessed Sept. 16, 2020.
• Comprehensive adult medical eye evaluation preferred pattern. American Academy of Ophthalmology. https://www.aao.org/preferred-practice-pattern/comprehensive-adult-medical-eye-evaluation-ppp. Accessed Aug. 24, 2022.
• Ferri FF. Glaucoma, open angle. In: Ferri's Clinical Advisor 2023. Elsevier; 2023. https://www.clinicalkey.com. Accessed Aug. 24, 2022.
• Jacobs D, et al. Open-angle glaucoma: Treatment. https://www.uptodate.com/contents/search. Accessed Aug. 24, 2022.
• Alternative medication. Glaucoma Research Foundation. https://glaucoma.org/alternative-medicine. Accessed Aug. 24, 2022.
• Does marijuana help treat glaucoma or other eye conditions? American Academy of Ophthalmology. https://www.aao.org/eye-health/tips-prevention/medical-marijuana-glaucoma-treament. Accessed Aug. 24, 2022.
• Mayo Clinic Research Finds Risk of Glaucoma Blindness Drops by Half

News from Mayo Clinic

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Glaucoma Case Studies

Nov 18, 2014

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Glaucoma Case Studies. James C. Tsai, M.D. Associate Professor of Ophthalmology Director, Glaucoma Division Edward S. Harkness Eye Institute Columbia University. LD: Clinical History &amp; Exam. 78 y/o woman with glaucoma x 7 months PMHx: hypothyroid; Meds: Synthroid, Premarin

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Glaucoma Case Studies James C. Tsai, M.D. Associate Professor of Ophthalmology Director, Glaucoma Division Edward S. Harkness Eye Institute Columbia University

LD: Clinical History & Exam • 78 y/o woman with glaucoma x 7 months • PMHx: hypothyroid; Meds: Synthroid, Premarin • Ocular Hx: negative; on Xalatan qhs OU • Va: 20/40 OU, Ta: 17 OD, 22 OS (9:25 AM) • SLE: 2+ NSC OU (+ PXE flakes), A/C D&Q • Gonio: Grade II-III OU; CCT: 518 OD, 533 OS • C/D ratio: 0.75 OD, 0.85 OS; thin temporally OU

LD: Clinical Assessment • HVF: OD: WNL, OS: inf. arcuate defect/nasal step • OCT3: OD: 88.0 microns, OS: 74.75 microns • Imp: PXF glaucoma w/ uncontrolled IOP (OS>OD) ? Thin CCT OU a risk factor Target IOP: mid-teens OU • Treatment Plan: ??

Patient: J.D. • 47 y.o. M w/ COAG & recurrent erosions • FHx of POAG, Myopia (-4 to -6 D) • Va 20/20 OU; IOP 18 OD, 16 OS • cc: grayer & darker vision (OD > OS) • C/D = 0.8 OD, 0.7 OS (cupped temporally) • Meds: Betaxolol, Propine

Patient: J.D. • Initial ALT OD, followed by ALT OS • 1 year later: c/o worse vision (OS > OD) • Va 20/20 OU; IOP 10 OD, 11 OS • Diurnal curve: peak of 13 OU • HVF: worse OU • C/D = 0.9 OD; 0.85 OS

Patient: J.D. • Neuro-ophthalmology consult: B-12 and folate: WNL CT of orbits: WNL • 3 months later: IOP 16 OU; cc: OS dimmer • TBX w/ MMC OS & OD 2 months later • 5 year F/U: Va 20/20 OU; IOP 10 OD, 9 OS HVF stable OU; No visual loss

Visual Fields Pre-Surgery

Visual Fields Post-Surgery

Case Presentation • 15 year old boy S/P trauma OD (tennis ball) • Cc: Blurred vision OD x 3 months • PMHx: negative • Va: 20/200 OD, 20/20 OS • IOP: 4 mm Hg OD, 15 mm OS • SLE (OD): deep A/C, trace RBCs

Anterior Ultrasound

Assessment • Ocular hypotony OD (with maculopathy) • Cyclodialysis cleft with concomitant angle recession • Treatment:1. Argon laser closure of cleft2. Surgical closure of cleft • Need to monitor for post-op IOP spike(? Concurrent Stage 1 glaucoma tube)

Followed in glaucoma clinic for COAG Noted progressive ↓ invision Referred to retina clinic to evaluate macula VA: 20/50 OD 20/80 OS 0.6 log unit RAPD OS Color 1/15 OU 74 Year Old Female

Optic Disc Exam

Humphrey Visual Fields

Neuroimaging

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Uveitic Glaucoma

Case presentation.

A 40-year-old man was referred for unilateral glaucoma in his left eye. Medical history was unremarkable for systemic disorders and medications.The patient had undergone uneventful phacoemulsification and posterior chamber intraocular lens (PCIOL) implantation in the same eye two years ago. Six months postoperatively intraocular pressure (IOP) was inadequately controlled with topical medications.The most recent examination revealed bestcorrected visual acuity of 10/10 with plano −0.5×100° and plano −1.75×60° in the right and left eyes, respectively. Slitlamp examination was unremarkable in the right eye. Examination in the left eye disclosed a normal tear film,intact and mobile conjunctiva, fine diffuse keratic precipitates (KPs), trace cells but no flare in the anterior chamber, diffuse iris atrophy with no synechiae, a well-positioned PCIOL, mild fibrotic posterior capsule opacification, and trace cells in the anterior vitreous. IOP was 13 mmHg in the right eye with no medications and 27 mmHg in the left eye with timolol BID,dorzolamide BID and brimonidine TID.Gonioscopy revealed wide open angles with no synechiae in both eyes. Fundus examination revealed cup/disc (C/D) ratio of 0.2 with healthy appearing neural rim and macula,normal vessels and peripheral retina in the right eye; and vertical C/D ratio of 0.8 with significant neural rim loss particularly in the inferior pole, but normal appearing macula,vessels and periphery in the left eye ( Fig. 1 ).Central corneal thickness was 579 and 559 μm in the right and left eyes, respectively. Standard achromatic perimetry was completely normal in the right eye but impaired in the left eye ( Fig. 2 ).

Optic disc appearance in the left eye.

2 Standard achromatic perimetry of the left eye.

Herein, we present the views of three glaucoma specialists regarding the diagnosis and management of the condition in this patient and whether adjunctive diagnostic tests or systemic evaluation is justified.

Heydar Amini, MD

Clinical findings consisting of low grade unilateral uveitis, cataract, fine diffuse KPs, iris atrophy and the absence of posterior synechiae are compatible with Fuchs heterochromic iridocyclitis (FHI). Despite diffuse iris atrophy, heterochromia has not been present; the absence of which may be due to a dark brown iris which is frequent in our patients. Differential diagnosis includes other causes of uveitic glaucoma such as herpetic keratouveitis, Posner-Schlossman syndrome, sarcoidosis and toxoplasmosis.Long-term steroid use may also cause steroid induced glaucoma. With a probable diagnosis of FHI, no additional laboratory or imaging studies are useful; the diagnosis is clinical solely based on history and examination. Recent studies, have suggested an association between FHI and the rubella virus and toxoplasmosis. Therefore, in unusual cases,laboratory tests for rubella virus or toxoplasmosis may help confirm the diagnosis. Considering treatment, laser trabeculoplasty is not effective and I would prefer trabeculectomy with adjunctive mitomycin-C. However, glaucoma drainage implants may be as effective as trabeculectomy. With both surgical approaches,chronic intraocular inflammation may ultimately lead to failure.

Kouros Nouri-Mahdavi, MD

The patient is a 40-year old man with history of unilateral cataract surgery in his left eye and subsequent (or pre-existing) glaucoma, now unresponsive to medical treatment. There are signs of mild persistent inflammation along with diffuse iris atrophy. The first and foremost task in this case is to clarify possible issues underlying the persistent uveitis, which is the most likely cause of glaucoma. The clinical presentation, including stellate KPs, diffuse iris atrophy, lack of posterior synechiae and evidence of mild vitritis are all in favor of FHI.There are few uveitic entities that resemble FHI. Herpetic uveitis can cause iris atrophy and indolent uveitis but the iris atrophy is usually more localized, involves the full thickness of the iris and is often accompanied by signs of corneal involvement. Glaucomatocyclitic crisis can also sometimes resemble FHI. However, at least in the beginning, IOP rise is episodic and readily responds to treatment. Moreover, the KPs tend to be localized and plumper. In this particular case, the presentation does seem typical of FHI.

The main question at this point is whether we need to perform additional tests to establish the diagnosis or for therapeutic purposes.There is strong evidence that FHI is likely the final result of a viral involvement of the eye,years or decades earlier in life. Rubella virus RNA and high anti-rubella antibody titers in the anterior chamber of eyes with FHI have been recently reported. Less commonly, cytomegalovirus (CMV) has been implicated as a cause of FHI. There is no known treatment for rubella virus but the possibility of treating CMV and potentially treating the secondary glaucoma is very appealing. Therefore, if polymerase chain reaction (PCR) were readily available,I would perform an anterior chamber tap and request PCR tests for rubella, CMV, and herpes viruses. In case of a positive result for CMV or herpes, I would initiate a trial of antiviral therapy for at least a few weeks and observe the response. If PCR is not available, its results are negative or if the above-mentioned trial is inconclusive, we are left with the option of treating the secondary glaucoma since there is no known treatment for rubella virus infection.

The patient does demonstrate obvious signs of glaucoma in his left eye both at the level of the optic disc and visual field. We are unaware how high the IOP had been prior to treatment. We can only assume that it was quite higher than mid-20s since the last IOP has been 27mmHg on 3 glaucoma medications.Given the severity of glaucomatous damage, I would classify it as moderately to severely advanced.Therefore, I would require a relatively low target IOP. I think the initial target IOP could to be set around mid- to upper teens considering the purely high-tension nature of the glaucoma in this case.

The patient is already on maximally tolerable medical treatment except for a prostaglandin (PG) analog. Although one would rather not use a PG analog in this setting, there are reports that a PG analog may not necessarily intensify the inflammation especially given the chronicity and mild nature of the inflammation in FHI. However, I doubt that adding a PG analog as a fourth medication will improve IOP control as much as we would like it to. But since we are left with no other nonaggressive treatment options at this point, it may be worth a short trial.Most likely the patient will require incisional surgery since laser trabeculoplasty is unlikely to help and not indicated. There is no firm evidence in the literature to guide us in the choice of surgery in this particular case. Young age, pseudophakia, and especially presence of chronic inflammation are factors that could lead some glaucoma specialists to do a primary glaucoma drainage procedure. However, given the intact nature of the superior perilimbal conjunctiva and the fact that the patient will likely need more than one glaucoma procedure in his lifetime, personally I would prefer a trabeculectomy with mitomycin-C as initial surgery. Intensive preoperative treatment with steroids is not required since the uveitis in FHI is typically not responsive to steroids. If the first trabeculectomy fails despite optimal perioperative care, I would then implant a glaucoma drainage device in the superotemporal quadrant. My device of choice would be a 350 mm2 Baerveldt implant with no antimetabolites.

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Navid nilforoushan, md.

Based on the available data, this is a fairly young patient with unilateral mild chronic iridocyclitis, moderately advanced open angle glaucoma and history of cataract surgery.Apparently the patient has had no symptoms of ocular discomfort such as redness, pain and photophobia. In a patient with chronic unilateral iridocyclitis and glaucoma, three differential diagnoses should be considered: FHI,glaucomatocyclitic crisis and herpetic uveitis.No signs or symptoms of corneal involvement in the past and present, diffuse uniform iris atrophy, and lack of synechiae formation all point against a diagnosis of herpetic uveitis.The first two diagnoses can be quite similar in signs: diffuse iris atrophy and hypochromia, no tendency for synechiae formation and fine diffuse KPs. The main cause for seeking medical attention in FHI is decreased vision from cataract formation; in contrast patients with glaucomatocyclitic crisis (Posner-Schlossman syndrome) usually have recurrent attacks of mild ocular discomfort associated with blurred and halo vision. Between episodes, the eye is quiet and there are no signs of inflammation such as KPs, anterior chamber cells and flare. In this patient with open angle glaucoma, unilateral iridocyclitis, lack of synechiae, clear cornea, fine diffuse KPs and past history of cataract surgery, one would consider an initial diagnosis of FHI and therefore, further systemic evaluation is not required. Regarding treatment, my initial choice would be trabeculectomy with high concentrations of mitomycin-C (0.04%). In addition, 7–10 days before surgery I would prescribe topical and systemic steroids to stabilize the blood-aqueous barrier and decrease postoperative inflammation. If this fails I would opt for a shunt procedure.