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Focus on glaucoma

Marc B. Taub OD and Brian Gardner OD

Angle recession glaucoma


Case reports and literature review
The introduction of the prostaglandin analogues have made unmanageable cases manageable, and have allowed us to successfully avoid surgical intervention in more of our patients. The Ocular Hypertensive Treatment Study (OHTS) identified multiple risk factors for developing glaucoma, including decreased central corneal thickness. Pachymetry has emerged as the new standard of care in the management of glaucoma patients. The introduction of diagnostic equipment such as the GDx nerve fibre analyser, optical coherence tomography (OCT), and the Heidelberg Retinal Tomograph II (HRT II) have proven to be useful adjuncts. The following cases describe the evaluation, diagnosis and management of angle recession glaucoma. Each patient presented with unique clinical findings and was successfully managed with various therapies.

ur understanding and management of glaucoma has progressed immensely in the past few decades. Although the true aetiology of glaucoma remains elusive, the treatments and diagnostics have made leaps and bounds.
16mmHg LE. Gonioscopy showed ciliary body in both eyes of 360 with angle recession of the inferior angle in the right eye from five to seven oclock. The optic nerves were asymmetric with cup to disc ratios of 0.55/0.60 (H/V) with superior temporal thinning in the right eye and 0.35/0.35 in the left. Also noted was pallor of the optic nerve head in the right eye with a posterior vitreous detachment (PVD). The macular area in the right eye exhibited drusen and an epiretinal membrane. A perimacular scar secondary to a longstanding choroidal rupture was also seen in the right eye. 24-2 SITA Fast Humphrey visual field of the right eye (Figure 1) indicated a nasal step with other isolated missed points. There were several non-specific missed points in the left eye, which were noted to be evaluated for repeatability on the next visit. HRT II (Figures 2 and 3) showed asymmetry of the cup/disc ratio, but were within normal limits per Moorfields regression analysis. GDx results (Figure 4) showed significant asymmetry of the nerve fibre layers between the two eyes.

Temporal) graph and chart. With this added information, the missed visual field points in the left eye became questionable. The contradiction of the two instruments exemplifies why practitioners must interpret test results for themselves, rather than simply rely on the normative database of each particular diagnostic software analysis.

Case history two


A 54-year old black male presented for a routine eye examination with a positive history of primary open angle glaucoma. He had discontinued his drops three years earlier. His complaints included itching, tearing, burning, flashing lights, and floating spots in both eyes. His last eye examination was three and a half years ago. His ocular history included trauma in the right eye as a child. His systemic history was positive for arthritis and post-surgical prostate cancer.

Examination
Best corrected visual acuities at distance and near were 6/6 in both eyes. Pupils were equal, round and reactive to light with no afferent defect. Colour vision and confrontation fields were normal. Extraocular muscles were full and smooth, and blood pressure was 136/82. Anterior segment revealed a corneal scar in the right eye, along with pinguecula, papillae and capped meibomian glands in both eyes. Goldmann applanation tonometry revealed IOPs of 26mmHg RE and 17mmHg LE. The optic nerves showed asymmetry, RE>LE with cup to disc ratios of 0.6/0.75 and 0.25/0.25 respectively. Gonioscopy revealed recession of the angle nasally in the right eye. SITA Std 24-2 SITA Standard Humphrey visual fields (Figures 5 and 6) indicated possible superior arcuate scotoma in both eyes. Fields were repeated two months later and indicated less extensive defects in both eyes. GDx (Figure 7) revealed normal nerve fibre in the left eye with significant defects in the right eye.

Case history one


A 45-year old Hispanic female was referred by her optometrist for asymmetrical cupping of the optic nerves, increased IOP, and a perimacular scar in her right eye. Her ocular history was positive for a corneal abrasion in her left eye at nine years of age and a car accident 11 years ago, which resulted in the need for reconstructive surgery to the right side of her face and periocular area. The patient did not report any ocular complaints. Her past medical history was positive for intermittent tension headaches. She took no medications and had no allergies to food or drugs.

Discussion
The patient was diagnosed with angle recession glaucoma and treatment was initiated with Alphagan P twice a day in the right eye. The patient was instructed to return for a follow-up after two weeks for an IOP check and to repeat visual fields. Also diagnosed were corectopia, PVD, optic atrophy, and longstanding choroidal rupture in the right eye all presumably secondary to trauma. Upon follow-up, IOPs were 18mmHg RE and 17mmHg LE, which represented a 28% decrease in the right eye. Serial visual fields were not performed at this visit due to patient time constraints. An interesting point concerning this case was the comparison of the GDx and HRT II results. Although asymmetry of the cup/disc ratio was present, both eyes still fell within normal limits on the HRT II. GDx results showed general nerve tissue loss in the right eye, consistent with the optic nerve head atrophy and glaucomatous axonal loss. Inter-eye symmetry fell outside of normal limits. The left eye showed normal range of nerve fibre layer thickness values surrounding the optic nerve, as shown by the TSNIT (Temporal, Superior, Nasal, Inferior,

Examination
Best corrected distance visual acuities were 6/9 RE and 6/6 LE. Her left pupil was round and reactive, while her right pupil was reactive with corectopia (a displacement of the pupil). An afferent pupillary defect was observed in her right eye. Colour vision was normal with slower responses in her right eye. Extraocular motility was full and smooth with normal confrontation fields in both eyes. Anterior segment evaluation revealed mild anterior and posterior blepharitis in both eyes, with trace pigmentation of the endothelium in the left eye. Corectopia of the iris in the right eye was observed. Goldmann applanation tonometry revealed IOPs of 25mmHg RE and

Discussion
Treatment was initiated with Lumigan once a day at night in the right eye only. Goldmann applanation tonometry was taken at a two-month follow-up and showed IOPs of 19mmHg RE and 20mmHg LE. This represented a 27.6% reduction in the right eye. The patient was advised to continue to return for follow-up every three months. At first glance, the visual field did not reveal a large difference between the eyes.

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Focus on glaucoma

Figure 1
Right visual field shows a nasal step and other isolated missed points

Figure 2
Right HRT II shows a larger cup/disc ratio but within normal database limits

Figure 3
Left HRT II shows a smaller cup/disc ratio within normal database limits

Figure 4
Right GDx (left side) shows diffuse nerve fibre layer loss with abnormal TSNIT values. Left GDx (right side) shows normal nerve fibre layer thickness with normal TSNIT values

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Focus on glaucoma

Marc B. Taub OD and Brian Gardner OD

Figures 5 and 6 Visual fields show a possible arcuate scotoma with GHT outside of normal limits in both eyes

When the GDx was brought into the mix, the nerve fibre layer defect in the right eye jumped off the page. The visual field defect in the left eye was believed to be an artifact because a nerve fibre layer defect was not present on the GDx. Both eyes were noted for close monitoring in the future with continued follow-ups. When comparing the first and second visual fields, it must be kept in mind that there was most likely a learning curve. The glaucomatous defects did not resolve with treatment the patient worked out how to take the test. One bad field does not represent glaucoma; several must be performed to truly diagnose this disease.

Background
Approximately 1.8-5.6 per thousand Americans over the age of 40 suffer ocular injuries. The annual incidence of ocular trauma requiring in-patient hospital treatment is 13.2 per 100,000 per year. Trauma to the eye, face and head is generally due to several activities. With regard to age, ocular trauma occurs in a bimodal distribution. The maximal risk occurs in young children and adults over the age of 70. The causes for the trauma also differ among these age groups. Falling, leading to secondary open globe trauma, is the most common cause among the over-70 population, while assault, car accidents and occupational hazards are more common in young adults. Children suffer trauma due to organised sports, domestic accidents, and from simply playing1. The first description of angle recession was by Collins in 1892. He described a split between the circular and longitudinal muscle fibres in two patients2. Wolf and Zimmerman reviewed 300 traumatised eyes in 1962, pointing out the clinical association among trauma, angle recession and glaucoma. They reported the presence of six patients who suffered from unilateral glaucoma and who had a history of blunt trauma with angle recession3.

Figure 7
GDx indicates a nerve fibre layer asymmetry in the right eye (right side) versus the left eye (left side). TSNIT values are abnormal in the right eye and normal in the left

Aetiology
When a blunt object hits the cornea, a pressure wave is formed. This wave causes the iris to strike the anterior surface of the lens, closing the iris-lens diaphragm. Since the fluid is not able to

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Focus on glaucoma

travel posteriorly, the only option is for the fluid to move laterally into the anterior chamber angle. This can cause a breakage, or cleavage, between the circular and longitudinal fibres of the ciliary body. This shockwave also causes damage to the trabecular meshwork, producing micro-tears. Scarring of the trabeculum results from these tears. While the scars cannot be seen via gonioscopy, they have been seen on histopathological examination4. Other mechanisms are also responsible for decreasing outflow. Descemets membrane may be stimulated to grow over the trabeculum due to the trauma4,5. Furthermore, the injury to the ciliary body may lessen the ability of the longitudinal ciliary body to apply tension to the trabeculum4.

Epidemiology
It is unknown why some patients with angle recession develop glaucoma and others do not. Even the incidence of angle recession following blunt trauma/ contusion injuries varies from 20% to 100%. Studies have shown that between 0-20% of patients with angle recession go on to develop glaucoma6-12. The main risk factor for the development of glaucoma in individuals with angle recession is the degree of recession. In studies, most patients who ultimately develop glaucoma had 240-360 of recession7. Those with less than 180 have a very low risk to develop glaucomatous changes11. The lifetime risk of developing primary open angle glaucoma in the non-traumatised fellow eye may be as high as 50%. A greater increase of IOP in the fellow eye with steroid provocative testing has been found6,7. One thing to keep in mind is that even though the patient in your chair has angle recession glaucoma in one eye, it does not preclude them from having POAG in both eyes. It is possible that the injury merely accelerated the glaucomatous changes in the traumatised eye7.

anterior subcapsule, Vossius ring, dislocation and phacodonesis7,14. Retinal detachments or tears can also occur13. Performing gonioscopy is the gold standard for evaluation of the angle. Whether you use a one, three or four-mirror lens makes no difference. Whichever you choose, perform this procedure on normal patients to hone your skills. The more you do, the better you will become at picking up the subtle differences. As is the case when looking at a questionable optic nerve head, look at the normal eye angle first to better judge the variations. Depending on the force of the injury, the view through a gonio-lens may vary. Minor injuries may present as torn iris processes or small tufts of uveal tissue observed on the iris root, or on the trabecular meshwork just above the scleral spur. Physical separation of the ciliary body at the apex of the angle is present in more severe cases. In these cases, the grey portion of the ciliary body appears broadened and the scleral spur is white and prominent13,14. Small peripheral anterior areas of synechiae can appear at the lateral limits of the angle recession and may extend into the peripheral areas of the recession14. A different clinical picture will be present on gonioscopy years after the initial assault. A marked, wedge-like contour of the ciliary muscle will be present due to the atrophying of inner circular muscles which were separated from the longitudinal fibres. The trabecular meshwork undergoes degeneration leading to atrophy, fibrosis and hyalinization. Peripheral anterior synechiae may also be present13.

Treatment
Because glaucoma secondary to angle recession can occur up to 50 years after the initial insult, patients must be monitored at least yearly. Gonioscopy should be considered for all patients presenting with history of ocular trauma regardless of intraocular pressure. If greater than 180 of angle recession is present, closer monitoring may be warranted. The standard of treatment for angle recession glaucoma is similar to that of primary open angle glaucoma. The first-line of treatment involves topical medications which decrease aqueous formation, such as beta-blockers, carbonic anhydrase inhibitors and alpha 2-agonists. Prostaglandin analogues, such as Xalatan, Lumigan and Travatan, which increase uveoscleral output, may prove useful13,14. Surgical management can be quite challenging in these cases. Argon laser trabeculoplasty (ALT) usually fails to lower IOP in this population. Traditional trabeculectomy has a lower success rate in this group. These patients require more post-operative glaucoma medications, develop more bleb fibrosis and have less of a decrease in IOP versus primary open angle glaucoma patients. The use of mitomycin-C or 5-florouracil and other metabolites appear to increase the success rate of this procedure. While filtering implants have shown some success, they too are prone to failure14.

Conclusion
Despite the incidence of ocular trauma, very few patients will go on to develop angle recession glaucoma. Even with this evidence, patients who have recessed angles require close monitoring of not only the traumatised angle but also the fellow eye. Determining if and what type of glaucoma is present relies solely on the abilities of the practitioner. In POAG and NTG, making a diagnosis can be straightforward at times, or very challenging in cases where true glaucomatous damage is questionable. Secondary open angle glaucomas can mimic POAG, but careful history and evaluation of the anterior segment using biomicroscopy and gonioscopy will help to determine the true aetiology and type of glaucoma present. With your care and hard work, your patients can continue to live their lives seeing all the world has to offer.

Differential diagnosis
One angle anomaly which can be confused with angle recession is cyclodialysis. In contrast to the changes found in angle recession, in which cleavage is between the circular and longitudinal fibres of the ciliary body, the separation in cyclodialysis occurs between the longitudinal muscle fibres of the ciliary body and the sclera. Clinically, there will be an area of white posterior to the scleral spur. Iridodialysis, trabecular tears and other abnormalities secondary to trauma must be ruled out14. Other forms of unilateral or asymmetrical glaucoma must be investigated as well. That list includes pigmentary dispersion and pseudoexfoliative syndromes, uveitic or inflammatory glaucoma, lens induced pressure changes, tumours of the iris or ciliary body, and iris or angle neovascularisation13. These various types of glaucoma will be ruled out during the examination and case history, which includes a full medical and ocular history14.

Clinical findings
As we all know, a good examination begins with a great case history. In some cases, the trauma may be so long ago, or not in the forefront of the patients thoughts, that they forget about it. One thing to keep in the back of your mind when you have a patient who denies a traumatic event is the emotional aspect. They may have been, or are currently in, an abusive relationship or the trauma may be part of a bigger picture of which you are unaware. In addition to trauma to the angle, other parts of the eye may also reveal damage. Iris injuries include iris sphincter tears, atrophy, iridogenesis, heterochromia iridis and mydriasis. The cornea can show signs of insult in the form of scars and pigment on the endothelium. The lens may form a cataract, most likely in the

References
For a full set of references, email nicky@optometry.co.uk

About the authors


Dr Marc B. Taub is a paediatric resident at Nova Southeastern University in Ft. Lauderdale, Florida. Dr Brian Gardner is a primary care resident also at Nova Southeastern University.

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