Ординатура / Офтальмология / Английские материалы / Clinical Pathways in Glaucoma_Zimmerman, Kooner_2001

quadrants. In spite of these anatomic changes, none of these patients developed complete angle closure or glaucoma. Another reason may be linked to a scleral buckle that is positioned too anteriorly.

What Causes Glaucoma Following Pars

Plana Vitrectomy?

There are a variety of reasons why pars plana vitrectomy may result in glaucoma. Oftentimes, the reasons why one may decide to perform the pars plana vitrectomy may be linked to the causes of glaucoma following the procedure. First, consider blood in the anterior chamber. If there was a vitreous hemorrhage either preor postoperatively, then ghost cell glaucoma may develop 10 to 14 days following a fresh bleed. One may observe a layer of khaki-colored cells in the anterior chamber. Second, if a lensectomy was performed at the same time as a vitrectomy, then retained lens material may be present. Third, consider a diabetic patient who may have undergone a pars plana vitrectomy due to proliferative disease. It is not unusual to see iris and angle neovascularization occur prior to or following the procedure. Fourth, steroid-induced glaucoma is another important consideration in this setting as well as preexisting glaucoma. Finally, trauma can result in significant damage to not only the posterior segment but also the trabecular meshwork. Thus, signs of angle recession may be observed on gonioscopy.31

Malignant glaucoma has also been reported following vitrectomy. A 65-year- old without a previous history of malignant glaucoma developed aqueous misdirection following pars plana vitrectomy, scleral buckle, and extracapsular cataract extraction with posterior chamber intraocular lens implantation, despite medical therapy, Nd:YAG laser capsulo-hyaloidotomy, and surgical disruption of the anterior hyaloid face. The patient’s condition resolved after a repeat vitrectomy, which included hyaloido-capsulo-iridectomy.32 Thus, the management of ciliary block glaucoma can be challenging.

262 Glaucoma Associated with Ocular Surgery

Because Intraocular Gas and Silicone Oil Are Placed in the Posterior Segment, How Can These Surgical Adjuncts Cause Problems in the Anterior Segment?

Intraocular pressure can increase within the eye if the intraocular gas bubble expands. If the patient is required to lie in a prone position, then blood and fibrin can clog the trabecular meshwork directly.33 On the other hand, if the patient is allowed to lie on his or her back, then the anterior chamber can shallow and obstruct egress of aqueous from the anterior chamber. Pupillary block can occur if the flow of fluid from the posterior segment to the anterior segment has been completely blocked.34

When silicone oil begins to emulsify, small bubbles can block the trabecular meshwork.35 Histologically, obstruction of the trabecular meshwork has been noted due to small silicone bubbles, pigmented cells, and silicone-laden macrophages.36 Higher viscosity silicone oil, the use of 5,000 centistokes, has been noted to result in fewer emulsified silicone droplets in the anterior chamber and a lower risk of glaucoma.36

Henderer et al37 of the Bascom Palmer Eye Institute in Miami, Florida, assessed the risk factors for the development of sustained IOP in a series of 532 patients who underwent silicone oil injection for the management of complex retinal detachments. Patients were further subdivided into two groups—those with and without cytomegalovirus. Among those patients with cytomegalovirus, 10% had hypotony by 6 months. By 1 year, 5.9% evidenced an elevation in IOP and 10% were noted to be hypotonous. On the other hand, among those patients without cytomegalovirus, 12.9% had an elevated IOP and 14.1% developed hypotony by 6 months. At 1 year, there were 21% of patients with an elevation in IOP and 27.3% evidenced hypotony. Risk factors for an elevation in IOP include previously diagnosed glaucoma, diabetes mellitus, and an alreadyhigh IOP.

How Are Such Difficult Glaucomas Managed?

One’s initial approach should be medical management, beginning with adrenergic antagonists and topical carbonic anhydrase inhibitors. Depending on the magnitude of the pressure elevation, then systemic carbonic anhydrase inhibitors may be required. Acetazolamide 250 mg q.i.d. will often control the pressure more consistently than the sequels in this acute period. It may be necessary in these acutely inflamed eyes to use topical steroids and even systemic steroids.

If there is pupillary block due to a gas bubble, for example, then a laser iridotomy should be performed. In the setting of silicone oil and pupillary block, an inferior laser iridotomy should be performed. If there is anterior rotation of the ciliary body due to a tight buckle, then peripheral iridoplasty or gonioplasty should be attempted. In those patients in whom the silicone oil is a problem, laser cycloablation may be the first choice. If the silicone oil is fairly compartmentalized, consider a filtration device.

Evidence of ghost cell glaucoma would suggest the need to wash out the anterior chamber. Similarly, retained lens material that is problematic should be removed. In patients who chronically have an increase in IOP and loss or antic-

264 Glaucoma Associated with Ocular Surgery

Even Following Glaucoma Surgery, Can There Be

a Sustained Increase in IOP?

Yes, any time the eye is mechanically changed, there can be an undesirable outcome. Consider the possibilities of a sustained increased in IOP following trabeculectomy, glaucoma filtration device surgery, and laser cycloablation.

In a trabeculectomy, if the anterior chamber is deep and the pressure is high, one must consider the following: (1) blocked sclerostomy, (2) tight flap sutures,

(3) choroidal effusion or hemorrhage, (4) steroid responder, (5) Tenon’s cyst or encapsulated bleb, (6) failed bleb, or (7) endophthalmitis. If the anterior chamber is shallow and the IOP is elevated, then consider the following: (1) pupillary block glaucoma, (2) malignant or ciliary block glaucoma, or (3) choroidal effusion or hemorrhage. The management of these entities is covered in other chapters.

When glaucoma filtration devices are used, there is a hypertensive phase that occurs 3 to 4 weeks following surgery, after which the IOP decreases. However, over time there may be a steady increase in pressure, which will require the initiation of antiglaucoma medications or potentially additional surgery. Entities to consider if faced with a sustained increase in IOP include the following: (1) blocked tube, (2) encapsulated bleb, and (3) steroid responder.

Finally, with regard to cycloablation the following scenarios should be considered: (1) inadequate treatment or (2) steroid responder.

Future Considerations

With the advent of newer techniques for performing cataract surgery, the risks of sustained elevation in IOP will continue to diminish over time. Smaller incisions and less reliance on viscoelastic substances throughout the procedure will minimize the distortion of the anatomy of the globe. Preventive measures such as pupilloplasty and larger donor grafts for avoiding glaucoma following penetrating keratoplasty are commonly employed. The introduction of valved filtration devices, which are easier to insert and manage postoperatively, facilitate one’s ability to control those patients who were once considered refractory to treatment.

There are new antiglaucoma medications, including combination drugs such as CoSopt (combination of timolol maleate and dorzolamide hydrochloride), and a drug which combines latanaprost and timolol. Medications on the horizon such as hypotensive topical lipids, new prostaglandin analogues, and neuroprotective agents such as systemic memantine will also provide additional therapeutic options for our patients.

Antifibrotic agents such as mitomycin-C and 5-fluorouracil have changed the number of patients who are now successfully filtered; future agents, however, which include antibodies to cytokines and growth hormones, may cause less hypotony than what is generally seen with these current agents. There have been many advances in ocular surgery that have improved the outcomes of our patients. There are still many more advances we can expect in the future.

References

1.Shields MB, Ritch R, Krupin T: Classifications and mechanisms of the glaucomas. In: Ritch R, Shields MB, Krupin T (eds): St. Louis: CV Mosby, 1989:751–755.

2.Higginbotham EJ, Lee DA (eds): Management of Difficult Glaucoma. Boston: Blackwell Scientific, 1994.

3.Lewis R, Perkins TW, Gangnon R, et al: The rarity of clinically significant rise in intraocular pressure after laser peripheral iridotomy with apraclonidine. Ophthalmology 1998;105: 2256–2259.

4.Chung HS, Shin DH, Birt CM, et al: Chronic use of apraclonidine decreases its moderation of post-laser intraocular pressure spikes. Ophthalmology 1997;104:1921–1925.

5.Cashwell LF, Martin TJ: Malignant glaucoma after laser iridotomy. Ophthalmology 1992;99: 651–659.

6.Aminlari A, Sassani JW: Simultaneous bilateral malignant glaucoma following laser. Graefes Arch Clin Exp Ophthalmol 1993;231:12–14.

7.Epstein DL (ed): Chandler and Grant’s Glaucoma, 3d ed. Philadelphia: Lea & Febiger. 1986.

8.Steinert RF, Puliafito CA, Kumar SR, et al: Cystoid macular edema, retinal detachment and glaucoma after Nd:YAG laser posterior capsulotomy. Am J Ophthalmol 1991;112:373–380.

9.Richter CU, Arzeno G, Pappas HR, et al: Intraocular pressure elevation following Nd:YAG laser posterior capsulotomy. Ophthalmology 1985;92:636–640.

10.Richter CU, Arzeno G, Pappas HR, et al: Prevention of intraocular pressure elevation following neodymium-YAG laser posterior capsulotomy. Arch Ophthalmol 1985;103:912–915.

11.Mastropasqua L, Ciancaglini M, Carpineto P, et al: Aqueous misdirection syndrome: a complication of neodymium: YAG posterior capsulotomy. J Cataract Refract Surg 1994;20:563–565.

12.Mardelli PG, Piebenga LW, Whitacre MM, et al: The effect of excimer laser photorefractive keratectomy on intraocular pressure measurements using the Goldmann applanation tonometer. Ophthalmology 1998;105:759.

13.Emara B, Probst LE, Tingey DP, et al: Correlation of intraocular pressure and central corneal thickness in normal myopic eyes and after laser in situ keratomileusis. J Cataract Refract Surg 1998;24:1320–1325.

14.Glaucoma Laser Trial Research Group: The Glaucoma Laser Trial. I. Acute effects of argon laser trabeculoplasty on intraocular pressure. Arch Ophthalmol 1989;107:1135–1142.

15.Elsas T, Johnsen H, Stang O, Fygd O: Pressure increase following primary laser trabeculoplasty. Effect on the visual field. Acta Ophthalmol 1994;72:297–302.

16.Ruiz RS, Eilson CA, Musgrove KH, et al: Management of increased intraocular pressure after cataract extraction. Am J Ophthalmol 1987;103:487–491.

17.Rothkoff L, Beidner B, Blumenthal M: The effect of corneal section on early increased intraocular pressure after cataract extraction. Am J Ophthalmol 1978;85:337–338.

18.Kirsch RE, Levine O, Singer JA: The ridge at the internal edge of the cataract incision. Trans Am Acad Ophthalmol Otolaryngol 1977;83:224–231.

19.Shrader CE, Belcher CD 3d, Thomas JV, et al: Pupillary and iridovitreal block in pseudophakic eyes. Ophthalmology 1984;91:831–837.

20.Linn DK, Zimmerman TJ, Nardin GF, et al: Effect of intracameral carbachol on intraocular pressure after cataract extraction. Am J Ophthalmol 1989;107:133–136.

21.Wise JB: Long-term control of adult open angle glaucoma: a pilot study. Ophthalmology 1981;95:197–202.

22.Reiss G, Wilensky J, Higginbotham EJ: Laser trabeculoplasty. Surv of Ophthalmol 1991;35: 407–428.

23.Campbell DG, Grant WM: Trabecular deformation and reduction of outflow facility due to cataract and penetrating keratoplasty sutures. Invest Ophthalmol Visual Sci 1977;suppl: 126.

24.Irvine AR, Kaufman HE: Intraocular pressure following penetrating keratoplasty. Am J Ophthalmol 1969;68:835–844.

25.Olson RJ, Kaufman HE: A mathematical description of causative factors and preventing keratoplasty. Invest Ophthalmol Visual Sci 1977;16:1085–1092.

26.Goldberg DB, Schanzlin DJ, Brown SI: Incidence of increased intraocular pressure after keratoplasty. Am J Ophthalmol 1981;92:372–377.

27.Van Meter WS, Allen RC, Waring GO, et al: Laser trabeculoplasty for glaucoma in aphakic and pseudophakic eyes after penetrating keratoplasty. Arch Ophthalmol 1988;106:185–188.

28.Diddie KR, Ernest JT: Uveal blood flow after 360° constriction in the rabbit. Arch Ophthalmol 1980;98:729–730.

29.Hayreh SS, Baines JA: Occlusion of the vortex veins: an experimental study. Br J Ophthalmol 1973;57:217–238.

30.Pavlin CJ, Rutnin SS, Devenyi R, et al: Supraciliary effusions and ciliary body thickening after scleral buckling procedures. Ophthalmology 1997;104:433–438.

31.Wilensky JT, Goldberg MF, Alward P: Glaucoma after pars plana vitrectomy. Trans Am Acad Ophthalmol Otolaryngol 1977;83:114–121.

32.Zacharia PT, Abboud EB: Recalcitrant malignant glaucoma following pars plana vitrectomy, scleral buckle, and extracapsular cataract extraction with posterior chamber intraocular lens implantation. Ophthamic Surg Lasers 1998;29:323–327.

266 Glaucoma Associated with Ocular Surgery

33.Abrams GW, Swanson DE, Sabates, et al: The results of sulfur hexafluoride gas in vitreous surgery. Am J Ophthalmol 1982;94:165–171.

34.Chang S, Lincoff HA, Coleman DJ, et al: Perfluorocarbon gases in vitreous surgery. Ophthalmology 1985;92:651–654.

35.McCuen BW 2d, de Juan E Jr, Landers MB 3d, et al: Silicone oil in vitreoretinal surgery. Part 2: results and complications. Retina 1985;5:198–205.

36.Ni C, Wang WJ, Albert DM, et al: Intravitreous silicone injection. Histopathologic findings in a human eye after 12 years. Arch Ophthalmol 1983;101:399–401.

37.Henderer JD, Budenz DL, Flynn HW, et al: Elevated intraocular pressure and hypotony following silicone oil retinal tamponade for complex retinal detachment. Arch Ophthalmol 1999;117:189–195.

13

Traumatic Glaucoma

Mohamed-Sameh H. El Agha

Definition

How Is Traumatic Glaucoma Defined?

Traumatic glaucoma is the occurrence of elevated intraocular pressure (IOP) secondary to ocular trauma. However, not every posttraumatic IOP elevation is necessarily due to trauma; for instance, the eye may have harbored primary glaucoma prior to the trauma. Furthermore, traumatic glaucoma may be masked by coincidental pathology that lowers the IOP. Table 13–1 shows how the IOP level may be interpreted following trauma.

Table 13–2 lists the different types of trauma that may be sustained by the eye. Glaucoma complicating intraocular surgery is discussed in Chapter 12. Head injury may lead to a carotid-cavernous fistula, which may give rise to glaucoma

Table 13–1. Interpretation of Intraocular Pressure (IOP) Level Following Trauma

High IOP

Preexisting primary glaucoma*

Preexisting primary glaucoma + traumatic glaucoma*

Pure traumatic glaucoma

Low IOP

Missed rupture globe (e.g., posterior scleral rupture)

Cyclodialysis

Ciliary shutdown

Choroidal effusion

Retinal detachment

Normal IOP

No ocular damage leading to glaucoma

Combination of high and low IOP

268 Traumatic Glaucoma

Table 13–2. Types of Ocular Trauma

Mechanical injury

Direct

Nonpenetrating (blunt) trauma

Penetrating trauma (± intraocular foreign body)

Surgical trauma

Cataract surgey

Glaucoma surgery (incisional and laser)

Penetrating keratoplasty

Scleral buckling

Pars plana vitrectomy

Nd:YAG laser surgery

Indirect

Head injury

Chemical injury

Alkali burns

Acid burns

Radiation injury

Electrical injury

Thermal injury

Nd:YAG, neodymium:yttrium-aluminum-garnet.

by raising episcleral venous pressure; this is discussed in Chapter 6. Otherwise, all other forms of traumatic glaucoma are discussed in detail in this chapter.

What Are the Mechanisms of Traumatic Glaucoma?

Much like primary glaucoma, traumatic glaucoma may be of the open-angle or closed-angle type. In open-angle varieties, the obstruction to aqueous outflow may be pretrabecular (e.g., epithelial down-growth), trabecular (e.g., glaucoma complicating hyphema, and ghost cell glaucoma), or posttrabecular (e.g., elevated episcleral venous pressure secondary to a carotid-cavernous fistula). Angle closure results from apposition or adherence of peripheral iris to the trabecular meshwork or peripheral cornea. In the anterior (“pull”) mechanism, an abnormal tissue in the angle contracts and pulls the iris into the angle (e.g., a fibrovascular membrane associated with neovascular glaucoma). Posterior (“push”) mechanisms include pupillary block (e.g., by a swollen cataractous lens) and forward movement of the iris-lens diaphragm (secondary to ciliochoroidal effusion or ciliary block).

How Long After Trauma Does the IOP Rise Occur?

Depending on pathogenesis, the onset of IOP elevation following trauma is variable. The IOP may rise in the first few hours following trauma, as in hyphema. Lens particle glaucoma, for example, will only appear a few days after penetrating trauma. Ghost cell glaucoma requires at least 2 weeks to develop. Angle recession glaucoma typically develops years after the traumatic incident. Therefore, a patient presenting with traumatic glaucoma may have even forgotten the traumatic incident that caused the IOP elevation. The