34

Glaucoma After Vitreoretinal Procedures

Ron A. Adelman, MD, MPH, MBA, FARVO and Martin Wand, MD

Vitreoretinal surgery is the third most common ocular surgery following cataract surgery and laser vision correction with more than 200,000 procedures performed each year in the United States.¹ There is a complex relationship between intraocular pressure (IOP) and vitreoretinal procedures.^1–10 Ocular hypertension may present after vitrectomy, scleral buckle, and/or intravitreal injections.^1,2 Although transient or persistent ocular hypertension following vitreoretinal procedures is not infrequent, vitrectomy may be helpful in the treatment of a select group of glaucoma patients, such as those with aqueous misdirection. Of interest is that reversible loss of light perception after vitreoretinal surgery does occur in some patients.⁹ In postvitrectomy patients with high IOP and no light perception, decreasing the IOP may be associated with return of light perception.⁹

Glaucoma after vitreoretinal surgery requires special attention to its etiology, pathophysiology, diagnosis, treatment, and prevention. Direct communication between the retina surgeon and glaucoma specialist will result in early diagnosis and appropriate management based on the likely etiology. It is important to distinguish between early (first week) and late (second week and later) ocular hypertension following vitreoretinal procedures. In the early postoperative period, ocular hypertension is usually due to viscoelastics, expanding gas bubble, pupillary block, angle closure, inflammation, hemorrhage, choroidal edema, silicone oil, or steroid response.¹ Late glaucoma may be a result of angle closure, neovascularization of the angle, emulsified silicone oil, or new open-angle glaucoma. As a rule, the more complicated the vitreoretinal surgery, the higher the risk of development of ocular hypertension.

Soon after a retina operation, the eye is often congested, painful, and with poor vision; the patient may be uncomfortable, somnolent, and at times nauseated, particularly if the surgery is performed under general anesthesia. Thus, the signs and symptoms of a secondary glaucoma in the early postoperative period can be confused with the expected side effects of vitrectomy or scleral buckle surgery. An awareness of this complication and its different presentations will facilitate recognition as well as allow for timely treatment and, in some instances, prevention of the complication.

ANGLE-CLOSURE GLAUCOMA

The reported incidence of clinically detectable angle narrowing after scleral buckle procedures ranges from 11.9% at 1 month¹¹ to 29% at 2 months after surgery¹²; the incidence reaches 50% in eyes examined within 1 week after surgery.¹³ The reported incidence of actual angle-closure glaucoma ranges from 1% to 4%.^11,14–16 The etiology of the angle shallowing is probably multifactorial (Table 34-1). Experimentally, occlusion of vortex veins in monkey eyes results in uveal tract congestion, forward movement of the iris-lens diaphragm, shallowing or closure of the anterior chamber angle, and, in some eyes, elevated IOP.¹⁷ Grant has shown that fluid injected into the choroid of human eye bank eyes results in choroidal detachment and angle closure.¹⁸ Clinically, a choroidal detachment is frequently, but not always, detectable after retinal detachment surgery.¹⁶ Ultrasound biomicroscopic studies have shown that choroidal effusion is present in eyes after scleral buckling procedures even when there are no signs of anterior chamber shallowing or clinical findings of choroidal detachment (Figure 34-1). This confirms the impression of retinal surgeons that virtually all eyes undergoing retinal surgery have some degree of choroidal effusion. Angle narrowing and angle closure are just at one end of the spectrum of choroidal effusion after retinal detachment.

Other clinical situations where there is inflammation and/or swelling of the uveal tract have also been shown to result in shallowing of the anterior chamber axially, anterior rotation of the ciliary body, and shallowing or closure of the anterior chamber angle. A similar pathophysiologic process may be implicated in the following conditions, all of which have been associated with angle-closure glaucoma: panretinal photocoagulation,19,20 uveal²¹ and orbital pseudotumor,²² uveal effusion,²³ central retinal vein occlusion,^24,25 choroidal hemorrhage,²⁶ and idiopathic ciliary body swelling.²⁷ The ciliary body is firmly attached to the scleral spur. With uveal swelling from these diverse causes, including postscleral buckling, there is an anterior rotation of the ciliary body with anterior movement of the lens-iris diaphragm (see Figure 34-1). In phakic or pseudophakic eyes, there may be enough forward movement to produce pupillary block with resultant angle-closure glaucoma.

However, angle closure may also occur in the absence of pupillary block. In such cases, anterior rotation of the ciliary body may be limited to pushing the peripheral iris against the trabecular meshwork (TM). The result is similar to the plateau iris syndrome (ie, there is a relatively deep central anterior chamber depth, flat iris plane, and peripheral angle closure).²⁸ This is attested to by the finding that angle-closure glaucoma has been noted in aphakic as well as phakic eyes and in eyes with patent iridectomies.^11,16 The incidence and extent of angle shallowing and closure has been related to myriad conditions including a preexisting narrow angle,^11,15 high myopia,¹⁵ older age of patient,¹⁵ use of an encircling band vs a scleral implant without an encircling band,¹³ large buckle elements, intravitreal injection of gas, placement of the encircling band anterior to the equator,¹¹ episcleral implants vs intrascleral implants,¹⁶ choroidal detachment extending to the ciliary body,¹¹ and the extent of the surgical procedure.¹⁵ In most cases, the shallowing of the angle resolves with time as the choroidal effusion is absorbed.^11–13,15

Prevention and Treatment

The critical point in the treatment of this problem is an awareness of the potential for angle closure after retinal detachment surgery. Frequently, there is no more discomfort or pain than from the normal sequelae of retinal surgery. Findings are minimal, and a hazy cornea with a mid-dilated pupil is often the only clue that glaucoma may be present.¹⁶ Ocular rigidity is decreased to one-quarter normal after a scleral buckle,²⁹ and Schiotz tonometry gives a falsely low IOP.¹² Thus, an IOP measurement by applanation or Tono-Pen (Reichert Technologies) and slit-lamp examination should be done preferably within the first 24 hours after surgery. If the cornea is not clear enough for gonioscopy, and the IOP is elevated, angle closure must be presumed to be present. With the advent of anterior segment optical coherence tomography, the diagnosis of angle closure in such cases may be easier.

Treatment of angle-closure glaucoma after scleral buckling surgery progresses from medical management through surgical intervention (Table 34-2). Maximal dilation and cycloplegia with atropine and phenylephrine should be aggressively continued, along with topical steroids, which may decrease ocular and choroidal congestion and effusion. Miotics should be avoided; beta-blockers, carbonic anhydrase inhibitors, and alpha-adrenergics should be used as tolerated. Regardless of the medical therapy, a laser iridotomy is indicated. With mild corneal haziness, a neodymium:yttrium-aluminum-garnet (Nd:YAG) laser may often be successful in iris penetration where the argon laser might fail.30 If the cornea is very hazy, clarity can frequently be achieved with topical glycerin. When the cornea is too hazy to allow even Nd:YAG laser iridotomy, argon laser peripheral iridoplasty might be helpful, as this has been reported to be successful in primary angle-closure glaucoma under such circumstances.³¹ As a last resort, angle closure from pupillary block may require a surgical iridectomy, but the advent of the different lasers has virtually eliminated the need for such intervention.

When a patent laser iridotomy does not resolve the angle closure, then choroidal detachment with anterior rotation of the ciliary body is commonly the cause of the angle closure. With the availability of argon laser gonioplasty,32 the angle can often be opened enough to lower the IOP, keeping in mind that once past the acute crisis, the choroidal effusion and secondary angle closure will resolve with time. However, there can be so much choroidal effusion that the only solution is to drain the choroidal fluid, the traditional technique of treating this type of glaucoma.¹⁴ Surgical anterior chamber deepening and mechanical breaking of peripheral anterior synechiae can be performed at the time of this surgery, if persistent angle closure is present (see Chapter 24).

Case 34-1

A 69-year-old man with a rhegmatogenous retinal detachment underwent a successful scleral buckle operation with a 200-degree scleral implant and a 360-degree encircling band. The course of his postoperative hospital stay was not well documented, but at his 1-week postoperative visit, the visual acuity was counting fingers, the IOP was 40 mm Hg, and the eye was congested. Various antiglaucoma medications were instituted without success. At 7 weeks after the retina surgery, the visual acuity was 20/100, the IOP was 57 mm Hg, the cornea clear, the anterior chamber deep, and the iris was flat with a 6-mm pupil. No pupillary block was evident, but the angle was closed 360 degrees (Figure 34-2). Argon laser gonioplasty was performed 360 degrees with immediate opening of the angle, and the IOP decreased to 31 mm Hg. The next day, the IOP was 21 mm Hg, and the angle remained open (Figure 34-3). Subsequently, his IOPs have remained under control on a topical beta-blocker only.

This case illustrates several important points. Angle closure after retinal detachment surgery is easily overlooked if not specifically sought for and may persist long after the acute postoperative inflammatory period. It can occur in the absence of pupillary block, making the diagnosis more elusive. With the availability of laser iridotomy and laser gonioplasty, many, if not most, cases of angle closure, even of several weeks’ duration, can now be resolved without further surgical intervention.

OPEN-ANGLE GLAUCOMA

Postoperative open-angle glaucoma requires special consideration because it frequently is a reflection of the preoperative status of the eye. The prevalence of open-angle glaucoma in eyes that develop retinal detachment is reported to be 4 to 12 times higher than that in the general population.³³ The reason is unknown, but the commonality of high myopia³⁴ and the use of miotics in open-angle glaucoma resulting in retinal detachment³⁵ have been cited as possible explanations. A higher incidence of both open-angle glaucoma and retinal detachment in persons with diabetes may be another factor. Because the IOP is often lower in eyes with retinal detachment due to decreased aqueous formation or increased outflow through the retinal break and uvea, successful reattachment usually, but not always, results in a return to at least the predetachment level of IOP. Additionally, debris, inflammation, blood breakdown products, and steroid response contribute to the decreased facility of outflow postoperatively.36 All things considered, reemergence of preexisting open-angle glaucoma should be looked for carefully after retinal detachment surgery and appropriately treated.

Chang¹ has reported that vitrectomy increases the risk of unilateral open-angle glaucoma in the operated eye. Following vitrectomy, up to 15% to 20% of eyes may develop open-angle glaucoma. Given the fact that there are more than 200,000 vitrectomies per year in the United States, up to 30,000 new cases of glaucoma following vitrectomy may develop each year. The open-angle glaucoma may present months or years after vitrectomy. In a large series, the average time from vitrectomy to open-angle glaucoma in phakic eyes and pseudophakic eyes was 46 and 18 months, respectively. The presence of a crystalline lens may have a protective effect. The etiology of delayed-onset open-angle glaucoma following vitrectomy may be due to inflammation and debris that reduce aqueous outflow, increased susceptibility of the optic nerve to damage, or alteration in the biochemical environment of the eye. Chang¹ postulated that the high level of oxygen in the vitreous cavity after vitrectomy results in oxidative stress of the TM.

Postoperative open-angle glaucoma may also be associated with Schwartz’s syndrome,³⁷ in which the preoperative IOP elevation is caused by obstruction of the TM by photoreceptor outer segments from a retinal tear or dialysis³⁸ and is improved by retinal surgery. If the retinal break is sealed and the retina reattached, the source of TM obstruction (photoreceptor outer segments) is eliminated, and the secondary open-angle glaucoma usually resolves. In this unique situation, persistent postoperative open-angle glaucoma should lead one to suspect an undetected persistent retinal detachment.

NEOVASCULAR GLAUCOMA

Chronic retinal detachment with its resultant retinal hypoxia has long been recognized as a cause of neovascular glaucoma (NVG).³⁹ Occasionally, the surgery for retinal detachment has been implicated in neovascularization of the iris, presumably due to anterior segment ischemia from damage to the anterior ciliary vessels.^40,41 Recently, vitrectomy in diabetic eyes has been associated with a high incidence of NVG if the eye is already aphakic or has concurrent lensectomy.⁴² Aphakia may have resulted in the elimination of a diffusion barrier for the passage of some angiogenic substance from the posterior to the anterior segment.⁴³ Subsequently, although the presence of the lens does seem to provide a relative protective barrier, of greater importance in the development of NVG is the presence of an angiogenic stimulus.^44,45 In both diabetic and nondiabetic eyes⁴⁶ where there is posterior segment hypoxia from a persistent retinal detachment, aphakia is only of secondary importance. The highest incidence of NVG after vitrectomy for complications of diabetic retinopathy is in eyes with a persistent retinal detachment and aphakia (92%); the lowest incidence is in phakic eyes with an attached retina (0%), and intermediate incidence in phakic eyes with a detached retina (40%)45 (see Chapter 32).

In eyes already predisposed toward the development of NVG, such as eyes with diabetic retinopathy, previous central retinal vein occlusion, or carotid obstructive disease, retinal detachment surgery, with or without vitrectomy, further stimulates the inflammatory and angiogenic responses.^47,48 One must be alert to the potential development of NVG postretinal detachment surgery, and one should specifically look for neovascularization of the iris on slit-lamp examination. If neovascularization of the iris is detected, a dilated fundus examination with scleral depression must be performed. When a retinal detachment is found, a successful reattachment will usually resolve the anterior segment neovascularization.⁴⁹ Occasionally, neovascularization of the iris and NVG may appear after successful retinal detachment surgery. If this occurs in eyes with preexisting diabetic retinopathy or previous central retinal vein occlusion, intravitreal anti–vascular endothelial growth factor injections and/or panretinal photocoagulation either must be performed, if not already done, or if done, it must be augmented. Indirect laser ophthalmoscopy and photocoagulation can be useful in treating the peripheral retina in this situation. With the extra inflammatory and angiogenic stimuli from the surgery, supplemental panretinal photocoagulation often needs to be performed. We and others have noted resolution of neovascularization of the iris and NVG after supplemental panretinal photocoagulation in such cases.^40,44 In recent years, development of anti–vascular endothelial growth factor has improved the outcome of patients with rubeosis. Intravitreal bevacizumab (Avastin) and ranibizumab (Lucentis) quickly improve recent-onset neovascularization of the iris. However, the duration of the therapeutic effect of these medications is about 1 month. Thus, multiple intravitreal injections may become necessary.⁷

GLAUCOMA AFTER INTRAVITREAL GAS

The use of various intraocular gases in vitreoretinal surgery has become increasingly popular over the past decades.⁵⁰ Because of their surface tension, all gases exert a tamponading effect on the retinal breaks. However, air has the disadvantage of being absorbed (in 2 to 7 days⁵¹) before firm choroidal-retinal adhesions can develop. Fluorinated hydrocarbon gases have an advantage over air because they are expansile and have a longer intraocular duration, attributed to their high molecular weight, low diffusion coefficient, and low water solubility. The most commonly used gases are sulfa hexafluoride (SF6) and perfluoropropane (C3F8). SF6 remains in the eye for about 2 weeks; C3F8, with a higher molecular weight than SF6, remains in the eye for about 2 months.^50,51 When injected into the vitreous cavity, the volume of these gases expands because of diffusion of nitrogen, oxygen, and carbon dioxide from ocular tissue. Pure SF6 expands to 2 to 2.5 times its original volume within 24 to 36 hours, and pure C3F8 expands to 3 to 4 times its original volume within the first 3 days.^50,51 With both gases, the maximum expansion occurs within the first 6 hours. When the gas gets diluted to a 40% concentration, further expansion occurs slowly and is balanced by vitreous loss.^52,53 The nonexpansile concentration for SF6 is 18% and for C3F8 is 14%.

With an expansile intravitreal gas bubble, anterior displacement of the lens can occur, despite proper positioning of the patient’s head in a prone position, resulting in pupillary block. This can occur even after the period of maximum expansion, and one must be aware of this possibility for the duration of the intravitreal gas. Because the gas bubble is compressible, high-displacement tonometers, such as the Schiotz tonometer, result in significant underevaluation of the true IOP.⁵⁴ With 1 mL of intraocular gas, there is a 7- to 8-mm Hg underevaluation when the IOP is in the 30- to 40-mm Hg range.⁵⁰ Even with low-displacement applanation tonometers, there can be a significant underevaluation of the true IOP. The Tono-Pen was found to underestimate true IOP (as measured in eye bank eyes with an intraocular manometer) by 15% and the pneumotonometer by 21%.⁵⁵ Therefore, not only is it imperative that only a low-displacement tonometer, such as the Goldmann applanation tonometer (Haag-Streit) or Tono-Pen, be used, but to realize that there could still be up to a 20% underestimation in eyes with intraocular gas.

More common than pupillary block is the glaucoma resulting directly from the expansile gas. The highest incidence and the highest IOP are during the rapid expansile phase when egress of liquid vitreous and aqueous cannot keep pace with the increasing gas volume. In an early study, 45% of 101 patients who had SF6 during surgery developed IOPs greater than 30 mm Hg within the first postoperative day; in 33 patients, the elevated IOPs persisted beyond the second postoperative day. More alarmingly, 11 of the 101 patients developed central retinal artery occlusion, 10 of whom had elevated IOPs; none of these eyes achieved functional vision.⁵⁶ Eyes that developed postoperative anterior chamber fibrinous exudates appear more likely to develop elevated IOPs, and diabetic eyes are more likely to develop these exudates.⁵⁶ Thus, eyes likely to have retinal vascular diseases, such as with diabetes, hypertension, sickle cell trait, or chronic open-angle glaucoma, may be at even greater risk for vascular occlusion associated with an elevated IOP.⁵⁷

Patients with intraocular gas who subsequently have surgery under general anesthesia with nitrous oxide will have a significant increase in IOP during anesthesia. Wolf and colleagues⁵⁸ found that SF6 gas volume in an eye increased 300% with nitrous oxide ventilation compared with a 50% increase with air ventilation and 35% increase with oxygen ventilation. Fu et al5 reported 4 out of 5 patients with intraocular gas and subsequent nitrous oxide anesthesia had final visual acuity of 20/200 or worse and significant optic atrophy. Hart and associates⁵⁹ also reported that 3 patients who had C3F8 in their eyes from vitreoretinal surgery 10 to 30 days earlier experienced loss of vision from central retinal artery occlusion after general anesthesia with nitrous oxide. Thus, nitrous oxide anesthesia should be contraindicated in all patients who still have expansile gas in their eyes.

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