Ординатура / Офтальмология / Английские материалы / Clinical Ophthalmology A Systematic Approach 7th Edition_Kanski, Bowling_2011

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Treatment

1Medical treatment is similar to that of POAG. Miotics would theoretically be of particular benefit because they decrease iridozonular contact in addition to facilitating aqueous outflow. They have the disadvantages, however, of exacerbating the myopia common in these patients and also of a risk of precipitating retinal detachment in myopia. They are not well tolerated by young patients. Topical thymoxamine, a selective alpha-adrenergic antagonist, induces miosis without causing spasm of accommodation, but is also poorly tolerated as it causes irritation.

2Laser trabeculoplasty is often initially effective although it is important not to over-treat eyes with heavily pigmented angles and to start at a relatively low power laser setting. At least one-third of patients will require trabeculectomy within 5 years of laser trabeculoplasty.

3Laser iridotomy has been proposed to retard pigment liberation by reversing iris concavity and eliminating iridozonular contact (see Fig. 10.50). It may have utility in patients under the age of 40 years but benefit has not been conclusively demonstrated.

4Trabeculectomy is indicated more commonly than in POAG although the results can be disappointing, perhaps at least partly because most patients are relatively young. The use of adjunctive antimetabolites may improve surgical outcome.

Prognosis

Over time the control of IOP becomes easier and occasionally the IOP may spontaneously revert to normal; this may or may not be associated with a decrease in trabecular pigmentation. Patients with undetected previous pigmentary glaucoma may later be erroneously diagnosed as having NPG.

Differential diagnosis

1POAG may be associated with a hyperpigmented trabeculum. However, the pigment tends to be concentrated in the inferior sector of the angle, in contrast to the homogeneous distribution in PDS. Patients with POAG are also usually older and lack Krukenberg spindles and iris transillumination defects.

2Pseudoexfoliation may exhibit trabecular hyperpigmentation and pigment dispersion. However, transillumination defects are evident at the margin of the pupil rather than in the periphery. Pseudoexfoliation glaucoma usually affects patients over the age of 60 years, is unilateral in 50% of cases and has no predilection for a myopic refractive error.

3Pseudophakic pigmentary glaucoma occurs in the context of rubbing of the haptics and optics of a posterior chamber intraocular lens against the posterior surface of the iris, with resultant pigment dispersion and outflow obstruction.

4Anterior uveitis may result in trabecular hyperpigmentation and iris atrophy. Clustered old pigmented keratic precipitates may be mistaken for a Krukenberg spindle on cursory examination.

5Subacute angle-closure glaucoma may be associated with a heavily pigmented trabeculum where the iris root has been in contact with the angle.

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Neovascular glaucoma

Introduction

Pathogenesis

Neovascular glaucoma (NVG) is an aggressive condition which occurs as a result of iris neovascularization (rubeosis iridis). The common aetiological factor is severe, diffuse and chronic retinal ischaemia. It is postulated that hypoxic retinal tissue produces growth factors in an attempt to revascularize hypoxic areas; the most important of these is vascular endothelial growth factor (VEGF). Apart from inducing retinal neovascularization (proliferative retinopathy) such factors also diffuse into the anterior segment and initiate rubeosis iridis and neovascularization in the angle of the anterior chamber. The latter initially impairs aqueous outflow in the presence of an open angle and later contracts to produce a secondary angle-closure glaucoma which is usually severe and relentless (Fig. 10.52A).

Fig. 10.52 Neovascular glaucoma. (A) Rubeosis iridis and angle-closure by PAS; (B) tiny capillary tufts on the pupil margin; (C) invasion of angle structures by new vessels; (D) progressive synechial angle-closure

(Courtesy of J Harry and G Misson, from Clinical Ophthalmic Pathology, Butterworth-Heinemann 2001 – fig. A)

Causes of rubeosis iridis

1Ischaemic central retinal vein occlusion accounts for about a third of cases. Approximately 50% of eyes develop NVG following ischaemic central retinal vein occlusion. Extensive peripheral retinal capillary non-perfusion on fluorescein angiography is the most valuable predictor of the risk of subsequent NVG, although in some patients non-ischaemic occlusion may subsequently become ischaemic. Glaucoma typically occurs 3 months after the occlusion (‘100-day glaucoma’) but intervals from 4 weeks to 2 years have been documented.

2Diabetes mellitus accounts for a slightly smaller proportion. Patients with long-standing diabetes (10 years or more) with proliferative retinopathy are at particular risk. The risk of glaucoma is decreased by appropriate panretinal photocoagulation and increased by cataract extraction. Pars plana vitrectomy may also precipitate rubeosis iridis if inadequate laser therapy is applied or tractional retinal detachment remains.

3Arterial retinal vascular disease such as central retinal artery occlusion and ocular ischaemic syndrome are uncommon causes.

4Miscellaneous causes include intraocular tumours, long-standing retinal detachment and chronic intraocular inflammation.

Classification

Despite a degree of overlap it is convenient to divide NVG into the following three stages: (a) rubeosis iridis, (b) secondary open-angle glaucoma and (c) secondary synechial angle-closure glaucoma. Systemic investigation and treatment should be tailored to individual causes.

Rubeosis iridis

Diagnosis

In chronological order rubeosis develops as follows:

•Tiny dilated capillary tufts or red spots develop at the pupillary margin and may be missed unless the iris is examined carefully under high magnification (Fig. 10.52B).

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•The new vessels grow radially over the surface of the iris towards the angle, sometimes joining dilated blood vessels at the collarette. At this stage the IOP may still be normal and the new vessels may regress either spontaneously or with treatment.

•Angle neovascularization in the absence of pupillary involvement may occur, particularly after an ischaemic central retinal vein occlusion. It is therefore important to perform careful gonioscopy without mydriasis in eyes at high risk even when the pupillary border is uninvolved.

Treatment

1Panretinal photocoagulation (PRP), if performed early, is often effective in inducing regression of the new vessels and preventing subsequent progression to glaucoma.

2Intravitreal vascular endothelial growth factor (VEGF) inhibitors such as bevacizumab (Avastin®) at a dose of 1.25 mg in 0.05 mL may decrease neovascularization at this stage and thus improve IOP control, although the duration of control is often limited, requiring further injections or definitive control with PRP.

3Retinal surgery. If rubeosis develops or persists following vitrectomy in a diabetic patient with residual retinal detachment, reattachment should be attempted, since if successful, the rubeosis will frequently regress. Additional panretinal photocoagulation is also beneficial.

Secondary open-angle glaucoma

Diagnosis

Neovascular tissue proliferates across the face of the angle (Fig. 10.52C). Here the new blood vessels arbourize and form a fibrovascular membrane which blocks the trabeculum, giving rise to secondary open-angle glaucoma.

Treatment

1Medical treatment is as for POAG but miotics should be avoided, and prostaglandin derivatives used with relative caution due to their inflammation-promoting potential. Topical atropine 1% and intensive topical steroids should be given if significant inflammation is present. Topical apraclonidine and/or oral acetazolamide may be required as short-term temporizing measures.

2Intravitreal VEGF inhibitor injection may be effective if fibrovascular angle-closure has not yet supervened.

3Cyclodiode should be performed if medical control of IOP is not possible, particularly if the eye is uncomfortable, has useful visual potential or corneal oedema prevents an effective retinal view for PRP.

4PRP should still be performed even if the IOP is adequately controlled medically, although this will not reverse the fibrous component of the fibrovascular membrane. If the retinal view is poor, indirect ophthalmoscopic application may provide better access, if necessary in the operating theatre with iris hooks to open a small pupil caused by posterior synechiae. Trans-scleral cryotherapy or diode laser are options.

Secondary angle-closure glaucoma

Diagnosis

If rubeosis continues to progress the angle becomes progressively closed by contraction of fibrovascular tissue with pulling of the peripheral iris over the trabeculum (Fig. 10.52D and see Fig. 10.52A). The angle thus closes circumferentially in a zipper-like fashion resulting in very high IOP, severe visual impairment, congestion of the globe and pain. The prognosis for visual function is generally poor by this stage, though aggressive management can achieve comfort and retain useful sight in some cases.

Treatment

1Medical treatment is as discussed above for the secondary open-angle stage. Steroids and atropine alone may be adequate if there is no potential for vision.

2 Intravitreal VEGF inhibitor injection is generally not thought to be effective once synechial angle-closure is present.

3Cyclodiode should be considered in the circumstances discussed above.

4PRP is performed if the fundus can be adequately visualized (see above). Eyes with opaque media can be treated by trans-scleral cryotherapy or cyclodiode, if appropriate.

5Filtration surgery may be considered if vision is hand movements or better. The options are trabeculectomy with adjunctive mitomycin C and artificial filtering shunts (glaucoma drainage devices).

6 Retrobulbar alcohol injection is useful in relieving pain but it may cause permanent ptosis and does not relieve congestion.

7Enucleation may be considered if all else fails.

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Inflammatory glaucoma

Introduction

Overview

Elevation of intraocular pressure (IOP) secondary to intraocular inflammation frequently presents a diagnostic and therapeutic challenge. The elevation of IOP may be transient and innocuous, or persistent and severely damaging. The prevalence of secondary glaucoma increases with chronicity and severity of disease. Secondary glaucoma is particularly common in Fuchs uveitis syndrome and chronic anterior uveitis associated with juvenile idiopathic arthritis. Posterior uveitis is less likely to affect the aqueous outflow pathway and consequently less likely to lead to IOP elevation.

Classification

1 Angle-closure with pupillary block.

2 Angle-closure without pupillary block.

3 Open-angle.

4 Posner–Schlossman syndrome.

Diagnostic dilemmas

1IOP fluctuation may be dramatic in uveitic glaucoma and phasing may be helpful in patients with borderline IOP.

2Ciliary body shutdown caused by acute exacerbation of chronic anterior uveitis is frequently associated with lowering of IOP that may mask the underlying tendency to glaucoma. Even eyes with considerably elevated IOP (30–35 mmHg) may become hypotonous during acute exacerbations of uveitis. Return of ciliary body function with subsidence of uveitis may be associated with a rise in IOP in the presence of permanently compromised outflow facility.

3Pathogenesis of elevation of IOP may be uncertain; multiple mechanisms may be involved. Steroid-responders often represent a therapeutic challenge.

4Assessment of glaucomatous damage may be hampered by a small pupil or opacities in the media. Poor visual acuity may also compromise accurate perimetry.

5Iris vessels may give rise to diagnostic confusion with NVG.

Angle-closure glaucoma with pupillary block

Pathogenesis

Secondary angle-closure is caused by posterior synechiae extending for 360° (seclusio pupillae) which obstruct aqueous flow from the posterior to the anterior chamber (Fig. 10.53A). The resultant increased pressure in the posterior chamber produces anterior bowing of the peripheral iris (iris bombé – Fig. 10.53B) resulting in shallowing of the anterior chamber and apposition of the iris to the trabeculum and peripheral cornea (Fig. 10.53C). Such an inflamed iris easily sticks to the trabeculum and the iridocorneal contact may become permanent with the development of PAS.

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Fig. 10.53 Secondary angle-closure with pupillary block. (A) Seclusio pupillae; (B) iris bombé; (C) iridocorneal contact

Diagnosis

1Slit-lamp biomicroscopy shows seclusio pupillae, iris bombé and a shallow anterior chamber.

2Gonioscopy shows angle-closure from iridotrabecular contact. Indentation may be used to assess the extent of appositional as opposed to synechial angle-closure.

Angle-closure glaucoma without pupillary block

1Pathogenesis. Chronic anterior uveitis causes the deposition of inflammatory cells and debris in the angle (Fig. 10.54A and B). Subsequent organization and contraction pulls the peripheral iris over the trabeculum, thereby causing gradual and progressive synechial angle-closure (Fig. 10.54C) and eventual elevation of IOP. The eye with a pre-existing narrow angle may be at higher risk, as may one with granulomatous inflammation with inflammatory nodules in the angle.

2 Diagnosis. The anterior chamber is deep but gonioscopy shows extensive angle-closure by PAS.

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Fig. 10.54 Secondary angle-closure without pupillary block. (A) Deposition of inflammatory cells in the angle; (B) gonioscopy shows inflammatory debris; (C) synechial angle-closure

(Courtesy of J Harry and G Misson, from Clinical Ophthalmic Pathology, Butterworth-Heinemann 2001 – fig. A)

Open-angle glaucoma

In acute anterior uveitis

In acute anterior uveitis the IOP is usually normal or subnormal due to concomitant ciliary shutdown. Occasionally, however, secondary open-angle glaucoma develops due to obstruction of aqueous outflow, most commonly as the acute inflammation is subsiding and ciliary body function is returning. This effect, which is often transient and innocuous, may be steroid-induced or caused by a combination of the following mechanisms:

1Trabecular obstruction by inflammatory cells and debris which may be associated with increased aqueous viscosity due to leakage of proteins from the inflamed iris blood vessels.

2Acute trabeculitis involving inflammation and oedema of the trabecular meshwork with secondary diminution of intertrabecular porosity may result in a reduction in outflow facility. It is thought that this is especially relevant in anterior uveitis associated with herpes zoster, herpes simplex and toxoplasma retinitis.

In chronic anterior uveitis

In chronic anterior uveitis the main mechanism for reduced outflow facility is thought to be trabecular scarring and/or sclerosis secondary to chronic trabeculitis. The exact incidence and importance of this mechanism is, however, difficult to determine as most eyes also have some degree of synechial angle-closure. Because of the variable appearance of the angle on gonioscopy, definitive diagnosis of trabecular damage is difficult. Theoretically, the angle should be open and, in some eyes, a gelatinous exudate resembling ‘mashed potatoes’ is seen on the trabeculum. Treatment is as for secondary synechial angle-closure glaucoma.

Treatment

Medical

•Medical control of IOP is more likely to be achieved if the angle is completely open.

•The aim of therapy in terms of IOP level to be attained depends on the health of the optic nerve head; eyes with advanced damage require a low target IOP.

•In steroid-reactors it is important not to sacrifice control of inflammation for fear of steroid-induced IOP elevation. Long-acting depot preparations should be used with great caution in patients with a history of a steroid response.

•The IOP-lowering effect of ocular hypotensive drugs is less predictable in uveitis and some cases may be unexpectedly sensitive to topical carbonic anhydrase inhibitors (CAI).

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•The use of prostaglandin analogues in uveitic glaucoma is tempered by the small risk of precipitating a uveitic episode and CMO.

•A beta-blocker is therefore usually the drug of first choice.

•The choice of a second line agent often depends on the IOP level. If the IOP is very high, systemic acetazolamide may be required in the short-term. If elevation of IOP is moderate (e.g. less than 35 mmHg on a beta-blocker) in the absence of significant glaucomatous damage, an alpha-adrenergic agonist or a topical CAI might be appropriate.

•Miotics are contraindicated as they increase vascular permeability and may promote inflammation, and miosis enhances the formation of posterior synechiae.

Laser iridotomy

•Laser iridotomy is performed to re-establish communication between the posterior and anterior chambers in eyes with pupillaryblock angle-closure glaucoma. The resulting hole is usually quite small and likely to become occluded in the presence of active uveitis.

•It is important to bear in mind that correction of pupillary block may not control the IOP if there is insufficient open-angle for drainage. In cases of progressive angle closure, iridotomy may nevertheless prevent further PAS formation.

•Intensive topical steroid therapy should be used to minimize post-laser inflammation.

•Surgical iridectomy is the definitive method of preventing further pupil block.

Surgery

1Preoperative preparation

•Control of uveitis for a minimum of 3 months before surgery is ideal but often impractical.

•Preoperative topical steroids should be used, not only as prophylaxis against recurrent inflammation, but also to reduce the conjunctival inflammatory cell population.

•In patients with particularly labile inflammatory disease systemic steroids should be considered (0.5 mg/kg/day of oral prednisolone).

2Trabeculectomy is usually the procedure of choice.

•Combined cataract and glaucoma surgery is not appropriate. Ideally cataract surgery should be deferred for about 6 months after trabeculectomy.

•Adjunctive antimetabolites, particularly mitomycin C, are required since these eyes carry a high risk of failure.

•Postoperative hypotony is a risk as a delicate balance may exist between reduced aqueous production and severely restricted aqueous outflow. If production drops in the early postoperative period, any filtration may be excessive.

•After trabeculectomy steroids are tapered according to the level of inflammation and the appearance of the filtering bleb, and usually discontinued after 3–6 months, although earlier tapering may be necessary in cases of overfiltration.

3Glaucoma drainage devices should be considered in cases where trabeculectomy, even with adjunctive antimetabolites, has a poor success rate. This includes aphakic eyes, children with chronic anterior uveitis, or a previously failed trabeculectomy.

5Cyclodestructive procedures should be used with caution because they may not only exacerbate the intraocular inflammation but can result in profound hypotony, which may proceed to phthisis bulbi. Even eyes with seemingly intractable uveitic glaucoma may paradoxically develop ciliary body insufficiency in the longer term.

6Angle procedures include trabeculodialysis and goniotomy may be successful in children. The former involves making an incision along Schwalbe line in order to establish communication between the anterior chamber and Schlemm canal (Fig. 10.55).

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Fig. 10.55 Trabeculodialysis

Posner–Schlossman syndrome

Posner–Schlossman syndrome (glaucomatocyclitic crisis) is characterized by recurrent attacks of unilateral, acute secondary open-angle glaucoma associated with mild anterior uveitis. The cause of the raised IOP is presumed to be acute trabeculitis. There is some evidence that the herpes simplex virus may play a pathogenic role. Posner–Schlossman syndrome is a rare condition typically affecting young adults, 40% of whom are positive for HLA-Bw54. Males are affected more frequently than females. The IOP is elevated for between a few hours and several days. The attacks are unilateral, although 50% of patients have bilateral involvement at different times. The intervals between attacks vary and, with time, usually become longer. Patients should be followed even after the attacks have completely subsided, because a significant percentage will develop chronic open-angle glaucoma.

Diagnosis

1Presentation is with mild discomfort, haloes around lights and slight blurring of vision.

2Slit-lamp biomicroscopy shows corneal epithelial oedema due to a high IOP (40–80 mmHg), a few aqueous cells and fine white central keratic precipitates (Fig. 10.56).

3Gonioscopy shows an open angle.

Fig. 10.56 Keratic precipitates in Posner–Schlossman syndrome

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Treatment

Topical steroids are used to control the inflammation and aqueous suppressants for the raised IOP. Oral non-steroidal anti-inflammatory agents may also be beneficial.

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Lens-related glaucoma

Phacolytic glaucoma

Pathogenesis

Phacolytic glaucoma (lens protein glaucoma) is open-angle glaucoma occurring in association with a hypermature cataract. Trabecular obstruction is caused by high molecular weight lens proteins which have leaked through the intact capsule into the aqueous humour. Macrophages containing lens proteins may also contribute to trabecular blockage (Fig. 10.57A and B). Phacolytic glaucoma should not be confused with phacoanaphylactic (phacoantigenic) uveitis which is an autoimmune granulomatous reaction to lens proteins occurring in an eye with a ruptured capsule.

Fig. 10.57 Phacolytic glaucoma. (A) Lens protein-containing macrophages in the angle; (B) lens protein-containing macrophages on the corneal endotheliumsimilar to keratic precipitates; (C) hypermature cataract and lens protein-containing macrophages floating in the aqueous; (D) neglected end-stage glaucoma with corneal vascularization and a small pseudohypopyon

(Courtesy of J Harry – figs A and B)

Diagnosis

1Presentation is with pain; vision is already poor due to cataract.

2Slit-lamp biomicroscopy shows corneal oedema, a hypermature cataract and a deep anterior chamber. The aqueous may manifest floating white particles (Fig. 10.57C), which may form a pseudohypopyon if very dense (Fig. 10.57D).

3Gonioscopy shows an open-angle.

Treatment

Once the IOP is controlled medically, the proteinaceous material is flushed out and the cataract removed. Care should be taken not to rupture the zonules when performing anterior capsulotomy.

Phacomorphic glaucoma

Pathogenesis

Phacomorphic glaucoma is an acute secondary angle-closure glaucoma precipitated by an intumescent cataractous lens. Equatorial agerelated growth of the lens slackens the suspensory ligament and allows the lens to move anteriorly. Associated anteroposterior growth leads to increased iridolenticular contact and potentiates pupillary block and iris bombé.

Diagnosis

1Presentation is similar to acute PACG with a shallow anterior chamber and dilated pupil; cataract is usually evident (Fig. 10.58).

2Examination of the fellow eye may demonstrate a deep anterior chamber and an open angle, thus making PACG unlikely, although phacomorphic glaucoma is more likely in eyes with a shorter axial length and shallower anterior chamber.

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