Ординатура / Офтальмология / Английские материалы / Handbook of Glaucoma_Azuara-Blanco, Costa, Wilson_2001

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Figure 9.8A and 9.8B Lens particle glaucoma. In this patient, the surgeon attempted phacoemulsification of the lens and abandoned the surgical procedure because of technical difficulties. The patient developed increased intraocular pressure and was then referred to the glaucoma unit.

Figure 9.9

Anterior capsule rupture following a penetrating injury, leading to lens-particle glaucoma.

outflow. Lens material may gain access to the anterior chamber following incomplete removal of the lens after phacoemulsification or extracapsular cataract extraction, penetrating lens injury, Nd:YAG laser posterior capsulotomy, and even without antecedent intraocular manipulation (Figures 9.8 and 9.9).

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Slit-lamp biomicroscopy shows cortical lens material circulating in the aqueous humor, lens debris deposited on the corneal endothelium, corneal edema depending upon the acuteness of the IOP rise, and significant inflammation, which may lead to a hypopyon. On gonioscopy, the angle is open, but cortical lens material usually can be identified. IOP is raised because of mechanical obstruction by the lens particles and by the inflammation associated with the process. Macrophages are also present in the anterior chamber and, in a similar manner to phacolytic glaucoma, are thought to participate minimally in the pathophysiology of the IOP increase.

Medical therapy with aqueous suppressants is indicated to reduce IOP, eventually in association with hyperosomotic agents. Cycloplegics and topical steroids are also given, whereas miotics and prostaglandin-related drugs should be avoided. If lens particle glaucoma does not respond to medical therapy or if a large amount of lens material is present, surgical removal should be prompt.

Phacoanaphylaxis

Phacoanaphylaxis can be defined as a granulomatous inflammatory response secondary to the presence of lens material. Prior sensitization to isolated lens proteins is mandatory to initiate phacoanaphylaxis, and it may occur after extracapsular cataract extraction or traumatic rupture of the lens capsule.

Although glaucoma may develop after phacoanaphylaxis, hypotony is more common. Clinical diagnosis is very difficult, and is commonly made only after enucleation and histopathology. It is characterized by a unilateral anterior uveitis that may develop days or months after lens injury.

Lens proteins are normally isolated within the lens capsule. If the capsule is ruptured, sensitization to the proteins may precipitate the granulomatous reaction. Initially, the accumulation of a polymorphonuclear infiltrate is followed by epithelioid and giant cells surrounding the damaged area. Raised IOP may be a result of several mechanisms, including trabecular obstruction by lens particle material, inflammation causing trabeculitis, or peripheral anterior synechiae.

Medical therapy with aqueous suppressants, topical and systemic steroids can be given to quiet the eye and lower the IOP before surgery. To treat this disorder, all lens particle material should be removed to stop the phacoanaphylactic response.

Phacomorphic glaucoma

Phacomorphic glaucoma is a secondary angle closure glaucoma caused by lens intumescence. Lens enlargement increases relative pupillary block and pushes the peripheral iris forward. Both mechanisms result in narrowing of the anterior chamber angle and increased IOP. The typical picture includes an asymmetrical cataract, with the contralateral eye showing a deeper anterior chamber.

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Medical treatment with aqueous suppressants can be effective. Miotics are contraindicated since they increase both iridolenticular contact and the lens axial diameter, exacerbating angle closure. Since an element of pupillary block is generally present, laser iridotomy is indicated. After laser iridotomy, gonioscopy should be done to measure how wide the angle is. Major widening suggests that the pupillary component is important, whereas an angle that does not change implies that lens intumescence is the main mechanism. Subsequently, since lens intumescence is generally associated with low visual acuity, lens extraction alone may be effective in the control of IOP if peripheral anterior synechiae are not extensive.

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Lens subluxation or dislocation

Lens subluxation (partial rupture of the zonules) or dislocation (complete rupture of the zonules) may cause glaucoma by several mechanisms:

a)Pupillary block by lens and/or vitreous resulting in acute or chronic angle closure.

b)Lens in the anterior chamber.

c)Lens in the vitreous causing phacolytic or lens particle glaucoma.

Several disorders are associated with ectopia lentis (Figure 9.10), such as microspherophakia (Figure 9.11), Weill–Marchesani syndrome, Marfan’s syndrome (Figure 9.12)—(supero-temporal subluxation), homocystinuria (infero-nasal subluxation), simple ectopia lentis, and ectopia lentis et pupilae. Slit-lamp examination findings may vary from a discrete shift in lens position to a complete dislocation to the anterior chamber or to the vitreous. Iridodonesis and phacodonesis may also be detected. Differences in anterior chamber depths may also alert the examiner to the possibility of lens subluxation.

Figure 9.10 Simple ectopia lentis.

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Figure 9.11

Microespherophakia, seen by trans-illumination (A), and with the lens luxated into the anterior chamber (B).

Dislocation of the lens to the anterior chamber is an emergency, since a series of complications may develop, including severe pupillary block and corneal decompensation. Medical treatment with cycloplegics with the patient in a supine position may be used when the lens is clear, to reposition it behind the iris plane, but recurrence is common. Lens extraction is the definitive treatment and is indicated in the presence of cataract, or when repositioning is unsuccessful. Pupillary block can be relieved with laser iridotomy. A lens dislocated to the vitreous may remain for many years without causing damage. Hence, conservative treatment should be encouraged, unless phacolytic glaucoma develops.

Neovascular glaucoma

Neovascular glaucoma is a secondary glaucoma caused by the presence of new vessels in the anterior chamber angle. The new vessels develop as a

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Figure 9.12

Marfan’s syndrome, with characteristic long fingers (A), and superiorly subluxated lens (B).

result of retinal ischemia, secondary to diabetic retinopathy, central retinal artery or vein occlusion, intraocular tumors, retinal detachment, or occlusive carotid artery disease. Ultrasound examination in patients with neovascular glaucoma and media opacities is mandatory to rule out intraocular tumors. The first signs of incipient neovascular glaucoma are discrete tufts of new vessels in the pupillary

margin (Stage I). At this stage, the angle is not yet involved. Subsequently, new vessels extend radially toward the angle (Stage II) until they finally cross over the scleral spur onto the trabecular meshowork. Occasionally, new vessels may be seen first in the anterior chamber angle. At this stage, the angle is still open, but may be crowded with new vessels, which mechanically obstruct the trabecular outflow and increase the IOP (Stage III). In a more advanced stage, the fibrovascular tissue that covers the angle pulls the peripheral iris and forms peripheral anterior synechiae that gradually lead to complete angle closure and severe IOP increase (Stage IV, Figure 9.13).

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Figure 9.13A and 9.13B Neovascular glaucoma. Observe the new vessels at the peripheral iris, and a closed anterior chamber angle due to diffuse peripheral anterior synechiae.

When managing neovascular glaucoma, the critical aspect is early diagnosis of patients at risk, investigating the presence of new vessels in the pupillary margin and detecting ischemic changes in the retina. Hence, patients with diabetic retinopathy or CRVO should be followed carefully to rule out rubeosis iridis. If rubeosis is detected, irrespective of the aspect of the angle, retinal panphotocoagulation must be started immediately to prevent later development of angle neovascularization and neovascular glaucoma. About 40% of patients with the ischemic type of CRVO may develop neovascular glaucoma if not treated.

Panretinal photocoagulation is the first line of therapy for most cases of neovascular glaucoma and should be done promptly at the early signs of rubeosis. In Stage III, panphotocoagulation effectively causes regression of rubeosis iridis and and new vessels in the angle, allowing an adequate IOP control without the need for surgical intervention. Aqueous suppressants, topical steroids, and cycloplegics can be used to reduce IOP and inflammation until the effect of the laser is achieved. In Stage IV, the effectiveness of panphotocoagulation in control of IOP depends on the extension of the peripheral anterior syncechiae. If the angle is circumferentially closed, panphotocoagulation is still indicated to treat retinal

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ischemia, but the ability to decrease IOP is limited. At this stage, medical therapy is usually unsuccessful, and filtration surgery with adjunct mitomycin C (when the rubeosis has regressed), implantation of an aqueous shunt (when the rubeosis is active), or cyclodestructive procedures (when the visual prognosis is poor) are indicated to promote adequate IOP control. In blind, painful eyes, topical steroids and atropine are often enough to reduce the pain to a tolerable level. However,

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cyclodestructive procedures and/or retrobulbar alcohol injection, or (rarely) enucleation are sometimes needed in painful eyes refractory to medical therapy.

Glaucoma associated with intraocular tumors

Intraocular tumors may cause glaucoma by several mechanisms:

a)Direct infiltration of the trabecular meshwork.

b)Neovascular glaucoma.

c)Secondary angle closure secondary to anterior displacement of the lens–iris diaphragm.

d)Free-floating tumor cells blocking conventional outflow (i.e. melanomalytic glaucoma).

e)Hyphema.

Tumor-induced glaucomas are usually unilateral and may be associated with several types of tumors, mainly uveal melanomas, uveal metastasis, and retinoblastoma. However, benign tumors, such as iris melanocytomas and medulloepitheliomas, can also cause glaucoma. Lymphoid tumors and leukemias may infiltrate the uveal tract and retina, resulting in blockage of aqueous outflow. Retinoblastoma, the most common malignancy of childhood, is associated with glaucoma in about 15% of cases.

Identifying the tumor as the cause of glaucoma is essential in establishing the best treatment strategy (Figure 9.14). Adequate gonioscopy, indirect ophthal-

Figure 9.14 Iris melanoma in a patient with secondary elevation of intraocular pressure. The lesion had invaded the adjacent anterior chamber angle, and there was increased pigmentation in the trabecular meshwork.

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moscopy, and ultrasound examination may disclose this uncommon but potentially life-threatening cause of glaucoma. Eyes with malignant tumors should not undergo filtration surgery. Cyclodestructive procedures or a retrobulbar alcohol injection should be considered in a painful eye in which the tumor cannot be treated.

Glaucoma secondary to increased episcleral venous pressure

The modified Goldmann equation, Po = F/C + Pev (where Po = intraocular pressure, F = aqueous production, C = outflow facility and Pev = episcleral venous pressure) illustrates the direct association between episcleral venous pressure and intraocular pressure. Hence, increasing the episcleral venous pressures (whose normal values range from 9 to 10 mmHg) leads to an increase in intraocular pressure.

Glaucoma may be caused by any disorder that causes compression of the venous drainage of the

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eye, especially the superior ophthalmic vein. Compression may be caused by retrobulbar tumors, thyroid ophthalmopathy, thrombosis of the cavernous sinus or the superior ophthalmic vein, jugular vein obstruction, and superior vena cava syndrome. Increased episcleral venous pressure may also be a consequence of arteriovenous anomalies such as carotid cavernous fistulas (Figure 9.15), or congenital abnormalities such as orbital varices. Episcleral hemangiomas seen in Sturge–Weber syndrome may also promote high episcleral venous pressure (Figure 9.16). Finally, idiopathic cases of increased episcleral venous pressure have been described (Figure 9.17).

Patients with raised episcleral venous pressure show dilated, tortuous episcleral veins. The angle is typically open, eventually allowing the visualization of blood in Schlemm’s canal. The glaucoma may be unilateral (when secondary to Sturge–Weber syndrome or orbital varices) or bilateral when the venous

Figure 9.15

Dilated, tortuous episcleral vessels, conjunctival chemosis and proptosis in a patient with a direct carotid cavernous fistula.

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Figure 9.16 Sturge–Weber syndrome. Episcleral hemangiomas are associated with high episcleral venous pressure.

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Figure 9.17

Idiopathic increased episcleral venous pressure, with prominent tortuous episcleral vessels.

compression is localized in the neck (i.e. superior vena cava syndrome). Carotid cavernous fistulas may result in unilateral or bilateral glaucoma, since there is a communication between the sinuses.

If possible, treatment of glaucoma should be directed to the cause of raised episcleral venous pressure. When this strategy is impossible or unsuccessful, medical therapy with aqueous suppressants and prostaglandin-related drugs should be commenced. Although aqueous suppressants will not decrease IOP below the episcleral venous pressure, prostaglandin-related drugs should be effective in doing so since they increase uveoscleral outflow. Laser trabeculoplasty is generally not effective. On the other hand, filtration surgery can be attempted, but is associated with a higher rate of complications, including

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choroidal effusions and suprachoroidal hemorrhage. Tight closure of the scleral flap combined with prophylactic sclerostomies may help reduce postoperative complications.

Inflammatory glaucomas

Intraocular inflammation alters the dynamics of aqueous humor, and may cause raised or reduced IOP. The latter is associated with decreased aqueous humor production and increased uveoscleral outflow. On the other hand, inflammatory glaucoma may be explained by a variety of mechanisms, including:

a)Obstruction of the trabecular meshwork by inflammatory cells and protein.

b)Trabeculitis (inflammation of the trabecular meshwork itself).

c)Formation of peripheral anterior synechiae.

d)Posterior synechiae leading to pupillary block (Figure 9.18).

e)Iris neovascularization and neovascular glaucoma.

f)Anterior rotation of the lens–iris diaphragm.

All forms of uveitis may result in glaucoma through one or more of the mechanisms above. In Fuch’s heterochromic cyclitis (Figure 9.19), the affected eye shows a triad consisting of heterochromia (lighter iris color than the contralateral eye), uveitis (low grade, usually symptom-free), and cataract. Keratic precipitates are fine, colorless, star-shaped, and scattered over the endothelium. Open-angle glaucoma may develop in later stages in 25% of cases. Patients may have fine neovascularization of the iris and the anterior chamber angle, which may bleed. Both eyes are affected in about 10% of patients.

Glaucomatocyclitic crisis, also known as Posner–Schlossman syndrome, is characterized by recurrent episodes of unilateral anterior uveitis and raised IOP. Symptoms include slight ocular

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discomfort, halos and blurred vision. As

Figure 9.18

Extensive peripheral anterior synechiae in a patient with inflammatory glaucoma.

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