Chapter 11: Glaucoma
SECONDARY GLAUCOMA
Increased intraocular pressure occurring as one manifestation of some other eye disease is called secondary glaucoma. These diseases are difficult to classify satisfactorily. Treatment involves controlling intraocular pressure by medical and surgical means but also dealing with the underlying disease if possible.
PIGMENTARY GLAUCOMA
This syndrome seems to be primarily a degeneration of the pigmented epithelium of the iris and ciliary body. The pigment granules flake off from the iris as a result of friction against the underlying packets of zonular fibers, resulting in iris transillumination. The pigment is deposited on the posterior corneal surface (Krukenberg's spindle) and becomes lodged in the trabecular meshwork, impeding the normal outflow of aqueous. The syndrome occurs most often in myopic males between the ages of 25 and 40 who have a deep anterior chamber with a wide anterior chamber angle.
The pigmentary changes may be present without glaucoma (pigment dispersion syndrome), but such persons must be considered "glaucoma suspects." A number of pedigrees of autosomal dominant inheritance of pigmentary glaucoma have been reported, and a gene for pigment dispersion syndrome has been mapped to chromosome 7.
The logical treatment in this condition is miotic therapy because it overcomes movement of the iris across the zonules. However, because the patients are usually young myopes, such therapy is poorly tolerated unless administered as pilocarpine once daily, preferably at bedtime. Beta-blockers and epinephrine are also effective.
The major problem, however, is the young age at which the disease develops, which increases the chance that drainage surgery will be necessary and enhances the advisability of combining such surgery with antimetabolite therapy. Laser trabeculoplasty is frequently used in this condition but is unlikely to obviate the need for drainage surgery.
EXFOLIATION SYNDROME (Pseudo-Exfoliation Syndrome)
In exfoliation syndrome, flake-like deposits of a fibrillary material are seen on the anterior lens surface (in contrast to the true exfoliation of the lens capsule caused by exposure to infrared radiation, ie, "glassblower's cataract"), ciliary processes, zonule, posterior iris surface, loose in the anterior chamber, and in the trabecular meshwork (along with increased pigmentation). These deposits can also be detected histologically in the conjunctiva, suggesting a more widespread abnormality. The disease usually occurs in patients over age 65. Treatment is as for primary open-angle glaucoma.
GLAUCOMA SECONDARY TO CHANGES IN THE LENS
Lens Dislocation
The crystalline lens may be dislocated as a result of trauma or spontaneously, as in Marfan's syndrome. Anterior dislocation may cause obstruction of the pupillary aperture, leading to iris bombé and angle closure. Posterior dislocation into the vitreous is also associated with glaucoma, though the mechanism is obscure. It may be due to angle damage at the time of traumatic dislocation.
In anterior dislocation, the definitive treatment is lens extraction once the intraocular pressure has been controlled medically. In posterior dislocation, the lens is usually left alone and the glaucoma treated as primary open-angle glaucoma.
Intumescence of the Lens
The lens may take up considerable fluid during cataractous change, increasing markedly in size. It may then encroach upon the anterior chamber, producing both pupillary block and angle crowding and resulting in angle-closure glaucoma. Treatment consists of lens extraction once the intraocular pressure has been controlled medically.
Phacolytic Glaucoma
Some advanced cataracts may develop leakiness of the anterior lens capsule, which allows passage of liquefied lens proteins into the anterior chamber. There is an inflammatory reaction in the anterior chamber, and the trabecular meshwork becomes edematous and obstructed with lens proteins, leading to an acute rise in intraocular pressure. Lens extraction is the definitive treatment once the intraocular pressure has been controlled medically and intensive topical steroid therapy has reduced the intraocular inflammation.
GLAUCOMA SECONDARY TO CHANGES IN THE UVEAL TRACT
Uveitis
The intraocular pressure is usually below normal in uveitis because the inflamed ciliary body is functioning poorly. However, elevation of intraocular pressure may also occur through a number of different mechanisms. The trabecular meshwork may become blocked by inflammatory cells from the anterior chamber, with secondary edema, or may occasionally be involved in an inflammatory process specifically directed at the trabecular cells (trabeculitis). Chronic or recurrent uveitis produces permanent impairment of trabecular function, peripheral anterior synechiae, and occasionally angle neovascularization, all of which increase the chance of secondary glaucoma. Seclusio pupillae due to 360-degree posterior synechiae produces iris bombé and acute angle-closure glaucoma. The uveitis syndromes that tend to be associated with secondary glaucoma are Fuchs's heterochromic cyclitis, HLA-B27-associated acute anterior uveitis, and uveitis due to herpes zoster and herpes simplex.
Treatment is directed chiefly at controlling the uveitis with concomitant medical glaucoma therapy as necessary, avoiding miotics because of the increased chance of posterior synechia formation. Long-term therapy, including surgery, is often required because of irreversible damage to the trabecular meshwork.
Acute angle closure due to seclusion of the pupil may be reversed by intensive mydriasis but often requires laser peripheral iridotomy or surgical iridectomy. Any uveitis with a tendency to posterior synechia formation must be treated with mydriatics whenever the uveitis is active to reduce the risk of pupillary seclusion.
Tumor
Uveal tract melanomas may cause glaucoma by anterior displacement of the ciliary body, causing secondary angle closure, direct involvement of the anterior chamber angle, blockage of the filtration angle by pigment dispersion, and angle neovascularization. Enucleation is usually necessary.
IRIDOCORNEOENDOTHELIAL (ICE) SYNDROME (Essential Iris Atrophy, Chandler's Syndrome, Iris Nevus Syndrome)
This rare idiopathic condition of young adults is usually unilateral and manifested by corneal decompensation, glaucoma, and iris abnormalities.
GLAUCOMA SECONDARY TO TRAUMA
Contusion injuries of the globe may be associated with an early rise in intraocular pressure due to bleeding into the anterior chamber (hyphema). Free blood blocks the trabecular meshwork, which is also rendered edematous by the injury. Treatment is initially medical, but surgery may be required if the pressure remains elevated.
Late effects of contusion injuries on intraocular pressure are due to direct angle damage. The interval between the injury and the development of glaucoma may obscure the association. Clinically, the anterior chamber is seen to be deeper than in the fellow eye, and gonioscopy shows recession of the angle. Medical therapy is usually effective, but drainage surgery may be required.
Laceration or contusional rupture of the anterior segment is associated with loss of the anterior chamber. If the chamber is not reformed soon after the injury-either spontaneously, by iris incarceration into the wound, or surgically-peripheral anterior syne-chiae will form and result in irreversible angle closure.
GLAUCOMA FOLLOWING OCULAR SURGERY
Ciliary Block Glaucoma (Malignant Glaucoma)
Surgery upon an eye with markedly increased intraocular pressure and a closed angle can lead to ciliary block glaucoma. Immediately after surgery, the intraocular pressure increases markedly, and the lens is pushed forward as a result of the collection of aqueous in and behind the vitreous body.
Treatment consists of cycloplegics, mydriatics, aqueous suppressants, and hyperosmotic agents. Hyperosmotic agents are used to shrink the vitreous body and let the lens fall more posteriorly.
Posterior sclerotomy, vitrectomy, and even lens extraction may be needed.
Peripheral Anterior Synechiae
Just as with trauma to the anterior segment (see above), surgery that results in a flat anterior chamber will lead to formation of peripheral anterior synechiae. Early surgical re-formation of the chamber is required if it does not occur spontaneously.
NEOVASCULAR GLAUCOMA
Neovascularization of the iris (rubeosis iridis) and anterior chamber angle is most often secondary to widespread retinal ischemia such as occurs in advanced diabetic retinopathy and ischemic central retinal vein occlusion. Glaucoma results initially from obstruction of the angle by the fibrovascular membrane, but subsequent contraction of the membrane leads to angle closure.
Treatment of established neovascular glaucoma is difficult and often unsatisfactory.
GLAUCOMA SECONDARY TO RAISED EPISCLERAL VENOUS PRESSURE
Raised episcleral venous pressure may contribute to glaucoma in Sturge-Weber syndrome, in which a developmental anomaly of the angle is also often present, and carotid-cavernous fistula, which may also cause angle neovascularization due to widespread ocular ischemia. Medical treatment cannot reduce the intraocular pressure below the level of the abnormally elevated episcleral venous pressure, and surgery is associated with a high risk of complications.
STEROID-INDUCED GLAUCOMA
Topical and periocular corticosteroids may produce a type of glaucoma that simulates primary open-angle glaucoma, particularly in individuals with a family history of the disease, and will exaggerate the intraocular pressure elevation in those with established primary open-angle glaucoma. Withdrawal of the medication usually eliminates these effects, but permanent damage can occur if the situation goes unrecognized too long. If topical steroid therapy is absolutely necessary, medical glaucoma therapy will usually control the intraocular pressure. Systemic steroid therapy is less likely to cause a rise in intraocular pressure.
It is imperative that patients receiving topical or systemic steroid therapy undergo periodic tonometry and ophthalmoscopy, particularly if there is a family history of glaucoma.
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10.1036/1535-8860.ch11