Angleclosure Glaucoma

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Angle closure is an anatomic disorder comprising a final common pathway of iris apposition to the trabecular meshwork. By recent convention, the term "glaucoma"

is applied to eyes with visual field and/or optic nerve damage, analogous to the differentiation between ocular hypertension and glaucoma in eyes with open angles. Angle closure results from various abnormal relationships of anterior segment structures. These, in turn, result from one or more abnormalities in the relative or absolute sizes or positions of anterior segment structures or posterior segment forces that alter anterior segment anatomy.1 Angle closure results from blockage of the meshwork by the iris, but the forces causing this blockage may be viewed as originating at four successive anatomic levels (figure 12.1):

1. Iris (pupillary block)

2. Ciliary body (plateau iris)

3. Lens (phacomorphic glaucoma)

4. Posterior to lens (aqueous misdirection, or malignant glaucoma)

The more posterior the level at which the angle closure originates, the more complex the diagnosis and treatment, because the operative mechanism specific to each level may also be accompanied by a component of the mechanism(s) peculiar to each of the levels preceding it and may require a combination of treatments appropriate to each of the mechanisms involved.

Indentation gonioscopy, or dynamic gonioscopy, is mandatory for accurate assessment and appropriate treatment of angle closure. Pressure applied to the cornea by the goniolens forces aqueous into the angle, widening it. The presence and extent of closure by peripheral anterior synechiae (PAS), the contour and insertion site of the iris, and the depth of the angle can be determined. Gonioscopy in a completely darkened room is of the utmost importance when assessing a narrow angle for oc-cludability (figure 12.2), because any light shining through the pupil may suffice to eliminate iris apposition to the trabecular meshwork. The slit beam should consist of the smallest square of light available to avoid stimulating the pupillary light reflex. The quadrant of angle to be assessed is examined with the four-mirror lens without pressure on the cornea and with the patient looking sufficiently far in the direction of the mirror so that the examiner can see as deeply into the angle as possible. The angle is observed while the pupil dilates in the dark. The narrowest quadrant is usually the superior angle (inferior mirror).

12.1.1 Acute Angle Closure. Therapy in acute angle closure (AAC) is directed at decreasing IOP rapidly and opening the angle. Both medical and laser treatments play a role in opening the angle and eliminating pupillary block.

Hyperosmotic agents lower IOP by causing a rapid but transient increase in serum osmolality of between 20 and 30 mOsm/L.2 The resulting blood-ocular osmotic gradient draws water from the eye via the retinal and uveal vasculature, primarily from the vitreous cavity. The decrease in vitreous volume lowers IOP and allows the lens to move posteriorly. Although the vitreous volume is decreased by only about 3%, this amounts to a volume of 0.12 mL, which is half the volume of the normal anterior chamber and twice the volume of the normal posterior chamber. IOP decreases within 30 to 60 minutes after administration, and the effect lasts about 5 to 6 hours. For maximal benefit, patients should limit fluid intake.

Figure 12.1. (A) Pupillary block (level 1). Force-producing iris apposition to the trabecular meshwork originates from the posterior chamber. Iridotomy provides definitive treatment. (B) Plateau iris (level 2). Force-producing iris apposition to the trabecular meshwork in this eye, which has already undergone laser iridotomy, originates from anteriorly positioned ciliary processes, holding the iris forward. Argon laser peripheral iridoplasty (ALPI) provides definitive treatment. (C) Phacomorphic glaucoma (level 3). Force-producing iris apposition to trabecular meshwork originates from an intumescent lens, pushing ciliary processes and the iris forward. ALPI can break an attack of acute angle-closure, and iridotomy can be performed to eliminate any component of pupillary block to give the eye time to quiet and the media time to clear so that lens extraction, the definitive procedure, can be safely performed. (D) Aqueous misdirection (level 4). Force-producing iris apposition to trabecular meshwork originates from behind the lens, pushing the lens, ciliary processes, and iris forward. Shallow supraciliary detachment is present, causing the lens-iris diaphragm to rotate anteriorly. The abnormal vitreociliary relationship that results causes posterior diversion of aqueous into the vitreous. Resultant increased posterior segment pressure pushes the lens farther forward, allowing more aqueous to be secreted into the vitreous and setting up a vicious cycle. Restoration of normal anatomic relationships is the definitive treatment, but achieving this can be difficult and entail complex combinations of medical, laser, and surgical treatment. Reprinted with permission from Ritch R, Lowe RF. Angle-closure glaucoma: mechanisms and epidemiology. In: Ritch R, Shields MB, Krupin T, eds. The Glaucomas. 2nd ed. St Louis, MO: CV Mosby Co; 1996:801-819.

Figure 12.2. (A) Ultrasound biomicrograph of anterior chamber angle in bright illumination. The iris is slightly convex, consistent with relative pupillary block. Aqueous has access to the trabecular meshwork, which is between Schwalbe's line and the scleral spur. (B) In the dark, the pupil dilates and the peripheral iris moves against the trabecular meshwork, closing the angle. Reprinted with permission from Ritch R, Lowe RF. Angle-closure glaucoma: mechanisms and epidemiology. In: Ritch R, Shields MB, Krupin T, eds. The Glaucomas. 2nd ed. St Louis, MO: CV Mosby Co; 1996:801-819.

Figure 12.2. (A) Ultrasound biomicrograph of anterior chamber angle in bright illumination. The iris is slightly convex, consistent with relative pupillary block. Aqueous has access to the trabecular meshwork, which is between Schwalbe's line and the scleral spur. (B) In the dark, the pupil dilates and the peripheral iris moves against the trabecular meshwork, closing the angle. Reprinted with permission from Ritch R, Lowe RF. Angle-closure glaucoma: mechanisms and epidemiology. In: Ritch R, Shields MB, Krupin T, eds. The Glaucomas. 2nd ed. St Louis, MO: CV Mosby Co; 1996:801-819.

Glycerol is administered as a liquid in dosages of 1 to 1.5 g/kg of body weight,3 either as a 100% solution mixed with an equal volume of iced juice or as a commercial preparation (Osmoglyn, 50% solution). Oral glycerol is rapidly absorbed, is distributed throughout the extracellular water, and penetrates the eye poorly. The drug is metabolized by the liver rather than excreted by the kidneys, producing less diuresis than do other hyperosmotic agents. Glycerol has an unpleasantly sweet taste and may cause vomiting. The caloric content is 4.32 cal/g, which, combined with the osmotic diuretic effect and resultant dehydration, mandates special caution when used in diabetic patients, who may develop hyperglycemia and ketosis.4

Isosorbide (Ismotic) is more palatable, causes less nausea and vomiting, and is not metabolized—a particular advantage in diabetic patients. Although isosorbide had advantages over other osmotic drugs (see chapter 8), this drug is not commercially available at this time. A solution of 20% mannitol (Osmitrol), 0.5 to 2 g/kg, given intravenously over 45 minutes, has a greater hypotensive effect and may be given when severe nausea and vomiting are present.

Administration of hyperosmotic agents is commonly accompanied by thirst and headache. Hyperosmolar coma can be a serious complication caused by severe dehydration of the central nervous system. Patients with renal or cardiovascular disease or those already dehydrated by vomiting are at risk. These agents should be used cautiously in patients with reduced cardiac function, because the sudden intravas-cular volume overload may lead to congestive heart failure and pulmonary edema.5 Acetazolamide (Ak-Zol, Dazamide, Diamox), a carbonic anhydrase inhibitor (CAI), is highly effective in AAC, even in the presence of ischemic iris atrophy and paralysis of the pupil. Rapid IOP reduction is most reliably achieved by giving 500mg intravenously. Adverse reactions are uncommon. Acetazolamide tablets may be given orally as an alternative, but the onset of action is not as rapid. Following oral therapy, the maximum effect occurs at 2 hours, and high plasma levels persist for 4 to 6 hours but then drop rapidly because of excretion in the urine. Topical aqueous suppressants are additive with acetazolamide but take longer to act, and their absorption through the cornea is slowed by corneal edema and markedly elevated IOP. They should be used in conjunction with, but not as an alternative to, systemic medications. These topical agents are more useful in later stages of treatment and in maintaining reduced IOP prior to laser iridotomy.

The liberal use of miotics to constrict the pupil and pull the peripheral iris away from the angle wall was long the main approach to AAC. A typical recommended regimen was pilocarpine 4% every 5 minutes for four doses, every 15 minutes for four doses, then every hour for four doses or until the attack was broken. However, when IOP is extremely high, the pupil is unresponsive to miotics because of ischemia and paralysis of the iris sphincter. Pilocarpine not only may be ineffective but, in some eyes, may paradoxically worsen the situation, triggering aqueous misdirec-tion.6 Although the miotic effect of pilocarpine is blocked, ciliary muscle contraction causes thickening of the lens and forward lens movement, which results in further shallowing of the anterior chamber. For this reason, some clinicians use lower concentrations of pilocarpine (1% or 2%) with less frequent dosing. In eyes with level 3 block (phacomorphic glaucoma) or level 4 block (aqueous misdirection), pilocarpine treatment should be considered contraindicated. Unequal anterior chamber depths, progressive increase in myopia, and progressive shallowing of the anterior chamber are clues to the correct diagnosis.

High doses of pilocarpine may produce cholinergic toxicity, which may not be noticed because of the nausea and vomiting associated with the AAC glaucoma attack. Strong miotics, such as echothiophate (Phospholine Iodide), can increase both the pupillary block and the vascular congestion. Immediate treatment with intravenous acetazolamide and repeated instillation of pilocarpine 2% was not more successful in breaking attacks of AAC glaucoma than was treatment with acetazolamide and a single drop of pilocarpine given 3 hours later.7 Similar results were obtained with topically administered timolol (Blocadren) in place of acetazolamide.8

Our preferred approach to the treatment of AAC is designed to prioritize reopening of the anterior chamber angle and to minimize the possibility of adverse responses to pilocarpine.9 Examination of the affected eye and fellow eye, with attention to central and peripheral anterior chamber depth as well as the shape of the peripheral iris, is performed in an attempt to determine the underlying mechanisms of the angle closure (pupillary block, plateau iris, phacomorphic glaucoma, or aqueous misdirection). A detailed analysis of these mechanisms has been published elsewhere.1

In the absence of oral isosorbide, we use glycerol as our preferred hyperosmotic agent, along with one or more topical aqueous suppressants. Intravenous acet-azolamide can be given according to the physician's preference. The patient is then placed supine to permit the lens to fall posteriorly with vitreous dehydration. The eye is reassessed after 1 hour. IOP is usually decreased, but the angle may remains appositionally closed. One drop of pilocarpine 4% is given and the patient is re-examined 30 minutes later. If IOP is reduced and the angle is open, the patient may be treated medically with topical low-dose pilocarpine, aqueous suppressants, and corticosteroids, until the eye quiets and laser iridotomy may be performed. However, if IOP is unchanged or elevated and the angle remains closed, lens-related angle closure should be suspected, further pilocarpine is withheld, and the attack is broken by argon laser peripheral iridoplasty (ALPI).10,11

AAC is associated with a marked inflammatory reaction. The instillation of prednisolone 1% or dexamethasone 0.1% is desirable from the start to reduce inflammation. Severe pain may be treated with analgesics, and vomiting with antiemetics.

Laser iridotomy is the procedure of choice for all cases of AAC with a component of pupillary block. Success requires gonioscopic confirmation of angle opening, because transient lowering of IOP may occur with medical therapy. Ideally, iridotomy should be performed after the acute attack has been terminated and the eye is no longer inflamed. Attacks of AAC that are unresponsive to medical treatment are almost always successfully broken with ALPI. Alternatively, ALPI with or without systemic medications may be used as immediate initial treatment, especially in eyes at risk for developing chronic angle-closure glaucoma, or eyes in which a dominant mechanism exists that is not pupillary block. It is highly effective in breaking the initial attack.12-15 In the absence of oral isosorbide and our current disinclination to use intravenous acetazolamide, we have moved to performing ALPI as an initial procedure.

ALPI does not eliminate pupillary block and is not a substitute for laser ir-idotomy, which must be performed as soon as the eye is quiet. However, even in eyes with extensive PAS, IOP is lowered sufficiently for a few days for the inflammation to resolve. ALPI is much safer than attempting surgical iridectomy on an inflamed eye with elevated IOP. The risks of intraoperative surgery are avoided and, even if aqueous misdirection is present, the angle remains open long enough for inflammation to clear. The alternative of waiting and prolonging medical therapy for several days seriously increases the possibility of irreversible damage to the iris, lens, drainage pathways, and optic nerve head.

12.1.2 Chronic Angle Closure. Chronic angle-closure (CAC) refers to an eye in which portions of the anterior chamber angle are permanently closed by PAS. In the era of surgical iridectomy, an attack of AAC could arise in an eye that had developed PAS because of gradual angle closure prior to the development of the attack. Conversely, a prolonged acute attack or a series of subacute attacks could lead to progressive PAS formation. The presence of PAS defined "chronic." At present, we prefer the term "combined-mechanism glaucoma'' for those eyes that have had angle closure eliminated by laser treatment and have residual elevated IOP, reserving the term "chronic angle-closure glaucoma'' for those eyes that develop gradual sealing of the angle with PAS and gradual elevation of IOP in the absence of an acute attack.

It is important to recognize early stages of appositional angle closure in the absence of PAS and to recognize circumferential (creeping) angle closure. Laser ir-idotomy is indicated for all stages of CAC, opening areas of the angle not involved by PAS and preventing further synechial closure.

Prolonged miotic treatment in eyes with open-angle glaucoma and narrow angles may lead to pupillary block and angle-closure glaucoma. Zonular relaxation leads to anterior lens movement and increased lens thickness in combination with increased pupillary block produced by pilocarpine. When miotic-induced angle closure occurs, the approach to treatment should be determined by assessing the medications necessary to control the glaucoma. If the patient has been treated with miotics alone, substitution of aqueous suppressants may suffice. If the patient requires miotics for IOP control, then laser iridotomy is warranted.

If the angle remains appositionally closed or spontaneously occludable after laser iridotomy, mechanisms other than pupillary block are likely responsible and ALPI is indicated to prevent progressive damage to, or further appositional and/or synechial closure of, the angle. The need for continued medical treatment after iridotomy with or without ALPI is determined by the level of IOP and the extent of glaucomatous damage. Treatment is similar to that of open-angle glaucoma. In two trials, lata-noprost lowered IOP more effectively than did timolol in patients with CAC glaucoma.16-18 Latanoprost was also effective in eyes with circumferential PAS to the level of the trabecular meshwork.19 Periodic gonioscopy is obviously warranted. Argon laser trabeculoplasty has been reported to be both successful20 and unsuccessful21 after iridotomy in combined-mechanism glaucoma. It remains to be evaluated whether selective laser trabeculoplasty is effective in this situation. If IOP remains uncontrolled and glaucomatous damage develops, filtration surgery is indicated. Patients who already present with glaucomatous optic neuropathy are unlikely to be adequately treated with iridotomy only and have a moderate chance to require filtration surgery. There is an increased chance of developing aqueous misdirection following filtration surgery in patients who have had angle-closure glaucoma.22

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