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Table 15-2.  Differential Diagnosis of Glaucoma-Like Optic Discs and Visual Fields

1.Missed elevated IOP

•diurnal variability

•Incorrect measurement

•thin central cornea (<500 μm)

2.Previous IOP elevation, no longer present

3.Shock-induced optic neuropathy

4.Compressive optic neuropathy

5.Ischemic optic neuropathy

6.Giant cell arteritis (temporal arteritis)

7.Optic nerve anomalies (pituitary tumors, etc.)

8.Macular degeneration

9.Juxtapapillary choroiditis

10.Myopia

11.Demyelinating disease

resonance imaging scan to evaluate for compressive lesions of the optic nerve or chiasm may be indicated. If history or symptoms suggest, rapid plasma reagin/Venereal Disease Research Laboratory, rheumatoid factor/antinuclear antibody, or erythrocytic sedimentation rate may be checked to look

for syphilis, autoimmune diseases, or temporal arteritis (giant cell arteritis) as potential causes. If a patient is on blood pressure medicines or has a history of hypotension, a 24-hour Holter monitor to check for nocturnal hypotension may be indicated.

33.How is average-pressure glaucoma treated?

The Collaborative Normal-Tension Glaucoma Study found that by reducing the intraocular pressure by 30% the rate of progression of visual-field loss was reduced from 35% to 12%. Lowering intraocular pressure is the mainstay of treatment for average-pressure glaucoma, as well as primary open-angle glaucoma.19

References

1.Tielsch JM, Sommer A, Katz J, et al.: Racial variations in the prevalence of primary open-angle glaucoma. The Baltimore eye survey, JAMA 266:369–374, 1991.

2.Caprioli J, Bateman J, Gaasterland D, et al.: Primary open-angle glaucoma: preferred practice pattern, San Francisco, 2003, American Academy of Ophthalmology.

3.Tielsch JM, Katz J, Sommer A, et al.: Family history and risk of primary open-angle glaucoma. The Baltimore eye survey, Arch Ophthalmol 112:69–73, 1994.

4.Wolfs R, Klaver C, Ramrattan R, et al.: Genetic risk of primary open-angle glaucoma: population-based familial aggregation study, Arch Ophthalmol 116:1640–1645, 1998.

5.American Academy of Ophthalmology: Basic and clinical science course, section 10, San Francisco, 2004, American Academy of Ophthalmology.

6.Colton T, Ederer F: The distribution of intraocular pressures in the general population, Surv Ophthalmol 25:123–129, 1980.

7.Dielemans I, Vingerling JR, Wolfs RC, et al.: The prevalence of primary open-angle glaucoma in a population-based study in the Netherlands. The Rotterdam study, Ophthalmology 101:1851–1855, 1994.

8.Coleman AL, Morrison JC, Callender O: Evaluation of the optic nerve head. In Higginbotham E, Lee D, editors: Clinical guide to glaucoma management, Boston, 2004, Elsevier, pp 183–191.

9.Kass MA, Kolker AE, Becker B: Prognostic factors in glaucomatous visual field loss, Arch Ophthalmol 94:1274–1276, 1976.

10.Mitchell P, Smith W, Attebo K, et al.: Prevalence of open-angle glaucoma in Australia. The Blue mountains study, Ophthalmology 103:1661–1669, 1996.

11.Sommer A, Tielsch JM, Katz J, et al.: Relationship between intraocular pressure and primary open angle glaucoma among white and black Americans. The Baltimore eye survey, Arch Ophthalmol 109:1090–1095, 1991.

12.Zeimer RC: Circadian variations in intraocular pressure. In Ritch R, Shields MB, Krupin T, editors: The glaucomas, ed 2, St. Louis, 1996, Mosby, pp 429–445.

13.Brandt JD, Beiser JA, Kass MA, et al.: Central corneal thickness in the ocular hypertension treatment study, Ophthalmology 108:1779–1788, 2001.

1.What landmarks are seen in the anterior chamber angle?

The structures noted in anterior-to-posterior sequence are as follows (numbered list corresponds to numbers in Fig. 16-1):

1.Schwalbe’s line: The peripheral or posterior termination of the Descemet’s membrane, seen clinically as the apex or termination of the corneal light wedge. May be visible inferiorly as the most anterior nonwavy pigmented line.

2.Anterior, nonpigmented, trabecular meshwork (TM): Clear whitish band.

3.Posterior, pigmented, TM: Variably pigmented band of homogeneous width. Usually most pigmented inferiorly (Fig. 16-2).

4.Schlemm’s canal: Variably visible light gray band at the level of the posterior TM. Elevated episcleral venous pressure or pressure from the edge of the goniolens will cause blood to reflux, making it appear as a faint red band.

5.Scleral spur: Narrow, white band of sclera invaginating between the TM and the ciliary body. Marks the insertion site of the longitudinal muscle fibers of the ciliary body to the sclera.

6.Ciliary body (CB) band: Pigmented band marking the anterior face of the ciliary body. Variably, iris processes may be seen as lacy projections crossing this band. By definition, iris processes do not cross the scleral spur. Projections that cross the scleral spur to the TM are peripheral anterior synechiae (PAS) and may be focal, pillar-like, or broad sheets.

7.Iris

2.Why is a goniolens necessary to visualize the anterior chamber angle?

Light from the anterior chamber (AC) angle undergoes total internal reflection at the cornea (tear)–air interface, preventing direct visualization. A goniolens changes the refractive index at the interface, enabling visualization.

3.What are the different kinds of gonioscopy? How do they differ?

•A Koeppe contact lens is used for direct gonioscopy. This technique is cumbersome, requiring the patient to be supine. A clear, viscous liquid such as methylcellulose is used as a coupling medium. By using a direct viewing system such as a binocular microscope, the anterior chamber angle is visualized.

•Indirect gonioscopy uses a mirrored contact lens. The Goldmann three-mirror lens vaults the central cornea and requires a viscous coupling liquid. The Zeiss (Fig. 16-3), Posner, or Sussman fouror six-mirror lenses directly contact the cornea and thus do not require a coupling agent beyond the patient’s normal tear film. These can be used at the slip lamp.

Figure 16-1.  Diagram of anterior chamber anatomy.

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Figure 16-2.  Inferior quadrant of heavily pigmented open angle.

Figure 16-3.  Zeiss goniolens.

4.Which goniolens is preferred by most glaucoma specialists and why?

The Zeiss, Posner, and Sussman lenses are preferred by a majority of glaucoma specialists for the following reasons:

•Speed and ease of use (they do not require a viscous coupling liquid and, because of their four or six mirrors, they do not need to be rotated to see all 360 degrees of the angle).

•The ability to perform indentation gonioscopy and the absence of a suction effect on the eye. Indentation cannot be performed with the Goldmann lens because of its larger diameter. The suction effect of the Goldmann lens can sometimes artificially widen narrow angles. These two qualities can be critically important when evaluating eyes with narrow angles.

•Elimination of the transient degradation of corneal clarity that is a consequence of the viscous liquid and Goldmann lens manipulation, which can make subsequent fundus examination difficult.

Warning: When first mastering gonioscopy, the Zeiss lens can be more difficult than the Goldmann

lens. In inexperienced hands, excessive indentation can easily occur, which will make the angle appear wider than it really is. Zeiss gonioscopy demands a light touch. One way to make sure you are not pressing is for the contact to be so light that you occasionally lose part of the contact meniscus. If you see any corneal striae or if your view is not crystal clear, you are probably indenting.

5.How is gonioscopy performed?

1.Topical anesthesia is essential for patient comfort and cooperation.

2.Rest your elbow on the slit lamp platform and your ring and/or small fingers on the side bar or on the patient’s cheek to help stabilize your hand.

3.Examination can be facilitated by asking the patient to stare straight ahead with the fellow eye without blinking.

4.To facilitate viewing a particular quadrant of the angle with indirect gonioscopy, either tilt the mirror toward the quadrant or have the patient look toward that mirror. For example, when viewing the

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Table 16-1.  The Scheie and Schaffer Classification Systems

*The angle is graded as a slit when it is between grades 0 and I.

superior angle, either tilt the inferior mirror upward, toward the superior angle, or have the patient look down slightly, toward the inferior mirror.

5.The superior–inferior relationships in the nasal and temporal mirrors and the nasal–temporal (right–left) relationships in the superior and inferior mirrors are preserved, not inverted as in indirect ophthalmoscopy. For example, when viewing the superior angle through the inferior mirror, an area of PAS seen at five o’clock in the mirror is actually at one o’clock, not eleven o’clock.

6.How can I determine which patients may have narrow angles and need gonioscopy?

The van Herick technique uses a thin slit beam focused at the limbus to approximate angle depth by comparing the peripheral AC depth to corneal thickness. Grade I has a peripheral AC depth less than onequarter of the corneal thickness; grade II is one-quarter of the corneal thickness; grade III is one-half of the thickness; and grade IV is one corneal thickness or more. Patients who are grade I or II certainly have narrow angles and should have gonioscopy. This technique, however, should never replace gonioscopy in eyes with clear media as part of a glaucoma evaluation. It falsely gives the appearance of an open angle in some eyes with plateau iris or anterior rotation of the ciliary body (see classification below).

7.What are the different gonioscopic anterior chamber angle classification systems?

Table 16-1 summarizes the Scheie system, which is rarely used, and the Schaffer system, which is the most commonly used.

The Spaeth system, however, is the most descriptive. The first element is a capital letter (A to E), for the level of iris insertion:

•A = Anterior to TM

•B = Behind the Schwalbe’s line, or at the TM

•C = At scleral spur

•D = Deep angle, CB band visible

•E = Extremely deep

If during indentation gonioscopy, the true iris insertion is noted to be more posterior than originally

apparent, the original impression is put in parentheses, followed by the true iris insertion outside parentheses.

The second element is a number that denotes the iridocorneal angle width in degrees at the level of the trabecular meshwork, usually from 5 to 45 degrees.

The third element is a lower-case letter describing the peripheral iris configuration:

•f = Flat

•b = Bowed or convex

•c = Concave

•p = Plateau configuration

In addition, the pigmentation of the posterior TM is graded on a scale of 0 (none) to 4 (maximal). For

example, (A)C10b, 2+PTM refers to an appositionally closed 10-degree angle that, with indentation, opened to the scleral spur and revealed moderate pigmentation of the posterior TM.

8.How do I know if I can safely dilate a patient, with or without a slit lamp?

If no slit lamp is available, use a penlight and shine it from the temporal side perpendicular to the central visual axis. In an eye with a normal or “safe” anterior chamber depth, the entire nasal half of the iris will be illuminated as well as the temporal half. In an eye with a shallow or questionable anterior chamber depth, none or only part of the nasal half of the iris will be illuminated. This technique does not hold true in eyes with plateau iris.

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c.Carotid occlusive disease, comprises approximately 10% of cases

d.Miscellaneous (e.g., central retinal artery occlusion (CRAO), tumors, chronic retinal detachment)

4.Iridocorneal endothelial syndrome

a.Progressive iris atrophy

b.Chandler’s syndrome

c.Cogan-Reese syndrome

11.What do the terms PACS, PAC, APAC, and PACG signify? How are they related to acute, subacute, and intermittent angle closure?

PACS stands for primary angle closure suspect PAC stands for primary angle closure

PACG stands for primary angle closure glaucoma APAC stands for acute primary angle closure

The terms refer to a new classification system of angle closure, which is currently used in most clinical and epidemiological studies. This system was developed by the International Society of Geographical and Epidemiological Ophthalmology between 1998 and 2005. PACS refers to patients with narrow angle on gonioscopy but without elevated IOP or presence of PAS. PAC refers to patients with narrow angle and elevated IOP or PAS. PACG refers to patients with narrow angle and glaucomatous optic neuropathy and/or visual field defects (Table 16-2).

The purpose of this new classification system is to unify the definition of glaucoma. It reserves the term glaucoma for the presence of optic neuropathy. For example, a patient presenting with acute elevated IOP secondary to angle closure will be referred to as APAC instead of acute angle closure glaucoma, as the patient may not have developed (yet) glaucoma optic neuropathy at the episode of acute angle closure.

The new classification system relates to the traditional classification of angle-closure glaucoma to some degree. Acute angle-closure glaucoma is referred to as acute primary angle closure; chronic angle-closure glaucoma can be either PAC or PACG depending on the status of the optic nerve and visual field. Subacute or intermittent angle-closure glaucoma can be PACS, PAC, or PACG with self-limited symptoms. The status of the angle and optic nerve dictates the classification of angle closure instead of the patient’s symptomatology and probably has better prognostic value than the previous system.

The new classification intends to describe the natural history of angle closure. Anatomically narrow angles (i.e., PACS) are common; about 4 to 10% of the population above the age of 40 have some degree of narrow angle. Angles narrow with age as the lens thickens throughout life. Some (not all) PACS will progress to PAC and eventually to PACG. Some PACS will develop APAC. We are still trying to identify which subgroup of PACS will progress to PACG and evaluating effective preventive treatments.

PRIMARY ANGLE CLOSURE (RELATIVE PUPILLARY

BLOCK AND OTHER MECHANISMS)

12.What is the epidemiology of primary angle-closure glaucoma?

Inuit or Eskimos have the highest incidence of APAC, followed by Asians and then Caucasians and those of African descent. It is more common in Northern European Caucasians than in Mediterranean Caucasians. The peak incidence is between the ages of 55 and 65. In both Asians and

Table 16-2.  The International Society of Geographic and Epidemiological

Ophthalmology Classification of Angle Closure

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Between episodes, the IOP is normal and the ocular exam is usually normal, except for the presence of narrow angles and, sometimes, glaukomflecken, cataracts, and PAS on gonioscopy.

17.How does chronic angle closure present clinically?

It is usually asymptomatic, unless marked visual-field loss has occurred. Gradual closure of the angle, by simple apposition and/or PAS, leads to a more gradual rise in IOP. The IOP is more variable but can be as high as 60 mm Hg without any symptoms. The cornea is usually clear, because the IOP rises gradually, resulting in a lack of pain, redness, decreased vision, or other symptoms. This is the most dangerous form of angle closure. Because of the lack of symptoms and very high IOP, patients tend to present late with very advanced disease.

18.What are the anatomic characteristics of eyes with primary angle closure?

Anatomically, the eyes have short axial length, hyperopia, anterior segment crowding, including a thicker lens, and/or peripheral iris.

19.What is the pathophysiologic mechanism of relative pupillary block?

The crystalline lens grows thicker throughout life. In eyes that are predisposed, apposition between the posterior iris surface and the anterior lens capsule gradually increases. As the iridolenticular touch increases, the resistance to aqueous flow from the posterior to the anterior chamber increases, gradually increasing posterior chamber pressure. Under conditions in which the pupil is in a middilated position (e.g., from stress, low ambient light levels, sympathomimetic or anticholinergic medications), the elevated posterior chamber pressure causes the lax or floppy iris to bow anteriorly and occlude the trabecular meshwork. It is hypothesized that thinner or lighter-colored irises are more likely to cause an acute rise in IOP because they are thinner and floppier, causing acute angle closure. Less floppy, thicker irises are pushed anteriorly more gradually, especially peripherally. This leads to creeping chronic angle closure, with or without PAS, and a more gradual IOP rise (Fig. 16-4).

20.What nonmedical maneuver may help to lower intraocular pressure even before medicating the patient?

Even before starting medical treatment, indentation gonioscopy can sometimes help to lower IOP by pushing aqueous from the central AC peripherally, opening the angle if it is not sealed with PAS. This must be done carefully to avoid abrading the corneal epithelium, which is swollen and may abrade more easily than normal. An anterior chamber paracentesis with a blade or needle may more rapidly decompress the eye, and medications would further lower the IOP.

21.How would you treat the involved eye medically?

The “kitchen sink” approach is generally preferred, using some combination of the drugs listed below (Table 16-3). The use of miotics such as pilocarpine in narrow, potentially occludable, angles is a subject of some debate, even among glaucoma specialists. The rationale for miotic use is to pull the peripheral iris away from the TM, which opens the angle and prevents appositional closure. It may, however, make the angle narrower and potentially induce angle closure by causing the lens–iris diaphragm to move anteriorly with contraction of the ciliary muscle, which relaxes zonular tension and makes the pupillary block worse. If pilocarpine is used in such a patient, repeat gonioscopy should be performed 30 to 60 minutes after the

initial drop. If the angle is not any wider, some would argue that a laser PI should be performed right away. If this is not feasible, consider adding a β-blocker to decrease aqueous secretion until the PI is performed.

•Topical inhibitors of aqueous secretion: β-Blockers, carbonic anhydrase inhibitors (CAIs), and α2-adrenergic agonists.

•Uveoscleral outflow enhancers: The prostaglandin analogs, as well as the α2-agonist brimonidine, increase uveoscleral outflow. Their use in angle closure has not been studied as extensively as some of the other agents, but they can also help lower the IOP. There is some theoretical concern that prostaglandin analogs could increase ocular inflammation. It should be remembered that miotics cause ciliary muscle contraction and decrease uveoscleral outflow.

•Carbonic anhydrase inhibitors: In patients who are not nauseated, an oral CAI is administered. If intravenous (IV) medications are available and the patient is unable to tolerate oral medications, IV acetazolamide is preferred as an adjunct to topical therapy because of its faster onset of action.

•Hyperosmotic agents: Hyperosmotic therapy reduces vitreous volume and can be a very powerful weapon in lowering IOP and breaking an attack. Glycerin and isosorbide can be given orally. Intravenous mannitol is the most potent agent for lowering IOP, but it also increases blood volume and should be used with caution, especially in patients with systemic medical issues such as congestive heart failure or kidney failure.

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CHAPTER 16  ANGLE-CLOSURE GLAUCOMA  161

Angle 10°

A

Extremely narrow angle

B

Figure 16-4.  Mechanism of relative pupillary block closure. A, Extremely narrow angle with resistance to aqueous flow between the iris and the lens, leading to increased posterior chamber pressure. B, Closed angle.

•Topical steroids: Topical steroids (e.g., prednisolone 1% q.i.d.) are a useful adjunct to control the usually concurrent intraocular inflammation that may or may not be clinically apparent.

•Miotics: Pilocarpine helps to break the attack by pulling the peripheral iris away from the TM and increasing trabecular outflow. However, the pupillary sphincter (but not the ciliary muscle) usually becomes ischemic at IOPs above 40 to 50 mm Hg and therefore unresponsive to miotics until the IOP is lowered with other medications. The duration of IOP elevation and sphincter ischemia ultimately determines whether the sphincter will respond to miotics even after the IOP is lowered. The usual concentration used is 1% or 2%. Pilocarpine should be used with caution to avoid cholinergic toxicity. Also keep in mind that it may make some cases of angle closure worse, as noted above. Some believe it should not be used in aphakic or pseudophakic pupillary block.

•Topical glycerin: Topical glycerin can be quite helpful to clear the cornea, which facilitates detailed examination of the eye and also laser treatment.

•Others: The α2-agonist brimonidine increases uveoscleral outflow, as do the prostaglandin analogs.

KEY POINTS: BASIC TREATMENT OF ACUTE PRIMARY ANGLE CLOSURE

1. “Kitchen sink” approach of maximal medical topical therapy plus oral acetazolamide if patient not nauseated.

2. Oral hyperosmotics if above not effective and patient not nauseated, otherwise IV mannitol.

3.Laser peripheral iridotomy.

22.How would you treat the involved eye with laser?

Laser PI is the definitive procedure of choice to relieve pupillary block (Fig. 16-5). Angle closure from any etiology other than pupillary block will not respond to iridotomy. The argon or Q-switched YAG

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Table 16-3.  Treatment of Angle-Closure Glaucoma*

Continued on following page

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Table 16-3.  Treatment of Angle-Closure Glaucoma* (Continued)

Note: All topical medications apply to the affected eye. No therapy in the form of drops is to be used in the unaffected eye unless that eye also has glaucoma or other ocular problems. Specifically, pilocarpine is not to be used in the unaffected eye.

*Glaucoma Service, Wills Eye Hospital/Jefferson Medical College.

Figure 16-5.  Patent laser peripheral iridotomy.

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lasers are used. The Nd:YAG laser is preferred because it is faster, is easier, requires fewer bursts with less energy (causes less inflammation), is not dependent on iris color, and is less likely to cause complications such as posterior synechiae. The argon laser’s thermal effect can help prevent bleeding and facilitate penetration of thick irides.

There is also some difference of opinion regarding the timing of the laser peripheral iridotomy in acute angle closure. If the IOP cannot be reasonably controlled medically, then the PI must be performed immediately. If the pressure can be reasonably controlled medically, it may be better to defer the iridotomy for a few days for the following reasons:

•Corneal edema, from high pressure, and Descemet’s folds, from the abrupt lowering of pressure, can both make visualization and performing the iridotomy more difficult. In addition, because the anterior chamber is usually shallow, the corneal endothelium is closer to the point of laser energy focus and is more likely to be damaged from the concussion.

•The iris is usually somewhat congested, edematous, and inflamed during an attack. This can make the iridotomy more difficult to perform. More power may be required to successfully penetrate the iris, and this can be more uncomfortable for the patient than when the eye is not inflamed.

23.What are the most common complications of laser peripheral iridotomy?

The most troublesome problem is a ghost image resulting from light that has entered through the PI.

•Argon: Posterior synechiae and localized cataracts. Argon laser PIs are more likely to close than are Nd:YAG PIs.

•Nd:YAG: A hemorrhage may occur in up to 50% of eyes. It is usually small and localized to the area of the PI, but sometimes can form a significant hyphema. The bleeding may be controlled by applying gentle pressure on the eye with the contact lens. Even relatively large hyphemas are almost always gone the next day.

Transient IOP spikes of more than 6 mm Hg do occur in up to 40% of patients, most often within the first 1 to 2 hours. Perioperative treatment with apraclonidine decreases the incidence and severity of postlaser IOP spikes. β-Blockers and CAIs have been used, but with less success. The incidence and severity of postoperative IOP elevation are similar with argon and Nd:YAG lasers.

24.What if a peripheral iridotomy is unsuccessful? What other options are available for acute primary angle closure?

I. Other laser treatments for APAC

A.Laser iridoplasty: Using a goniolens, spots of argon or diode laser aimed at the peripheral iris pull the iris away from the angle.

B.Cyclophotocoagulation (CPC): mild cyclophotocoagulation using diode laser can abort cases of APAC refractory to medical and laser treatments (iridotomy and iridoplasty). It is not considered the first-line treatment for APAC but can be successful at aborting an episode of APAC when all options have failed before proceeding to surgery.

In most cases of APAC, the IOP can be brought down successfully with medical treatment (usually requiring systemic medication) and laser treatment; surgery is rarely indicated in resolving IOP in the acute phase of APAC. It is not infrequent, however, that after a crisis of APAC, the IOP is elevated chronically (i.e., APAC progresses into PAC/PACG). Studies from recent years have demonstrated the benefit of removing the lens in the treatment of APAC, PAC, and PACG even when there is an absence of significant cataract.

II.Surgical options for APAC

A.Clear corneal peripheral iridectomy: This procedure was the treatment of choice for angleclosure glaucoma (acute or chronic) prior to the introduction of laser iridotomy. It is rarely performed today. However, if laser is not available or unable to be performed successfully, surgical iridectomy can be an option.

B.Early cataract extraction for APAC: recent studies demonstrated the benefit of lens extraction in patients with APAC, PAC, and PACG. Unlike in POAG, the IOP-lowering effect of cataract extraction alone is significant in all primary angle closure cases (APAC, PAC, or PACG).

C.Cataract extraction combined with goniosynechialysis: Mechanical pulling of PAS from the angle is performed at the end of cataract extraction surgery using a goniolens and a forceps of the surgeon’s choice. The goal is to relieve the blockage of the trabecular meshwork from PAS and restore the outflow of aqueous humor. Some studies suggest that goniosynechialysis is more effective when the PAS are recent.

D.Cataract extraction combined with endocyclophotocoagulation (ECP): Laser treatment of the ciliary body is performed at the time of cataract extraction using an endoscope equipped with

CHAPTER 16  ANGLE-CLOSURE GLAUCOMA  165

a diode laser. Similar to CPC (which refers to external laser application on the ciliary body), ECP coagulates the ciliary body and reduces IOP. In addition, laser application shrinks the ciliary body and opens the angle further, sometimes referred to as endocycloplasty. Currently, there

is no evidence that cataract extraction combined with ECP or goniosynechialysis is superior to cataract extraction alone in the treatment of angle-closure diseases.

E.Trabeculectomy or tube shunts: Close to half the cases of APAC will progress into chronic PAC or PACG. In cases in which the IOP is consistently elevated despite laser iridotomy and medical treatment, lens extraction should be performed prior to filtering or tube shunt surgery, as the former carries fewer long-term complications and is often effective in reducing IOP. In advanced cases of PACG requiring very low IOP, combined lens extraction and filtering or tube surgery may be the best option.

When operating on these eyes, it is important to remember that they already have shallow chambers and are more likely to develop flat chambers and aqueous misdirection (malignant or ciliary block glaucoma). The use of miotics can also increase the chances of aqueous misdirection.

25.When can you consider an attack to be completely “broken”?

An attack can be considered “broken” when the intraocular pressure in the involved eye is lowered significantly and the patient’s symptoms are resolved. However, many of these eyes will have chronically elevated IOP and require further medical and surgical treatment over the long term.

26.What are the chances of the same thing happening to the fellow eye?

There is a 40 to 80% chance of an acute attack in the fellow eye over the next 5 to 10 years.

27.What would you recommend for the fellow eye?

Prophylactic laser PI would be recommended, if a gonioscopic evaluation reveals a potentially occludable angle. It may be appropriate to treat the fellow eye first (if the angle is occludable), while waiting for the involved eye to quiet down and for the cornea to clear. The use of pilocarpine in the fellow eye to try to prevent angle closure by pulling the peripheral iris away from the TM until PI is performed is not without risk, as discussed in question 21.

28.Describe the shortand long-term sequelae to the various structures of the eye after an acute angle-closure attack

•Cornea: Shortly after the IOP is lowered, the epithelial microcystic edema will resolve, and Descemet’s folds may be seen from the acute reduction in IOP (Fig. 16-6). The stromal edema takes longer to resolve. In most cases, significant endothelial damage occurs. If the attack has caused enough endothelial injury, epithelial and stromal edema may persist. Endothelial pigment may result from the pigment released during iridotomy or from any ischemic atrophic regions of the iris.

•Anterior chamber: Even after successful PI, the AC is usually still shallower than normal. Cataract extraction is the definitive treatment to deepen the anterior chamber.

•Iris: One may see a middilated, nonreactive, or sluggish pupil and sector atrophy and stromal necrosis from ischemia. Posterior synechiae may eventually develop long after a PI is performed owing to the alternate route available for aqueous humor flow. The pupil is often vertically oval.

•Lens: Glaukomflecken are small whitish anterior subcapsular opacities representing areas of necrotic lens epithelium with adjacent subcapsular cortical degeneration (see Fig. 16-6). Cataracts

Figure 16-6.  Photograph of an eye after resolution of an acute angle-closure attack. Note the corneal Descemet’s folds, the PI at twelve o’clock at the upper edge of the photograph, and the lacy pattern of glaukomflecken under the anterior lens capsule.

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