Care of the patient with primary angle closure glaucoma (clinical practice guideline 5)

OPTOMETRIC CLINICAL
PRACTICE GUIDELINE
OPTOMETRY:
THE PRIMARY EYE CARE PROFESSION
Doctors of optometry are independent primary health care providers who examine, diagnose, treat, and manage diseases and disorders of the visual system, the eye, and associated structures as well as diagnose related systemic conditions. Optometrists provide more than two-thirds of the primary eye care services in the United States. They are more widely distributed geographically than other eye care providers and are readily accessible for the delivery of eye and vision care services. There are approximately 32,000 full-time equivalent doctors of optometry currently in practice in the United States. Optometrists practice in more than 7,000 communities across the United States, serving as the sole primary eye care provider in Primary Angle
more than 4,300 communities. The mission of the profession of optometry is to fulfill the vision and eye Closure Glaucoma
care needs of the public through clinical care, research, and education, all of which enhance the quality of life. OPTOMETRIC CLINICAL PRACTICE GUIDELINE
CARE OF THE PATIENT WITH
PRIMARY ANGLE CLOSURE GLAUCOMA
Reference Guide for Clinicians
Prepared by the American Optometric Association Consensus Panel on Care of the Patient with Primary Angle Closure Glaucoma: Jimmy Jackson, O.D., M.S., Principal Author Reviewed by the AOA Clinical Guidelines Coordinating Committee: NOTE: Clinicians should not rely on the Clinical Guideline alone for patient care and management. Refer to the listed references and other sources for a more detailed analysis and discussion of research and patient care information. The information in the Guideline is current as of the date of publication. It will be reviewed periodically Approved by the AOA Board of Trustees June 23, 1994; Revised October, 1998; Reviewed 2001 American Optometric Association, 1994 243 N. Lindbergh Blvd., St. Louis, MO 63141-7881 Primary Angle Closure Glaucoma iii TABLE OF CONTENTS

INTRODUCTION. 1

I.
STATEMENT OF THE PROBLEM. 3
A.
Description and Classification of Primary Angle Closure Glaucoma . 3 Epidemiology of Primary Angle Closure Glaucoma . 6 Clinical Background of Primary Angle Closure Glaucoma . 8 Common Signs, Symptoms, and Complications. 9 PROCESS . 13
Management of Acute Primary Angle Closure Glaucoma. 18 iv Primary Angle Closure Glaucoma Management of Patients with Severe, Irreversible Vision INTRODUCTION
Optometrists, through their clinical education, training, experience, and CONCLUSION . 29
broad geographic distribution, have the means to provide effective primary eye and vision care for a significant portion of the American III. REFERENCES . 30
public and are often the first health care practitioners to examine a
IV. APPENDIX . 43
patient with, or at risk for developing, primary angle closure glaucoma Optometric Management of the Patient with Acute Primary Frequency and Composition of Evaluation and This Optometric Clinical Practice Guideline for the Care of the Patient with Primary Angle Closure Glaucoma describes appropriate ICD-9-CM Classification of Angle Closure Glaucoma . 46 examination and treatment procedures to reduce the risk of visual Abbreviations of Commonly Used Terms . 47 disability from primary ACG. It contains recommendations for timely diagnosis, treatment, and when necessary, referral for consultation with or treatment by another health care provider. This Guideline will assist optometrists in achieving the following goals: • Identify patients in whom primary ACG is present or who are at risk • Accurately diagnose primary ACG • Manage a patient who has an acute attack of primary ACG • Monitor and manage, as indicated, patients with intermittent or • Develop criteria for referral to the patient's primary care physician or other health care practitioner when management options dictate • Improve the quality of care rendered to patients with primary ACG • Minimize the adverse effects of primary ACG and its management • Inform and educate patients and other health care practitioners about the visual complications of primary ACG and the availability of treatment. STATEMENT OF THE PROBLEM

Primary angle closure glaucoma is a relatively uncommon condition in
the United States, accounting for less than 10 percent of all diagnosed
cases of glaucoma.1-3 However, its importance as a health care issue is
far greater than the relatively small number of cases would suggest. In
contrast to open angle glaucoma, in which vision loss is slow and
gradual, an acute attack of angle closure glaucoma can lead to blindness
within hours or days. Prompt diagnosis and correct treatment are,
therefore, critical. Accurate and timely diagnosis of the intermittent and
chronic forms of primary ACG is also important because prophylactic
treatment (peripheral iridotomy) can protect the eye against acute
episodes and prevent damage from repeated intermittent attacks or
chronic angle closure.
A.
Description and Classification of Primary Angle Closure
Glaucoma
Glaucoma represents not one single clinical entity but a group of ocular diseases with various causes that ultimately are associated with progressive optic neuropathy leading to loss of vision. The glaucomas can be separated by etiology: those not related to another underlying condition, which are classified as primary, and those that are secondary to ocular or systemic disease. The glaucomas are generally classified as angle closure, open angle, mixed or combined mechanism, and developmental. In primary angle closure glaucoma intraocular pressure becomes elevated because the peripheral iris prevents aqueous from reaching the anterior chamber drainage tissue, the trabecular meshwork. The meshwork itself is presumed to function normally. In open angle glaucoma (OAG) aqueous has ready access to the trabecular meshwork, but drainage is impaired due to other mechanisms. Mixed mechanism glaucoma exists when both forms of glaucoma are present, a combination of ACG and OAG. Developmental glaucoma is caused by some anomaly of the anterior chamber that is present at birth and is associated with other ocular or systemic anomalies.4,5 4 Primary Angle Closure Glaucoma Angle Closure Glaucoma with Pupillary Block
The scope of this Guideline includes the diagnosis, treatment, and management of primary angle closure glaucoma. See Appendix Figure 3 The classification of angle closure glaucoma is based upon the presence for ICD-9-CM classification of primary angle closure glaucoma. or absence of pupillary block and whether the angle closure mechanism _________________________________________________________ is primary or secondary (Table 1). With pupillary block, the normal flow of aqueous through the pupil from the posterior chamber to the anterior chamber is restricted. This block leads to increased pressure in the posterior chamber which pushes the peripheral iris forward (iris bombe) Classification of Angle Closure Glaucomas *
until it blocks the trabecular meshwork. Angle closure glaucoma with pupillary block
Primary ACG with pupillary block exists when there is a predisposing Primary angle closure with pupillary block anatomical basis, such as a narrow angle. Primary ACG may be further classified as suspect, subacute (intermittent angle closure with spontaneous resolution), acute (sudden blockage of the outflow of aqueous by the iris), or chronic (occlusion of the angle caused by the development of peripheral anterior synechiae or apposition of the iris). Secondary angle closure with pupillary block Secondary ACG with pupillary block is associated with some other Posterior synechiae to lens, vitreous, or IOL primary disease process, such as anterior chamber inflammation. Angle Closure Glaucoma without Pupillary Block
Primary ACG without pupillary block, or plateau iris, occurs in two distinct forms. Plateau iris configuration is a clinical entity in which the central anterior chamber depth is normal, the iris plane is flat, and the Angle closure glaucoma without pupillary block
anterior chamber angle is extremely narrow. Gonioscopy, which is Primary angle closure without pupillary block required to make the diagnosis, reveals that the peripheral iris takes a sharp turn posteriorly before inserting into the ciliary body. Plateau iris syndrome occurs when the anterior chamber remains capable of closure in the presence of a patent iridotomy.6,7 Secondary angle closure without pupillary block Secondary ACG without pupillary block can be classified as either an anterior pulling mechanism or a posterior pushing mechanism. In the anterior form (e.g., neovascular glaucoma) the peripheral iris is "pulled" against the meshwork by the contraction of fibrovascular membranes on the iris and in the angle. Posterior pushing mechanisms (e.g., malignant glaucoma and related conditions such as choroidal detachment) "push" (Malignant glaucomas and related causes) the peripheral iris against the meshwork.5,8 These conditions are invariably unilateral with little risk to the fellow eye. 6 Primary Angle Closure Glaucoma Some Mongoloid populations, such as Eskimos,21-25 East and Southeast Asians,26-29 and Southern Asians,30-32 have a very high rate of primary ACG. On the other hand, Pacific Islanders, while of similar ancestry, have a very low rate of primary ACG,33,34 and Australian aborigines, whose ancestry is Southeast Asian, have no reported primary ACG.35 South American Amazon Indians have a higher prevalence of primary ACG than American Indians (in whom it is virtually nonexistent), although they have similar Asian ancestry.36,37 The dissimilar rates of primary ACG among groups of similar ancestry make it apparent that no clear genetic pattern exists. Nevertheless, _________________________________________________________ numerous studies have shown that certain racial groups are at increased risk for primary ACG, as are those with small, crowded anterior Epidemiology of Primary Angle Closure Glaucoma
segments. The tendency toward shallower anterior chamber depths in individuals with primary ACG has been reported consistently among Prevalence and Incidence
Caucasians,38-40 Eskimos,21 and Asians.41,42 Asians also have a greater tendency toward plateau iris,26,43 which would increase the rate of Primary ACG accounts for less than 10 percent of all diagnosed cases of primary ACG. Other factors associated with the high prevalence of glaucoma in the United States. 1-3 An estimated 2-8 percent of the U.S. primary ACG in Asia are intumescent cataract in India32 and trachoma in population have anterior chamber angles narrow enough to close. Of those cases, 5 percent will actually progress to primary ACG.1-3 In other populations, primary ACG occurs more frequently and may exceed the b. Family
History
incidence of primary OAG. The prevalence of primary ACG within a particular population depends on a number of variables, including race, A positive family history of primary ACG is an additional risk factor. family history, age, gender, and refractive error. The frequency of occludable angles is 3.5-6 times higher in first-degree relatives of patients with primary ACG.26,45-49 The inheritance pattern of primary ACG is believed to be polygenic,50-53 although pedigrees with a high prevalence of primary ACG have been reported with both a. Race
autosomal dominant and recessive inheritance patterns.26,45,54 The configuration of the anterior chamber may be inherited under polygenic In Caucasian populations, the prevalence of primary ACG is one-twelfth influence. This, rather than a specific gene linked to the disease, may to one-sixth that of primary OAG.5,9-13 Primary ACG is thought to be explain the familial occurrence of primary ACG.39,55 However, most exceedingly rare among African Americans14-18 and when it does occur cases of primary ACG occur in patients with no known family history of in these individuals, it is usually as the chronic form of the disease.14,18-20 In addition, African Americans tend to have fewer symptoms than Caucasians during acute primary ACG attacks, which may lead to under 8 Primary Angle Closure Glaucoma c. Age
leading to an increase in intraocular pressure (IOP) within the posterior chamber. Eventually, if sufficient force is generated on the posterior The prevalence of primary ACG increases with age, with a peak surface of the iris, it is displaced forward. Especially when the frequency in the sixth and seventh decades of life.11,13,23,25,56,57 ACG is peripheral iris is lax and distensible as a result of pupillary dilation, it considered rare below age 40,26,39 although cases involving children have may balloon forward (iris bombe) and occlude the trabecular meshwork. been reported.58 Age-related factors that contribute to primary ACG Aqueous production continues, resulting in rapid, marked elevation in include increasing lens thickness, increasing anterior lens surface curvature, slight anterior displacement of the lens, and pupillary Only certain eyes have small enough anterior chambers and narrow enough angles for primary angle closure. Such susceptible eyes may d. Gender
undergo spontaneous pupillary block. More commonly, pupillary block is precipitated by a triggering mechanism such as pupillary dilation. In Women are considered more susceptible than men to primary ACG; at-risk individuals dilation, with resultant pupillary block, may occur reported female:male ratios vary from 2:1 to 4:1.13,19,21,26,64,65 In the naturally following emotional upset or in dim illumination as in a African American population, however, some studies have found the restaurant or theater. It may also be induced pharmacologically by a rates of primary ACG to be equal,14 although this finding is disputed.19 variety of systemic and topical medications. An explanation for gender-based differences is that women generally have shallower anterior chamber depths and narrower angles.26,64,65 During dilation the greatest iris-to-lens contact occurs when the pupil is in the mid-dilated state (3.5-4.0 mm).67,70 In contrast, when the pupil is e. Refractive
Error
widely dilated, there is little or no contact between the lens and the iris, therefore minimum pupillary block.59 The "high-risk" mid-dilation state Numerous studies have reported that narrow angles and primary ACG occurs after the pupil has reached maximal dilation and is returning to its occur more frequently in hyperopic eyes than in emmetropic or myopic normal size. With pharmacologic dilation this typically occurs from one eyes.1,61,64,66 Hyperopic eyes are generally smaller in globe volume, to several hours after administration of the dilating agent depending upon which results in a crowding of the anterior chamber when the lens size is Common Signs, Symptoms, and Complications
Clinical Background of Primary Angle Closure Glaucoma
The signs and symptoms of primary ACG vary with the nature of the 1. Natural
condition. Persons at risk for primary ACG are generally free of symptoms. A narrow anterior chamber angle is evident when viewed Most cases of primary ACG involve some form of pupillary block and with a gonioscopic lens in patients at risk for a future primary ACG occur primarily in eyes with narrow angles.1,59,60,67-69 There is always a small amount of relative pupillary block in phakic individuals because the iris rests against the anterior surface of the lens. This relative a. Subacute
ACG
pupillary block is usually of little importance; however, some circumstances can increase the force of contact between the iris and the In the subacute stage of primary ACG patients undergo incomplete angle lens. This contact increases resistance to aqueous flow through the pupil, closure that resolves spontaneously. Symptoms vary widely on the basis 10 Primary Angle Closure Glaucoma of IOP, the patient's pain threshold and level of awareness, and perhaps d.
Plateau Iris Configuration
race. Subacute attacks tend to increase over time and the patient may progress to chronic primary ACG or have an acute angle closure attack. Patients with plateau iris configuration typically have no symptoms until they develop an acute or subacute attack of primary ACG. The diagnosis b. Acute
ACG
of plateau iris requires biomicroscopic evaluation and gonioscopy which reveals a flat central iris and that the peripheral iris takes a sharp turn An acute angle closure attack is a true ophthalmic emergency and posteriorly before inserting into the ciliary body. In most cases appropriate therapy must be instituted immediately to prevent vision loss. peripheral iridotomy can cure the patient with plateau iris syndrome by The diagnosis of acute angle closure glaucoma is not difficult; the signs preventing future attacks of primary ACG, suggesting that pupillary and symptoms are fairly classic. An acute attack is almost always block plays a considerable role in the development of acute glaucoma in unilateral with the population most at risk consisting of elderly, these patients.56,71 However, others maintain that pupillary block hyperopic individuals.12,26 Typical signs and symptoms are: contributes little to IOP rise and that peripheral iridotomy is of no benefit.7 Despite a patent iridotomy, plateau iris syndrome patients remain at risk for primary ACG. Treatment of this condition includes the use of miotic agents and peripheral gonioplasty.71 Failure to diagnose and appropriately manage an attack of acute angle closure can result in permanent optic nerve damage and vision loss. Repeated episodes of subacute or chronic primary ACG that are not properly diagnosed and managed can produce PAS and permanent Early Detection and Prevention
In acute ACG, the development and progression of symptoms are typically rapid. The level of pain seems to be related more to the rapid Evaluation of the anterior chamber angle depth performed as part of a rise in pressure than to the absolute level of the IOP increase. Because comprehensive eye and vision examination serves to prevent inadvertent African Americans seem to experience less pain during an acute primary pupillary dilation in a patient at risk for angle closure and identifies those ACG attack, a relative lack of pain should not deter the clinician from a patients in need of further management. There are three main methods c. Chronic
ACG
• The penlight shadow test is a screening method for assessing anterior chamber depth and iris convexity.73,74 The result is an estimation of Chronic primary ACG is defined as permanent closure of parts of the anterior chamber angle by peripheral anterior synechiae (PAS). Closure of the entire angle may progress slowly. Symptoms may be mild or absent until very late in the disease. The diagnosis of chronic ACG may The van Herick angle estimation technique is an excellent screening therefore be made only on the basis of optic nerve and visual field procedure for assessing anterior chamber depth prior to dilation. changes and gonioscopic evidence of a narrow angle. This technique may be a part of the biomicroscopic evaluation.75 12 Primary Angle Closure Glaucoma • Gonioscopy is the definitive test for determining anterior chamber depth. It allows the clinician actual visualization of angle structures and permits the detection of anomalies such as angle recession, This Guideline describes the optometric care provided a patient with plateau iris, PAS, and neovascularization. primary angle closure glaucoma. The components of patient care described are not intended to be all inclusive. Professional judgement
and individual patient symptoms and findings may have significant
impact on the nature, extent, and course of the services provided. Some
components of care may be delegated.
A.
Diagnosis of Primary Angle Closure Glaucoma

Evaluation of a patient for ACG should begin with the assumption that
any of the four types of primary ACG could be present. Although the
identification of acute primary ACG rarely constitutes a diagnostic
dilemma, other types of ACG may escape detection if a thorough
evaluation is not done.
1. Patient

A thorough patient history is needed for diagnosis. Particular attention
should be paid to eliciting symptoms suggestive of prior angle closure
attacks. These symptoms include blurred vision, transient loss of vision,
colored halos around lights, headaches, mild to severe ocular pain,
photophobia, and congestion of the eye.6 These "attacks" are often
relieved by sleep, exposure to bright light, or induced miosis. It is also
important to determine whether there is a family history of primary
ACG.

2. Ocular
Examination

The evaluation of a primary ACG suspect may include, but is not limited
to, the following procedures:
• Refraction (unless the patient is in acute angle closure)
• Biomicroscopic evaluation of the anterior segment
• Stereoscopic evaluation of the optic nerve 14 Primary Angle Closure Glaucoma • Baseline photographs of the optic nerve photos may be taken (stereophotography, if available). A detailed description and drawing is an appropriate alternative if photography is not available or feasible. Baseline central visual fields utilizing threshold The optometrist should look for signs of prior angle closure attacks: peripheral anterior synechiae, posterior synechiae, glaukomflecken (anterior subcapsular lens opacities), iris atrophy, pigment anterior to Schwalbe's line, and possibly glaucomatous optic nerve and visual field Anterior Chamber Angle Grading Systems
changes. With intermittent attacks the optic nerve may appear more pale than cupped. Close examination of the depth of the anterior chamber van Herick
Becker-Shaffer Angle
Pigmentation
angle and central anterior chamber is needed. The van Herick angle estimation technique1 is commonly used to screen for the depth of the anterior chamber angle prior to dilation. The width of the black space formed by the anterior chamber angle interval is subjectively compared to the width of the corneal optic section. Angles are graded 1 to 4. Grades 3 and 4 are thought to be incapable of closure, while grades 1 or 2 should have gonioscopy performed before dilation (Table 2).1,73,76 Estimation of the anterior chamber axial depth may also be helpful because central chamber depth of less than 2.5 cm is the threshold for pupillary block primary ACG.64 When the angle appears The two methods of gonioscopy are direct and indirect. In the more commonly used indirect method, a mirrored goniolens and biomicroscope enable examination of the anterior chamber angle opposite the direction of view. Many indirect gonioscopy lenses are available and each requires a slightly different technique. Among the multiple methods of grading the anterior chamber angle via gonioscopy, the Becker-Shaffer system is most widely used (Table 2). The amount of ------ No
pigment in the angle is an important finding that is also usually graded _________________________________________________________ (Table 2). To describe the angle fully, the examiner should note other gonioscopic findings such as PAS, angle recession, and In chronic primary ACG, there is closure of only part of the angle. The patient may have an IOP that is normal or just slightly elevated at the time of examination. Such patients tend to develop optic nerve head and It is important to ascertain the type and amount of refractive error visual field changes identical to those of patients with primary OAG. because hyperopia is a definite risk factor for primary ACG. The The appropriate diagnostic procedure includes careful gonioscopy to examination should include measurement of intraocular pressure and reveal evidence of PAS in those patients who have primary ACG. stereoscopic evaluation of the optic nerve head. Baseline optic nerve 16 Primary Angle Closure Glaucoma 3. Provocative
iridotomy is recommended when the angle is narrow, the chamber is shallow, and any one of the following exists:6,79 Provocative testing to mirror "physiologic" conditions that induce dilation may help to determine which primary ACG suspects are at high risk for progression to an acute attack. These "high-risk" patients may benefit from a prophylactic iridotomy. The most commonly used • Symptoms associated with past closure • Positive provocative test with evidence of angle closure. • Dark room test. The patient is placed in a dark room for 60-90 4. Assessment
Diagnosis
minutes after measurement of baseline IOP and gonioscopy. Though problematic, it is important not to allow the patient to fall asleep The examination of the patient with ACG classically reveals because the miosis of sleep counteracts the mydriasis of dim circumlimbal injection, a mid-dilated nonreactive pupil, corneal edema, illumination. At the end of the prescribed time, the IOP is anterior chamber inflammation, and an IOP in the range of 40-90 mm remeasured. The examiner must be careful not to expose the patient Hg. It is crucial to determine whether the patient has primary acute ACG to bright light, which would constrict the pupil. A rise in IOP that with pupillary block rather than one of the secondary ACGs or some equals or exceeds 8 mm mercury (Hg) is a positive finding. other cause of acute rise in IOP. Conditions to be considered in the Gonioscopy should be repeated to confirm angle closure. • Prone test. The patient is placed in the prone position for 60-90 • Open angle glaucoma with unusually high IOP minutes and is instructed to remain awake and to avoid direct pressure on the globe or orbit. Criteria for determining a positive test Prone dark room test. The patient is placed in a dark room in the prone position for 60-90 minutes. Instructions to the patient and • Iridocorneal endothelial syndrome (ICE). criteria for a positive test are the same as for the previous two tests. Appropriate management of these conditions differs dramatically from Mydriatic test. After measurement of baseline IOP, the patient's that of acute primary ACG because pupillary block plays little or no role pupils are dilated with a weak cycloplegic agent such as 0.5% or 1% in their development. Gonioscopy and biomicroscopic evaluation are tropicamide. When IOP is remeasured 60-90 minutes later, a rise of crucial in diagnosing the etiology of a rise in IOP. If the cornea is edematous, the use of topical glycerin may temporarily clear it enough to permit an adequate view. Alternatively, gonioscopy and biomicroscopic Unfortunately, none of these provocative tests has demonstrated evaluation of the fellow eye may prove helpful in that anterior chamber adequate specificity and sensitivity in clinical trials. There is no anatomy is usually similar for both eyes. A review of the patient's consensus among glaucoma specialists regarding the use of provocative medical history is needed for management. Particular emphasis should testing. Most clinicians rely on gonioscopy and clinical judgement to be directed toward the patient's cardiac, renal, and pulmonary status to determine which patients can benefit from iridotomy. Prophylactic rule out contraindications to the medical treatment of primary ACG. 18 Primary Angle Closure Glaucoma Management of Acute Primary Angle Closure Glaucoma
• Miotics. Pilocarpine firms the peripheral iris and pulls it away from
the trabecular meshwork. Concentrations stronger than 2% are The extent to which an optometrist can provide treatment for angle generally not used because they may produce ciliary body closure glaucoma may vary depending on the state's scope of practice thickening, excess miosis, and vascular congestion, which can cause laws and regulations and the individual optometrist's certification. Care the anterior chamber to become shallow, increase pupillary block, of the patient with primary ACG may require referral for consultation and aggravate rather than relieve primary ACG.59,80 with or treatment by the patient's primary care physician or an ophthalmologist for services outside the optometrist's scope of practice. There is some controversy as to when pilocarpine should be The optometrist may participate in the comanagement of the patient, administered. When the IOP is above 40-50 mm Hg, the pupillary including preoperative and postoperative care when appropriate. sphincter muscle is ischemic and unresponsive to topical miotic agents.81-83 Once IOP has been reduced, normal blood flow returns Basis for Treatment
to the iris sphincter and it becomes responsive to pilocarpine.83 Some clinicians recommend that pilocarpine not be administered The treatment of acute primary ACG with pupillary block is directed until the pressure has been reduced to approximately 40 mm Hg.73,81,84 However, most experts still recommend giving pilocarpine at the first diagnosis of acute primary ACG to ensure its availability • Rapid breaking of the attack using medical therapy, laser therapy, or when sphincter muscle receptors regain function.59,68,77,85,86 The recommended dosage of pilocarpine is one drop of 2% solution • Performance of laser peripheral iridotomy or surgical iridectomy every 15-60 minutes up to a total of two to four doses.57,86 Care (usually after the attack has been broken medically) should be taken to avoid over treatment which may produce a • Evaluation for treatment of the fellow eye. cholinergic crisis (nausea, vomiting, diarrhea, sweating, bradycardia, and hypotension), especially in elderly patients.57 A predisposed 2. Available
Treatment
fellow eye should be maintained on pilocarpine, 2%, four times daily until laser peripheral iridotomy (LPI) is performed.59,87 a. Medical
(Pharmaceutical)
• Beta blockers. If the patient has no pulmonary or cardiac
Pharmaceuticals* used in the management of an acute primary angle contraindications, any of the nonselective beta blockers may be used, closure attack include topical, oral, and intravenous agents. Topical with Timolol, 0.5% (Timoptic) probably the most commonly agents include miotics (pilocarpine), beta- adrenergic blockers, an alpha- utilized. Betaxolol, 0.25% (Betoptic S) should be used for patients adrenergic agonist (apraclonidine), and steroids. Oral agents that may be with pulmonary contraindications. The recommended dose of any used are carbonic anhydrase inhibitors (CAIs) and hyperosmotics. beta blocker is one drop initially, repeated in 1 hour if necessary, and Hyperosmotics and CAIs may also be administered intravenously. continued as one drop every 12 hours until LPI is performed.69
• Alpha-adrenergic agonists. Approved for use in anterior segment
laser procedures to prevent IOP spikes, Apraclonidine 1% (Iopidine) * Every effort has been made to ensure the drug dosage recommendations are accurate at is an adjunct therapy in angle closure.77,88,89 It is an alpha-adrenergic the time of publication of this Guideline. However, as treatment recommendations agonist that lowers IOP by decreasing aqueous production. The change due to continuing research and clinical experience, clinicians should verify drug dosage schedules with product information sheets. 20 Primary Angle Closure Glaucoma usual dose, one to two drops in the affected eye at the time of These agents are best tolerated if given chilled (serve over crushed diagnosis, may be repeated once in 1 hour if necessary. ice), with the entire dose consumed in 5 minutes.69 Caution should be used when administering hyperosmotic agents in patients Dapiprazole hydrochloride 0.5% (Rev-Eyes) is an alpha-adrenergic susceptible to dehydration. Older patients, who may be particularly blocking agent used to reverse pharmacologically induced vulnerable, may suffer disorientation, confusion, diarrhea, or mydriasis. There is no benefit from adding dapiprazole to the seizures. Hyperosmotic drugs place stress upon the cardiovascular therapeutic regimen in cases of acute angle closure, but it is system because of the increased load created by higher fluid volumes recommended to reverse mydriasis in ACG suspects whose pupils within the vessels. As fluid is drawn from the tissues, intravascular are dilated.90 Dapiprazole is superior to pilocarpine for reversal of fluid volume increases. This additional stress on an elderly dilation because dapiprazole does not increase pupillary block or individual with a decompensating heart or kidney disease could be cause shallowing of the anterior chamber.90-92 fatal.77 When the patient is nauseated, an intravenous hyperosmotic agent such as urea or mannitol should be used. Most authorities • Topical Steroids. Although topical steroids are not efficacious
consider mannitol the drug of choice; the recommended dose is 2.5- during an acute angle closure attack, they are useful in managing 10 ml/kg of a 20% solution.77 Intravenous hyperosmotics should be inflammation once the attack has been broken medically. The usual used with caution due to their systemic complications. Although dose is one drop of 1% prednisolone acetate four times a day until a they are the same as those of the oral hyperosmotics, the systemic • Oral carbonic anhydrase inhibitors. An oral CAI should be given
b. Corneal
Indentation
immediately upon diagnosis when the patient is not nauseated. A 500 mg dose (two 250 mg tablets) of acetazolamide (Diamox) is Corneal indentation is an adjunct procedure in which a cotton-tipped most commonly used. The 500 mg Diamox Sequel should be applicator or gonioscopy lens is used to indent the central cornea.93 avoided because it is a timed-release formulation, and, therefore, it Repeated indentation, each time lasting approximately 30 seconds, has a slower onset of action. Acetazolamide should be avoided in followed by 30 second rest, over 10-15 minutes displaces aqueous patients with kidney problems for whom 100 mg of methazolamide peripherally into the angle and opens the angle mechanically. Although (Neptazane) becomes the CAI treatment of choice. CAIs are sulfa- this procedure may be successful, many patients suffering acute ACG based drugs and should be avoided in allergic patients. When the attacks are already in acute pain and unable to tolerate corneal patient is nauseous, 500 mg of intravenous acetazolamide should be administered. An antiemetic suppository may be used with oral medication to reduce nausea and avert the need for intravenous c. Laser
Treatment
In recent years, the use of lasers has largely replaced surgical iridectomy • Oral hyperosmotic agents. The most effective means of lowering
as the procedure of choice in most cases of ACG.94 IOP during acute angle closure attacks are oral hyperosmotic agents. If the patient is not nauseated or vomiting, 50% glycerin (Osmoglyn) • Laser peripheral iridotomy. Primary ACG, in which pupillary
may be administered in a dose of 1.5 ml/kg body weight. Because it block is the presumed cause, is an indication for LPI.95,96 is not metabolized, 45% isosorbide (Ismotic) can be substituted in Prophylactic LPIs are indicated for all fellow eyes after an acute equal doses for glycerin in patients with diabetes mellitus.59,68,69,77 angle closure attack.87,95-100 Intermittent and chronic pupillary blocks 22 Primary Angle Closure Glaucoma are also considered to be indications for LPI.96,99,100 Patients with produce significant contour changes in the iris because of their heat angle closure due to mechanisms other than pupillary block (such as and coagulative effects. This technique, which can be used to "open" neovascularization, inflammatory synechiae, or swelling of the sections of the angle, may be effective in treating cases of acute ciliary body) are not candidates for LPI.100 angle closure that do not respond to medical management. Such unresponsive cases are not appropriate for LPI due to extreme Corneal edema may preclude LPI in the patient suffering an acute corneal edema which renders precise focusing impossible. angle closure attack. It is generally preferable to manage the patient medically until the cornea clears and then proceed with the LPI. If Gonioplasty uses a larger spot size (300-500 microns vs. 25-50 an attack cannot be broken medically, the use of topical glycerin may microns for LPI), which makes precise focusing less critical. clear the cornea enough to permit LPI. A flat anterior chamber is Although this procedure may be used to break an attack of acute also a contraindication for LPI because it is very difficult to avoid angle closure secondary to pupillary block, it is not a cure. LPI will still be needed when the corneal edema resolves. Most patients are placed on a short course of topical steroids after gonioplasty.101 Complications following LPI are not uncommon; however, they are Complications are uncommon but, when they occur, are similar to not usually sight-threatening.101 A rise in postoperative IOP may those of other anterior segment laser procedures. occur88,98-100, 102-111 but can be minimized by prophylaxis.88,102-104,111 Transient anterior uveitis is very common,106,112 but typically d. Surgery
resolves with topical steroid treatment. Blurred vision occurs frequently after LPI secondary to released pigment, cell and flare, or When the acute ACG attack cannot be broken within 3-6 hours of microhyphema. The resolution of blurred vision is usually rapid initiating treatment, and laser gonioplasty (and perhaps LPI utilizing and spontaneous. Hemorrhaging, which can occur when the glycerin) has been unsuccessful, the patient requires Nd:YAG laser is used for iridotomy, can usually be controlled by surgical iridectomy. Other situations in which surgical iridectomy may the application of slight digital pressure to the globe. There are no reports of serious complications related to the hemorrhaging.98,106- 109,112 Retinal damage is a rare but potentially severe complication • When the laser fails to produce a patent iridotomy of LPI. Use of an iridotomy lens, careful focusing of the laser, and direction of the beam away from the fovea minimize this risk.101 The most common "serious" complication is closure of the • When the patient is uncooperative or has severe nystagmus.59,101 iridotomy. Closure rates following argon LPI's of up to 40 percent have been reported.105,108,110,113 Larger peripheral iridotomies with Some eyes that develop acute primary ACG with pupillary block the argon laser and control of inflammation can minimize closure.101 eventually require filtering surgery for IOP control.114-116 Consequently, Closure is very rare with the Nd:YAG laser,108,110,113 a leading primary filtering surgery is recommended for eyes that have had severe, reason many practitioners choose the Nd:YAG over the argon laser prolonged, or recurrent attacks of angle closure glaucoma in the presence of significant PAS.117-119 Several studies have demonstrated that iridectomy combined with medical treatment provides results equal to • Laser peripheral gonioplasty. Laser peripheral gonioplasty
those obtained by primary filtering surgery, but with fewer (iridoplasty) is a procedure in which the peripheral iris is contracted complications.115,116,120 When only 50 percent or less of the angle is or flattened to pull it away from the angle. Thermal lasers can closed, there is a good chance of controlling IOP with iridectomy. If 24 Primary Angle Closure Glaucoma PAS exceeds 70 percent, the patient may have greater success with a topical beta blocker twice a day in the affected eye. Miosis helps guard trabeculectomy, or with goniosynechialysis followed by gonioplasty. against reclosure; topical steroids reduce the inflammation associated with angle closure; and the beta blocker decreases aqueous production. In general, iridotomy is less likely to succeed when the attack is of long It is customary to wait 2-7 days after breaking the attack before duration, when the eye is congested, or when there is optic nerve damage performing the LPI to allow resolution of the iris congestion and the and visual field loss.6,121 These findings, plus the difficulty of predicting anterior chamber response.59,101 Appendix Figure 1 summarizes the which eyes will ultimately require filtering surgery, have made recommended management of an acute angle closure attack. iridectomy the surgical technique of choice. 4. Patient
Education
Recommended Management Protocol
The optometrist should review signs and symptoms of an acute angle Immediately after the diagnosis of acute primary angle closure, the closure in detail with patients suspected of having ACG and those who patient should receive the following medications, providing no have undergone an iridotomy. Patients should be instructed to seek care immediately if any of these signs or symptoms are noted. Because of the increased risk associated with a positive family history, all first-degree relatives of the patient should be encouraged to have a comprehensive Prognosis and Followup
While attempting to break an angle closure attack, the clinician should Patients with primary ACG should not be considered cured even after check IOP readings every 15-30 minutes. If the attack is not broken 1 successful LPI. Such patients should be considered glaucoma suspects hour after institution of treatment, oral hyperosmotics may be for life and receive appropriate followup care. Elevated pressure in the administered along with repeating all topical medications. When an immediate postiridotomy period can occur secondary to incomplete or attack is unbroken after 2 hours, the patient should have argon (or diode) closed iridotomy, inflammation or extensive PAS, or in response to laser gonioplasty. If the patient is still in angle closure 4-6 hours after steroid therapy. Late-stage IOP rise may be due to trabecular meshwork initiation of treatment, emergency LPI or surgical iridectomy should be damage that occurred during the period of appositional closure, or to attempted. When the IOP falls to 20 mm Hg or below, gonioscopy nonpupillary block components of angle closure, such as plateau iris and should be performed to confirm that the angle is open. malignant glaucoma. The development of open angle glaucoma is also An acute attack of angle closure glaucoma should not be considered broken until the IOP has returned to normal levels, the pupil is miotic, Patients who have undergone LPI should be evaluated in the immediate and the angle is open. Low pressure is not, by itself, indicative of a postprocedure period (1-7 days). The examination should be directed broken attack. When the angle is not open, IOP will again rise to very toward establishing patency of the iridotomy, IOP measurement and high levels in hours to days. When the attack can be broken medically, control, and gonioscopy to reaffirm that the anterior chamber angle the patient should be maintained on 2% pilocarpine four times a day remains open. These patients should also be examined at 1, 2, and 6 bilaterally, and 1% prednisolone acetate four times daily in the affected months following LPI. Most iridotomy closures occur within the first 2 eye until a LPI is performed. Most clinicians also keep the patient on a months, almost never past 6 months;105 therefore, evaluating patency of 26 Primary Angle Closure Glaucoma the iridotomy is critical in these examinations. The 1-month visit should • Response to selective absorption filters. include dilation with stereoscopic evaluation of the optic nerve head. Baseline photos of the optic nerve head and baseline threshold visual Once appropriate optical requirements have been determined, the fields may be conducted, if not previously obtained. Long-term followup clinician should educate and train the patient in methods of improving of patients who have undergone LPI should be every 6-12 months. visual function with and without optical devices. The patient should be encouraged to use prescription optical devices for work, home, and social Primary ACG suspects should undergo baseline gonioscopy with standard classification and drawing, careful biomicroscopic evaluation, stereoscopic evaluation of the optic nerve head with baseline photos, and The goal of low vision rehabilitation is to reduce ocular morbidity and baseline threshold visual fields. Clinicians should educate these patients enhance the quality of life. In addition to optical intervention, the regarding the signs and symptoms of an acute angle closure attack and evaluation should include the need for nonoptical devices, special instruct them to seek care immediately under those circumstances. lighting, posture aids, contrast enhancement, enlarged print, and Long-term monitoring of these patients should be every 3-4 months for nonvisual methods or devices when appropriate. These devices, which the first year and every 6-12 months thereafter. Appendix Figure 2 significantly enhance the rehabilitative process, are necessary to provides a summary of the frequency and composition of evaluations for When indicated, the optometrist should recommend blind rehabilitation, Management of Patients with Severe, Irreversible Vision Loss
occupational, vocational and independent living counseling services and psychosocial consultation. Patients should be informed of other Patients with primary ACG may suffer permanent vision loss. resources including agencies that register and provide services and Consultation with an optometrist who has advanced training or clinical advocacy to individuals with legal blindness or visual impairment. experience in low vision is advisable because patients may benefit from These agencies can provide information regarding large-print and talking low vision rehabilitation including the use of specialized optical devices books, independent travel aids, and other devices geared to improve quality of life and functional ability within the patient's household. The optometrist should provide the patient written documentation of his or Patients should be evaluated to determine the potential benefits from her status relating to legal blindness for state and federal (Internal comprehensive low vision rehabilitation which reduces the debilitating Revenue Service) tax requirements. Local and national support groups effects of vision loss from primary ACG. This task-oriented evaluation for the visually impaired assist many patients in coping with the anxiety and concerns of vision loss. Such groups also provide information regarding resources to help patients function safely and productively in • Expanded patient history and needs assessment • Low vision assessment of visual acuity (including eccentric viewing) • Low vision refraction • Binocular function assessment • Supplemental testing, including visual fields, contrast sensitivity, and • Response to optical and electro-optical magnification CONCLUSION
The presentation of primary ACG varies greatly; therefore, the
optometrist needs a broad understanding of the epidemiology,
pathophysiology, and clinical manifestations of this challenging group of
conditions. Prompt, appropriate diagnosis and aggressive treatment and
management are necessary to prevent, or minimize, significant ocular
morbidity in patients with primary angle closure glaucoma.
30 Primary Angle Closure Glaucoma III. REFERENCES
Lehrfeld L, Reber J. Glaucoma at the Wills Hospital. Arch van Herick W, Schaffer RN, Schwartz A. Estimation of width of angle of anterior chamber. Incidence and significance of the Bengtsson B. The prevalence of glaucoma. Br J Ophthalmol narrow angle. Am J Ophthalmol 1969; 68:626-9. Cockburn DM. Slit lamp estimate of anterior chamber depth as a Graham P, Hollows F. Intra-ocular pressure, glaucoma and predictor of the gonioscopic visibility of the angle structures. glaucoma suspects in a defined population. Br J Ophthalmol Spaeth GL. The normal development of the human anterior Alper MG, Laubach JL. Primary ACG in the American Negro. chamber angle: a new system of descriptive grading. Trans Au Shalom A. Israeli ophthalmologists in Africa. J Israeli Med Hoskins HD Jr, Kass MA. Becker-Shaffer's diagnosis and therapy of the glaucomas, 6th ed. St. Louis: CV Mosby, Newman E, Zauberman H. Glaucoma survey in Liberia. Am J Lewis TL. Definition and classification of glaucomas. In: Lewis TL, Fingeret M, eds. Primary care of the glaucomas. Olvrin O. Anterior chamber depth in Nigerians. Ann Norwalk: Appleton & Lange, 1993:3-5. Fisch BM. Primary angle closure glaucoma. In: Fisch BM, ed. Venable HP. Glaucoma in the Negro. J Natl Med Assoc 1952; Gonioscopy and the glaucomas. Boston: Butterworth- Luntz MH. Primary ACG in urbanized South African causacoid Tornquist R. Angle closure glaucoma in an eye with a plateau and negroid communities. Br J Ophthalmol 1973; 57:445-56. type of iris. Acta Ophthalmol 1958; 36:413-20. Venable HP. Recent advances in the diagnosis and therapy of Luntz MH, Rosenblatt M. Malignant glaucoma. Surv glaucoma. J Natl Med Assoc 1958; 50:79-96. Alsbirk PH. Primary angle closure glaucoma: oculometry, Bankes JLK, Perkins ES, Tsolakis S, Wright JE. Bedford epidemiology and genetics in a high-risk population. Acta Barkan O. Primary glaucoma: pathogenesis and classification. Clemmesen V, Alsbirk PH. Primary angle closure glaucoma in Greenland. Acta Ophthalmol 1971; 49:47-58. 32 Primary Angle Closure Glaucoma Cox JE. Angle closure glaucoma among the Alaskan Eskimos. Holmes WJ. Glaucoma in the Central and South Pacific. Am J Van Rens GH, Arkell SM, Charlton W, Doesburg W. Primary Genio CA, Gavino BC. Glaucoma profiles at the Philippine angle-closure glaucoma among Alaskan Eskimos. Doc General Hospital. Philippine J Ophthalmol 1983; 15:1-2. Murchland J. Anterior chamber depth of eyes of full blood Drance SM. Angle closure glaucoma among Canadian Eskimos. aborigines at a reserve in South Australia. Aust J Ophthalmol Arctic Ophthalmology Symposium 1973. Can J Ophthalmol Allen H. Amazonian ophthalmology. Am J Ophthalmol 1971; Congdon N, Wang F, Tielsch JM. Issues in the epidemiology and population-based screening of primary angle closure glaucoma. Surv Ophthalmol 1992; 36:411-23. Wilensky J. Glaucoma. In: Peyman G, Sanders D, Goldberg M., eds. Principles and practice of ophthalmology, vol 1. Shiose Y, Kitazawa Y, Tsukuhara S, et al. Epidemiology of Philadelphia: WB Saunders, 1980:671-737. glaucoma in Japan: a nationwide glaucoma survey. Jpn J Lowe RF. Causes of shallow anterior chamber in primary angle- closure glaucoma. Am J Ophthalmol 1969; 67:87-93. Hung PT. Aetiology and mechanism of primary ACG. Asia Pac Rosengren B. Studies in the depth of the anterior chamber of the eye in primary glaucoma. Arch Ophthalmol 1950; 44(4):523-38. Lim ASM. Primary ACG in Singapore. Aust J Ophthalmol Tornquist R. Shallow anterior chambers in acute glaucoma. Pararajasegaram R. Glaucoma pattern in Ceylon. Trans Asia Aizawa K. Studies in the depth of the anterior chamber. Jpn J Alsbirk PH. Prevention and control of visual impairment and blindness (with special reference to glaucoma) in India. Sood NN, Jain RC, Agarwal HC. Ocular biometry in primary Consultant Report. World Health Organization, Southeast Asia angle closure glaucoma in Indians. Indian J Med Res 1988; Linner E. Assessment of glaucoma as a cause of blindness, India. World Health Organization, Southeast Asia Region/Ophthalmology, 1982. 34 Primary Angle Closure Glaucoma Alsbirk PH. Oculometry in angle closure glaucoma. In: Wang RR, Guo BK, Chen SC . Genetic rules of primary angle National symposium on recent advances in the diagnosis and closure glaucoma. Chin Med J 1986; 99:535-43. management of glaucoma. New Delhi: All India Inst Med Sci, Phelps CD, Podes SM. Glaucoma. In: Goldberg MF, ed. Genetic and metabolic eye disease. Boston: Little, Brown, & Alsbirk PH. Prevention and control of visual impairment and blindness (with special reference to glaucoma) in Burma. Consultant Report. World Health Organization, Southeast Asia Tornquist R. Chamber depth in primary acute glaucoma. Br J Spaeth GL. Gonioscopy: Uses old and new: The inheritance of Lowe RF, Ritch R. Angle closure glaucoma. Mechanisms and occludable angles. Ophthalmology 1978; 85:222-32. epidemiology. In: Ritch R, Shields MB, Krupin T, eds. The glaucomas. St. Louis: CV Mosby, 1989:825-37. Leighton DA. Survey of the first-degree relatives of glaucoma patients. Trans Ophthalmol Soc UK 1976; 96:28-32. Hillman JS. Acute angle closure glaucoma: an investigation into the effect of delay of treatment. Br J Ophthalmol 1979; Lowe RF. Clinical types of primary angle closure glaucoma. Appleby RS Jr, Kinder RSL. Bilateral angle closure glaucoma in Paterson G. Studies on siblings of patients with both angle a 14 year old boy. Arch Ophthalmol 1971; 86(4):449-50. closure and chronic simple glaucoma. Trans Ophthalmol Soc Hoskins HD Jr, Kass MA. Becker-Shaffer's diagnosis and therapy of the glaucomas, 6th ed. St. Louis: CV Mosby, Perkins ES. Family studies in glaucoma. Br J Ophthalmol Tomlinson A, Leighton DA. Ocular dimensions in the heredity Alsbirk PH. Anterior chamber depth, genes and environment. of angle closure glaucoma. Br J Ophthalmol 1973; 57:475-86. Fontana SC, Brubaker RF. Volume and depth of the anterior Francois J. Multifactorial or polygenic inheritance in chamber in the normal aging human eye. Arch Ophthalmol ophthalmology. In: Henkind P, ed. Acta XXIV Proceedings of the International Congress of Ophthalmology, vol 1, 1982. Lowe RF, Clark BAJ. Radius of curvature of the anterior lens surface. Correlations in normal eyes and in eyes involved with Lowe RF. Primary angle closure glaucoma: inheritance and primary angle closure glaucoma. Br J Ophthalmol 1973; environment. Br J Ophthalmol 1972; 56:13-20. 36 Primary Angle Closure Glaucoma Brown N. The change in lens curvature with age. Exp Eye Res Fingeret M, Kowal D. Acute glaucomas: diagnosis and treatment. In: Classe JG, ed. Optometry clinics, vol 1. Norwalk: Appleton & Lange, 1991:165-91. Lowe RF. Aetiology of the anatomical basis for primary angle- closure glaucoma. Br J Ophthalmol 1970; 54:161-9. Bresler MJ, Hoffman RS. Prevention of iatrogenic acute narrow-angle glaucoma. Ann Emerg Med 1981; 10:535-7. Leighton DA, Phillips CI, Tsukahara S. Profile of presenting states of eyes in angle closure glaucoma. Br J Ophthalmol 1971; van Herick W, Shaffer RN, Schwartz A. Estimation of width of angle of anterior chamber. Incidence and significance of the narrow angle. Am J Ophthalmol 1969; 68:626-9. Drance SM, Morgan RW, Bryett J, Fairclough M. Anterior chamber depths and gonioscopic findings among Eskimos and Fingeret M, Casser L, Woodcome HT. Atlas of primary eyecare Indians in the Canadian Arctic. Arctic Ophthalmology procedures. Norwalk: Appleton & Lange, 1990; 26-7. Symposium 1973. Can J Ophthalmol 1973; 8:255-9. Stelmack T. Angle closure glaucoma. In: Lewis TL, Fingeret Chandler PA. Narrow angle glaucoma. Arch Ophthalmol 1952; M, eds. Primary care of the glaucomas. Norwalk: Appleton & Wollensak J, Zeisberg B. Pathophysiology, treatment, and Novak JM. Provocative testing. In: Onofrey BE, ed. Clinical prophylaxis of angle closure glaucoma. Glaucoma 1986; 8:3-11. optometric pharmacology and therapeutics. Philadelphia: JB Simmons RJ, Belcher CD, Dallow RL. Primary angle closure glaucoma. In: Tasman W, Jaeger EA, eds. Clinical Slamovits T, Dutton J. Should patients with anatomically ophthalmology, vol 3. Philadelphia: JB Lippincott, 1985; 53:1- narrow angles have prophylactic iridectomy? Surv Ophthalmol Mapstone R. Mechanics of pupil block. Br J Ophthalmol 1968; Wollensak J. Prophylaxis and treatment of narrow angle Hoskins HD Jr, Kass MA. Becker-Shaffer's diagnosis and Garnias F, Mapstone R. Miotics in closed angle glaucoma. Br J therapy of the glaucomas, 6th ed. St. Louis: CV Mosby, 1989; Anderson DR, Davis EB. Sensitivities of ocular tissues to acute Watson PG. Surgery of the glaucomas. Br J Ophthalmol 1972; pressure-induced ischemia. Arch Ophthalmol 1975; 93:267-74. Zimmerman TJ. Pilocarpine. Ophthalmology 1981; 88:85-8. 38 Primary Angle Closure Glaucoma Kramer P, Ritch R. The treatment of acute angle closure American Academy of Ophthalmology. Ophthalmic procedure glaucoma revisited. Ann Ophthalmol 1984; 16:1101-3. assessment: Laser peripheral iridotomy for pupillary-block Hillman JS. Management of acute glaucoma with pilocarpine- soaked hydrophilic lens. Br J Ophthalmol 1974; 58:674-9. Ritch R, Solomon IS. Laser treatment of glaucoma. In: L'Esperance F, ed. Ophthalmic lasers. St. Louis: CV Mosby, Greco JJ, Kelman CD. Systemic pilocarpine toxicity in the treatment of angle closure glaucoma. Ann Ophthalmol 1973; Alward WLM. Laser iridotomy. In: Weingeist TA, Sneed SR, eds. Laser surgery in ophthalmology. Norwalk: Appleton & Davidorf JM, Baker ND, Derick R. Treatment of the fellow eye in acute angle-closure glaucoma: A case report and survey of members of the American Glaucoma Society. J Glaucoma 1996; Rostron CK. Acute angle-closure glaucoma: surgery or laser? Robin AL, Pollack IP, deFaller JM. Effects of topical ALO 2145 Fleck BW, Dhillon B, Khanna V, et al. A randomized, (p-aminoclonidine hydrochloride) on acute intraocular pressure prospective comparison of Nd:YAG laser iridotomy and rise after argon laser iridectomy. Arch Ophthalmol 1987; operative peripheral iridectomy in fellow eyes. Eye 1991; 5:315- American Academy of Ophthalmology. Preferred practice Hoskins HD Jr, Kass MA. Becker-Shaffer's diagnosis and pattern primary angle-closure glaucoma. San Francisco: AAO, therapy of the glaucomas, 6th ed. St. Louis: CV Mosby, Johnson ME, Molinari JF. Efficacy of dapiprazole. Optom Vis Iwata K, Abe H, Sugiyama J. Argon laser iridotomy in primary angle-closure glaucoma. Glaucoma 1985:7:103-6. Doughty MJ, Lyle WM. A review of the clinical Jackson J. Clinical applications of lasers. In: Pitts D, Kleinstein pharmacokinetics of pilocarpine, moxisylyte (thymoxamine), R, eds. Environmental vision - interactions of the eye, vision and dapiprazole in the reversal of diagnostic pupillary dilation. and the environment. Stoneham: Butterworths, 1993:239-56. Krupin T, Stone RA, Cohen BH, et al. Acute intraocular Bonomi L, Marchini G, De Gregorio M. Ultrasonographic study pressure response to argon laser iridotomy. Ophthalmol 1985; of the ocular effects of topical dapiprazole. Glaucoma 1986; Schrems W, Eichelbronner O, Krieghtein GK. The immediate Anderson DR. Corneal indentation to relieve acute angle closure IOP response of Nd:YAG laser iridotomy and its prophylactic glaucoma. Am J Ophthalmol 1979; 88:1091-3. treatability. Acta Ophthalmol 1984; 62:673-80. 40 Primary Angle Closure Glaucoma Liu PF, Hung PT. Effect of timolol on intraocular pressure Bobrow JC, Drews RC. Long-term results of peripheral elevation following argon laser iridotomy. J Ocul Pharmacol Hyams SW, Friedman Z, Keroub C. Mixed glaucoma. Br J Assaf AA. Argon laser iridectomies. Glaucoma 1985; 7:75-83. Robin AL, Pollack IP. A comparison of neodymium:YAG and Krupin T, Mitchell KB, Johnson MF, Becker B. The long-term argon laser iridotomies. Ophthalmology 1984; 91:1011-6. effects of iridectomy for primary acute angle-closure glaucoma. Wise JB. Low-energy linear-incision neodymium:YAG laser iridotomy versus linear-incision argon laser iridotomy. A Forbes M. Indentation gonioscopy and efficacy of iridectomy in prospective clinical investigation. Ophthalmology 1987; angle-closure glaucoma. Trans Am Ophthalmol Soc 1974; Del Prioro LV, Robin AL, Pollack IP. Neodymium:YAG and Gelber EC, Anderson DR. Surgical decision in chronic angle- argon laser iridotomy. Long-term follow-up in a prospective, closure glaucoma. Arch Ophthalmol 1976; 94:1481-4. randomized clinical trial. Ophthalmology 1988; 95:1207-11. Playfair TJ, Watson PG. Management of acute primary angle- Gray RH, Honre Nairn J, Ayliffe WHR. Efficacy of Nd:YAG closure glaucoma: a long-term follow-up of the results of laser iridotomies in acute angle-closure glaucoma. Br J peripheral iridectomy used as an initial procedure. Br J Moster MR, Schwartz LW, Spaeth GL, et al. Laser iridectomy: Murphy MB, Spaeth GL. Iridectomy in primary angle-closure a controlled study comparing argon and neodymium:YAG. glaucoma: classification and differential diagnosis of glaucoma associated with narrowness of the angle. Arch Ophthalmol King MH, Richards DW. Near syncope and chest tightness after administration of apraclonidine before argon laser iridotomy. Tanihara H, Makoto N. Argon-laser gonioplasty following Letter. Am J Ophthalmol 1990; 110:308-9. goniosynechialysis. Graefes Arch Clin Exp Ophthalmol 1991; Schwartz LW, Moster MR, Spaeth GL, et al. Neodymium: YAG laser iridectomies in glaucoma associated with closed or occludable angles. Am J Ophthalmol 1986; 102:41-4. Prum BE, Shields SR, Shields MB, et al. In vitro videographic comparison of argon and Nd:YAG. Am J Ophthalmol 1991; 111:589-94. IV. APPENDIX
Optometric Management of the Patient with
Acute Primary ACG: A Brief Flowchart
Use every 15-60 minutes up to a total of Use two 250 mg tablets; avoid if patient methazolamide, if patient has kidney condition; if nauseated, consider Dosage is 1.5 ml/kg body wt (serve over ice) if nauseated, consider intravenous Topical glycerin may aid in clearing cornea 44 Primary Angle Closure Glaucoma Figure 2 (Continued)
Frequency and Composition of Evaluation and Management Visits
for Primary ACG *
Frequency of
Optic Nerve
Automated
Management
Examination
Tonometry
Gonioscopy
Slit Lamp
Assessment
Perimetry
* Figure 2 extends horizontally through page 45. 46 Primary Angle Closure Glaucoma ICD-9-CM Classification of Primary Angle Closure Glaucoma
Abbreviations of Commonly Used Terms
Primary angle closure glaucoma
Primary angle closure glaucoma, unspecified
Intermittent angle closure glaucoma
Acute angle closure glaucoma
Chronic angle closure glaucoma
Residual stage of angle closure glaucoma
48 Primary Angle Closure Glaucoma Glossary
Plateau iris syndrome A condition in which both plateau iris
Anterior chamber The space in the eye, filled with aqueous humor, that
configuration and a peripheral iridotomy or iridectomy are present and is bordered anteriorly by the cornea and a small portion of the sclera and the anterior chamber still remains capable of closure. posteriorly by a small portion of the ciliary body, the iris, and that portion of the lens which presents through the pupil. Posterior synechia An adhesion between the iris and the anterior lens
capsule, most commonly at the pupillary border. Anterior uveitis (iritis, cyclitis, iridocyclitis) Inflammation of the iris,
Pupillary block Blockage of the normal flow of aqueous humor from
the posterior chamber into the anterior chamber through the pupil. Biomicroscopy Examination of ocular tissue using a bright focal source
of light with a slit of variable width and height and a binocular Refraction Determination of refractive errors of the eye.
Tonometry A procedure for measurement of the pressure within the
Glaukomflecken Irregular white opacities in the subcapsular region of
the anterior portion of the lens which are considered a diagnostic sign Trabecular meshwork The meshwork of connective tissue located
between the Canal of Schlemm and the anterior chamber which is Gonioscopy A technique for examining the anterior chamber angle,
involved in drainage of aqueous humor from the eye. utilizing a corneal contact lens, magnifying device, and light source. Visual acuity The clearness of vision that depends upon the sharpness
Iridocorneal endothelial (ICE) syndrome Progressive atrophy of the
of focus of the retinal image and the integrity of the retina and visual iris tissue in which the formation of synechiae scars in areas around the Laser peripheral iridotomy (LPI) A hole created in the iris by
Cline D, Hofstetter HW, Griffin JR. Dictionary of visual science, 4th ed. different types of lasers (e.g., argon, Nd:YAG, diode) to relieve pupillary Peripheral anterior synechia (PAS) An adhesion between the
Coles WH. Ophthalmology: a diagnostic text. Baltimore: Williams & Wilkins, 1989. peripheral iris and the anterior chamber angle or peripheral cornea.
Peripheral iridectomy The surgical removal of a section of the
Cullom RD, Chang B, eds. The Wills eye manual: office and emergency room diagnosis and treatment of eye diseases, 2nd ed. Philadelphia: JB Lippincott, Plateau iris configuration A condition in which the central anterior
chamber depth is normal, the iris plane is flat, and the anterior chamber Grosvenor TP. Primary care optometry. Anomalies of refraction and binocular vision, 2nd ed. Boston: Butterworth-Heinemann, 1996:575-91 50 Primary Angle Closure Glaucoma Stedman’s medical dictionary, 26th ed. Baltimore: Williams and Wilkins, 1995. Vaughan D, Asbury T, Riordan-Eva P. General ophthalmology, 14th ed. Norwalk, CT: Appleton and Lange, 1995:419-22.

Source: http://www.grandlakeeyecarellc.com/wp-content/uploads/2012/07/CPG-glaucoma1.pdf