AUTHOR AND EDITOR INFORMATION

Section 1 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

INTRODUCTION

Section 2 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Background

Since the early 1900s, the status of the angle has been recognized as highly relevant in the analysis of glaucoma. In 1938, Barkan described peripheral anterior synechiae (PAS) between the peripheral iris and trabecular meshwork (TM), which could lead to increased intraocular pressure (IOP). In 1952, Chandler recognized that narrowing of the angle would decrease outflow, thereby increasing ocular tension.

Today, PAS are a well-recognized consequence of altered anterior chamber (AC) anatomy and AC inflammation. PAS subsequently can result in significant morbidity as a precipitant to secondary angle-closure glaucoma.

Pathophysiology

PAS may form under the following 2 circumstances: a nonproliferative state or a proliferative state.

Apposition of the iris against the TM as a result of pupil block or a posterior pushing mechanism without any inflammation can result in continuous PAS. These continuous PAS lead to "zippering" of the angle. Primary angle-closure glaucoma and the various posterior pushing mechanisms are examples of this process.

In the presence of inflammation or cellular proliferation, a membrane forms between the iris and the TM, creating the PAS. This membrane contracts, resulting in angle-closure glaucoma by an anterior pulling mechanism. Examples of this process include the fibrovascular membrane formed in neovascular glaucoma, proliferating abnormal endothelial cells in the iridocorneal endothelial (ICE) syndromes, epithelialization of the angle due to epithelial ingrowth, or inflammatory trabecular and keratic precipitates in contact with an inflamed iris. These processes can be accentuated by iris swelling and protein transudation and exudation

Frequency

United States

Infrequent

International

Infrequent

Mortality/Morbidity

The morbidity of PAS lies in its ability to occlude the angle and result in a pathological increase in IOP.

Race

Asians have the highest propensity for primary angle-closure glaucoma and, thus, PAS formation. This condition is not as common in blacks. Whites are least likely to develop primary angle-closure glaucoma.

Sex

Females have shallower ACs; therefore, they may have a greater disposition to forming PAS.

Age

The risk of PAS formation increases with age because of a reduction in AC depth. This is due to a combination of cataract formation, leading to an increase in the thickness of the lens, and laxity of the zonules, resulting in the forward displacement of the lens.

CLINICAL

Section 3 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

History

• PAS can present in the following manners:
• • Acute angle closure with the classic constellation of symptoms, including ocular pain, headaches, blurred vision, and halos.
  • Subacute: History of multiple transient attacks, which consist of mild ocular pain, reduced vision, and halos.
  • Chronic
    • Asymptomatic

    • Reduced vision due to corneal edema or end-stage glaucomatous optic neuropathy

• History may be valuable in trying to elucidate processes that may have lead to PAS formation. Specific inquiry should include the following:
• • History of ocular infection, surgery, or trauma
  • Family history of glaucoma or other eye disease
  • Past medical history, specifically inquiring about rheumatological disease and inflammatory syndromes
  • Ocular and systemic medications

Physical

As a general principle, examination of the nonaffected eye in unilateral presentations may prove to be valuable in trying to discern between primary and secondary etiologies of angle closure.

• Refraction: Hyperopia is a risk factor for angle closure.


• Gonioscopy
• • Zeiss compression
  • • Zeiss compression should be performed to distinguish appositional closure from synechial closure in narrow-angle glaucoma.
    
    
    • Areas where an abrupt change in the angle from open to closed is present suggest the presence of PAS.
    
    
    • If not visualized directly, synechial presence can be indicated by the lack of displacement of the focal lines reflected from the posterior surface of the cornea and the anterior surface of the iris. When PAS are not present, a displacement will be noted with compression gonioscopy.
    
    
    • It is imperative that the entire circumference of the angle be examined for an open, normal-looking angle and compared to the regions of PAS to estimate the filtration capabilities of the eye.
    
    
    • The point of anterior attachment of PAS should be noted because PAS that obstruct the central third of the TM are more likely to result in increased IOP.


• Table 1. Description of PAS on gonioscopy
  
  

  Description of PAS	Associations	Possible conditions
  Broad bands
  	PAS to all levels but not to cornea No bridging usually present	Angle-closure glaucoma
  	PAS to all levels, sometimes to cornea Bridging may be present	Posterior pushing mechanism, postoperatively shallow AC, or from iris bombé
  	PAS with new vessels, multiple sites	Neovascularization
  	Anterior PAS advancing irregularly on or beyond the TM onto cornea Bridging may be present	ICE syndrome, epithelialization of AC
  Scattered, irregular
  	PAS tent and form columns up to, but not on, the cornea	Iridocyclitis with keratic and trabecular precipitates
  	Small PAS to scleral spur	Post-argon laser trabeculoplasty (ALT)

• Prominent uveal meshwork (must be differentiated from PAS)
  
  
  • Can be confused for PAS
  
  
  • More common and extensive in brown irides compared to blue eyes
  
  
  • Has a lacy and porous appearance through which angle structures can be visualized; this can be enhanced with transillumination
  
  
  • Axenfeld and Rieger anomalies (anterior segment dysgenesis) may have anterior prominent uveal meshwork with an anterior displaced Schwalbe line, which is not believed to be true PAS.
  
  

• Cornea
  
  
  • Keratic precipitates would indicate an inflammatory etiology.
  
  
  • Polymorphous opacities at the Descemet membrane level suggest posterior polymorphous dystrophy (PPMD).
  
  
  • Corneal guttata and/or edema are suggestive of Chandler syndrome.
  
  
  • Congenital corneal opacities or sclerocornea suggest a congenital corneal defect (anterior segment dysgenesis).
  
  
  • Posterior embryotoxon


• AC depth
  
  
  • If the peripheral depth in this region has a corneal thickness of one fourth or less, the possibility of angle closure exists (Von Herrick law).
  
  
  • Distinction should be made between peripheral and central shallowing.
  
  
  • Pupil block commonly results in greater peripheral shallowing as compared to the central AC.
  
  
  • Posterior pushing mechanisms result in equal peripheral and central shallowing.
  
  


• Iris
  
  
  • Iris atrophy may suggest previous attacks of angle-closure glaucoma, uveitis, or anterior segment dysgenesis.
  
  
  • Koeppe and Busacca nodules suggest iritis.
  
  
  • Irregularity of the pupil may be secondary to trauma or inflammation.
  
  
  • New vessels along the anterior iris stroma and ectropion uveae suggest neovascular glaucoma.
  
  
  • Ectropion uveae, corectopia, iris stretch holes, and nevi suggest an ICE syndrome.
  
  
  • Anterior bowing of the iris may imply an element of pupil block or iris bombé.
  
  


• Lens
  
  
  • Glaukomflecken suggests previous attacks of angle-closure glaucoma.
  
  
  • Pseudoexfoliation is associated with zonule laxity, which can result in forward displacement of the lens.
  
  
  • Posterior synechiae may lead to iris bombé.
  
  
  • Intumescent lens may cause shallowing of the AC.
  
  


• Retina
  
  
  • Any cause of vascular compromise (eg, diabetic retinopathy, central retinal artery occlusion [CRAO], central retinal vein occlusion [CRVO]) can be a precipitant for rubeosis.
  
  
  • CRVO can lead to choroidal/supraciliary effusions.
  
  


• Choroid - Choroidal masses, effusions, or hemorrhage may result in a posterior pushing mechanism.


• Optic nerve
  
  
  • Pallor may suggest previous attacks of angle-closure glaucoma.
  
  
  • With or without cupping - May have cupping with persistent increased IOP with optic nerve damage; if IOP is normal or near-normal, optic nerve may not have evidence of cupping on clinical examination.
  
  


• Intraocular pressure
  
  
  • Rises when a significant portion of the angle is occluded by PAS (usually greater than two thirds).
  
  
  • IOP may be normal even if a significant portion of the angle has been closed by PAS due to the phenomenon of bridging, ie, when the iris has attached anterior to the TM, leaving a space in front of the TM allowing it to function. This typically occurs in ICE syndromes and congenital anomalies and is not seen in primary angle closure.
  
  
  • Postoperatively, low IOP in the presence of extensive PAS also warrants consideration for cyclodialysis.

Causes

Table 2: Summary of Important Mechanisms and Causes of PAS

• Congenital
• • Anterior segment dysgenesis (ie, Peters anomaly, posterior embryotoxon, Axenfeld anomaly, Rieger anomaly) - Associated with prominent uveal meshwork. See Gonioscopy in Physical.
  
  
  • ICE syndromes (essential iris atrophy, Chandler and Cogan-Reese syndromes) - Endothelial membrane (epithelial-like) over angle
  
  
  • Nanophthalmos (>10 diopters [D] hyperope or <20 mm axial length) - Pupil block or uveal effusion narrows angle.
  
  
  • Posterior polymorphous dystrophy - Endothelial membrane (epithelial-like) over angle
  
  
  • Aniridia - Iris stump may block TM.
  
  
  • PHPV - Associated with microphthalmia and elongated ciliary processes. Contracture of retrolental mass and lens intumescence also can lead to PAS and angle closure.
  
  
  • Retinopathy of prematurity
  
  
  • Neurofibromatosis - Possible mechanisms of PAS formation include the following: (1) high flat iris insertion or sweeping anterior insertion; (2) thickening of the ciliary body and choroid (up to 6-8 times normal) that can lead to anterior displacement of the iris diaphragm and narrowing of the angle; and (3) Lisch nodules blocking angle recess.

• Relative pupil block and iris bombé
• • Narrow-angle glaucoma - PAS can form while the iris is in contact with the TM or the cornea and can persist after an iridectomy. PAS also may form during an acute attack in which there would be scattered PAS formation, or they may occur in a chronic state in which case PAS would form in a continuous, creeping, angle-closure manner. This is a diagnosis of exclusion (ie, there cannot be any other etiologies for PAS formation).
  
  
  • Posterior synechiae resulting in iris bombé
  
  
  • Pseudophakic or aphakic pupil block


• Plateau iris
• • Flat, anterior iris insertion
  
  
  • Anteriorly displaced ciliary processes

• Uveitis
• • Mechanisms
  • • Contracting inflammatory precipitates in the angle
    
    
    • Posterior synechiae resulting in iris bombé
    
    
    • Posterior pushing mechanism as a result of choroidal effusion with posterior uveitis
    
    
    • PAS rarely is caused by acute episodes of uveitis but rather in chronic inflammatory states. If PAS develops in acute episodes, it is likely in eyes that have a concurrent narrow angle in which an edematous iris can come into contact with the cornea.
  
  
  • Etiology
  • • Inflammatory - Idiopathic (most common), specific inflammatory syndromes, including juvenile rheumatoid arthritis, interstitial keratitis, lens related (eg, phacolytic, lens particle, phacoanaphylaxis), sarcoidosis, pars planitis, and uveitis-glaucoma-hyphema syndrome. PAS typically is not found in glaucomatocyclitic crisis (Posner-Schlossman syndrome) or Fuchs heterochromic iridocyclitis.
    
    
    • Infectious - Herpes simplex, herpes zoster, toxoplasmosis, and syphilis.


• Postsurgical
• • Filtering surgery - A shallow AC can result after filtering surgery, leading to PAS due to early postoperative wound leaks or overfiltration. PAS usually occurs after 1 week of peripheral iris-cornea touch.
  
  
  • ALT - Higher risk of inflammation and PAS formation is associated with narrow angles, posterior burns, high-power burns, and brown eyes.
  
  
  • Scleral buckling surgery - Anterior displacement of the vitreous occurs, leading to a shallow AC. Also, compression of vortex veins with reduced venous drainage from the ciliary body leads to supraciliary effusion and anterior rotation of the ciliary body.
  
  
  • Intravitreal expansile gas injection - Intravitreal injection of an expansile gas (sulfur hexafluoride [SF₆], octafluoropropane [C₃F₈]) after vitrectomy and/or scleral buckling surgery can lead a shallow AC due a posterior pushing mechanism.
  
  
  • Silicone oil - May develop pupil block without peripheral iridotomy, particularly in aphake
  
  
  • Cryotherapy or panretinal photocoagulation - Can result in choroidal/ciliary body effusion, leading to a posterior pushing mechanism
  
  
  • Penetrating keratoplasty - May result in loss of angle support postoperatively, resulting in PAS
  
  
  • Cataract extraction/IOL insertion, including phacoemulsification
  • • Surgical-related processes that can lead to PAS - Epithelial ingrowth; wound leak, leading to a shallow AC; persistent postoperative uveitis; residual lens cortex "fluffing"; and pushing the iris forward
    
    
    • Pseudophakic-related processes that can lead to PAS - Pseudophakic pupil block, the haptics of a posterior chamber lens can push the iris forward, leading to PAS formation; increased incidence (65-85%) with anterior vaulted haptics, and, when these lenses are sulcus supported, the haptics of a sulcus or angle-supported lens may cause irritation and uveitis, leading to PAS formation (uveitis-glaucoma-hyphema syndrome); and PAS can form around the haptics of AC lenses


• Neovascular glaucoma
• • See Glaucoma, Neovascular for causes.
  
  
  • PAS preceded by rubeosis iridis and fibrovascular membrane - May have IOP elevation prior to obvious PAS formation
  
  
  • Contractile forces along new vessels lead to PAS.


• Epithelial or fibrous ingrowth - Secondary to epithelial membrane growing over angle after penetrating surgery/trauma


• Traumatic
• • Hyphema - A total hyphema that has not cleared by day 5 or a large hyphema persisting for more than 10 days can lead to PAS and should be evacuated.
  
  
  • Dialysis of the iris root can lead to PAS in the healing process.
  
  
  • Vitreous in the AC leads to inflammation that can cause PAS.
  
  
  • Wound healing after a corneal wound (eg, iatrogenic, traumatic) can lead to epithelial proliferation that results in PAS, particularly lacerations that cross the limbus.
  
  
  • Lens subluxation anteriorly


• Physical - Posterior pushing mechanisms resulting in appositional closure, then synechial closure
• • Choroidal effusions
  
  
  • Suprachoroidal hemorrhage
  
  
  • Ciliary bock (malignant) glaucoma (aqueous misdirection)
  
  
  • Posterior segment tumors (eg, retinoblastoma, choroidal melanoma, metastasis)
  
  
  • Iris cysts or tumors
  
  
  • Ciliary body tumor, cysts, or effusions
  
  
  • Intumescent lens (phacomorphic glaucoma)
  
  
  • Ectopia lentis - Marfan, homocystinuria, Weill-Marchesani syndrome, microspherophakia, Ehlers-Danlos syndrome, trauma, and pseudoexfoliation syndromes can lead to the anterior subluxation of the lens, leading to a shallow AC secondary to zonular laxity (see Ectopia Lentis).


• Medications
• • Miotics - Cause a forward displacement of the lens-iris diaphragm
  
  
  • Anticholinergic agents - Lead to pupillary dilation, which may result in increased pupil block in a predisposed eye (eg, topical cycloplegics or systemic atropine, antihistamines, antiparkinsonism, antipsychotics, botulism toxin)
  
  
  • Adrenergics - Lead to pupillary dilation, which may result in increased pupil block in a predisposed eye (eg, topical or systemic epinephrine, CNS stimulants, appetite depressants, bronchodilators, hallucinogenic agents)
  
  
  • Medications that can cause ciliary effusions (eg, sulfonamides, tetracycline)

DIFFERENTIALS

Section 4 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

WORKUP

Section 5 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Lab Studies

• Inflammatory and infectious workup as required

Imaging Studies

• Ultrasound biomicroscopy
• • Useful in evaluating the angle in angle-closure glaucoma
  • Can delineate PAS and determine their extent
  • May demonstrate a small space between PAS and the TM, suggesting that the TM may still be capable of normal function
  • May be useful in demonstrating supraciliary fluid

• Corneal specular microscopy - Useful in identifying ICE or PPMD cells

Other Tests

• Provocative testing - This test measures IOP while dilating or constricting the pupil to differentiate angle-closure glaucoma from open-angle glaucoma with narrow angles; however, it correctly identifies only 50-70% of patients with true angle closure.
• • Dark room - Increase in IOP with mydriasis implies pupil block
  • Pharmacologic mydriatic test - Increase in IOP with mydriasis implies pupil block
  • Thymoxamine and dapiprazole (alpha-adrenergic antagonists)
    • Blocks iris dilator muscles, resulting in miosis with no effect on outflow facility

    • Decrease in IOP implies miosis has reduced pupil block

Procedures

• An AC paracentesis with subsequent injection of viscoelastic into the AC in an attempt to deepen a narrow angle can be used to differentiate appositional closure versus synechial closure. By deepening the angle, a better view of the angle could be gained in the operating suite to determine the presence of PAS. Sometimes, this procedure may be therapeutic and diagnostic.

Histologic Findings

Histologic findings depend on the causative agent; they can be fibrovascular, epithelial endothelial, or inflammatory in nature.

Staging

No formal staging scale exists.

TREATMENT

Section 6 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Medical Care

No specific medical management exists pertaining to the treatment of PAS. In general, the treatment of the underlying etiology prevents the formation of PAS.

• The appropriate management of PAS depends on the disease process that leads to PAS formation. The following drug categories may be considered depending on the primary diagnosis: topical beta-blockers, topical alpha-agonists, topical carbonic anhydrase inhibitors, oral carbonic anhydrase inhibitors, topical prostaglandin analogs, miotics, cycloplegics, and topical corticosteroids.


• Treat IOP as necessary.
  
  
  • Topical alpha-agonists, beta-blockers, carbonic anhydrase inhibitors, and prostaglandin analogs may be useful in lowering IOP in eyes with PAS.
  
  
  • Miotics are useful in pupil block due to primary angle closure but may accentuate angle closure in posterior pushing mechanisms.
  
  
  • Miotics or prostaglandin analogs likely will not be useful in cases where 360° PAS exist.


• Inflammatory states
• • Topical steroids minimize inflammation and, therefore, PAS formation.
  
  
  • Cycloplegics should be used to prevent posterior synechiae.
  
  
  • Miotics and epinephrine should be avoided because they can increase inflammation.

Surgical Care

General principles

• If PAS are to be successfully surgically treated to increase aqueous outflow, treatment should be undertaken within the first 6 months of formation. After this time, significant scarring has occurred in the TM and synechialysis will open the angle, but the TM will not be able to function normally.

• The IOP of the contralateral eye will play a role in modifying the threshold for these procedures, ie, if the IOP is elevated or on the high end of normal, this would lower the threshold because it suggests poor baseline function of the exposed TM. The converse also would be true; with a low IOP, the threshold would be increased.
• AC compression with Zeiss gonioprism may be successful in breaking pupil block or early posterior synechiae.
• Nd:YAG/argon laser iridotomy
  • This treatment is indicated when angle-closure glaucoma is the identified etiology of PAS; consider even with nonelevated IOP.

  • Prophylactic treatment of the other eye should be considered in angle-closure glaucoma.

  • Second eye risk is 50% within 5 years without an iridotomy.
• Surgical iridectomy
  • Prophylactic iridectomy is recommended in patients who receive AC intraocular lenses (IOLs) or who are aphakic.

  • Surgical iridectomy is performed in cases where an iridotomy is indicated but unable to be performed.
• Argon laser peripheral iridoplasty
  • When PAS continue to form after an iridotomy has been performed, laser iridoplasty is indicated. By creating burns in the peripheral iris causing contraction of the iris, the iris is pulled away from the TM, rupturing PAS.

  • Argon laser peripheral iridoplasty also may be useful in preventing PAS formation in a persistent narrow angle after iridotomy.

  • Argon laser peripheral iridoplasty is useful in posterior pushing mechanisms, such as plateau iris and nanophthalmos.
• Argon laser pupilloplasty is used to expand/enlarge pupil, which may break acute angle-closure attack and/or posterior synechiae.
• Nd:YAG peripheral synechialysis can be attempted in early synechial closure but may not be effective if the synechiae are firm. Laser synechialysis should be attempted before surgical goniosynechialysis.
• Surgical goniosynechialysis
  • Using a smooth-tipped irrigating cyclodialysis spatula, the iris can be separated from the TM, rupturing the PAS. This is not recommended unless there is 270° or more of synechial closure.

  • If significant glaucomatous cupping associated with visual field loss is present, a filtering operation would be preferred to goniosynechialysis.
• Cataract extraction may be useful in intumescent or subluxed lens.
• Goniophotocoagulation/panretinal photocoagulation is used to treat neovascular glaucoma.
• Choroidal tap is used to treat choroidal effusions or hemorrhage.

• Filtration surgery is indicated in continuing uncontrolled pressure despite above measures.

Consultations

A rheumatologic consultation should be considered in patients with a sterile uveitis of unknown origin.

MEDICATION

Section 7 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

No specific medical management exists pertaining to the treatment of PAS. In general, the treatment of the underlying etiology prevents the formation of PAS.

Drug Category: Adrenergic agonists

Topical adrenergic agonists, or sympathomimetics, decrease aqueous production and reduce resistance to aqueous outflow. Adverse effects include dry mouth and allergenicity.

Drug Category: Beta-blockers

Topical beta-adrenergic receptor antagonists decrease aqueous humor production by the ciliary body. Adverse effects of beta-blockers are due to systemic absorption of the drug and include decreased cardiac output and bronchial constriction. In susceptible patients, this may cause bronchospasm, bradycardia, heart block, or hypotension. Pulse rate and blood pressure should be followed in patients receiving topical beta-blocker therapy, and punctal occlusion may be performed after administration of the drops.

Drug Category: Miotic agents (parasympathomimetics)

Contract the ciliary muscle, tightening the TM and allowing increased outflow of the aqueous. Miosis results from action of these drugs on pupillary sphincter. Adverse effects include brow ache, induced myopia, and decreased vision in low light.

Drug Category: Prostaglandin analogs

Increase uveoscleral outflow of the aqueous. One mechanism of action may be through induction of metalloproteinases in ciliary body, which breaks down extracellular matrix, thereby reducing resistance to outflow through ciliary body.

Drug Category: Sympathomimetics

Increase outflow of aqueous humor through the TM and possibly through uveoscleral outflow pathway, probably by a beta2-agonist action. Also may decrease aqueous production with long-term use. Up to one third of patients will not respond to these drugs.

Drug Category: Cycloplegics/mydriatics

Can relax any ciliary muscle spasm that can cause a deep aching pain and photophobia.

Drug Category: Carbonic anhydrase inhibitors

Reduce secretion of aqueous humor by inhibiting carbonic anhydrase in the ciliary body. In acute angle closure glaucoma, carbonic anhydrase inhibitors may be given systemically, but they are used topically in refractory open-angle glaucoma patients. Topical formulations are less effective, and their duration of action is shorter than many other classes of drugs. Adverse effects of topical carbonic anhydrase inhibitors are relatively rare, but they include superficial punctate keratitis, acidosis, paresthesias, nausea, depression, and lassitude.

Drug Category: Corticosteroids

Reduces intraocular inflammation.

FOLLOW-UP

Section 8 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Further Outpatient Care

• Further care depends on the disease process that leads to PAS formation.

Deterrence/Prevention

• Appropriate and timely management of the disease processes that leads to PAS almost certainly will preclude PAS formation. This is the most important aspect of PAS management, because once PAS has formed, treatment is focused on sequelae of PAS (ie, IOP) rather than PAS itself.

Complications

• Complications include elevated IOP leading to ocular pain, decreased visual acuity, and glaucomatous optic neuropathy with visual loss.

Prognosis

• PAS should be treated within 6 months of formation if the TM is to regain normal function. Beyond this, the TM will have incurred permanent damage.
• Ultimately, prognosis depends on the adequacy of management of the etiologic process that leads to PAS formation.
• Eyes with 360° PAS may not be treated adequately with medications and, thus, require a glaucoma filtering procedure.

Patient Education

• Patient education depends on the disease process that leads to PAS formation.

MISCELLANEOUS

Section 9 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Medical/Legal Pitfalls

• It is important to use gonioscopy on any patient with elevated IOP, although the AC may appear deep, to rule out an angle closure component of the increased IOP, thus indicating specific treatment (ie, laser peripheral iridectomy).

REFERENCES

Section 10 of 10

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

• Albert DM, Jakobiec FA. Principles and Practice of Ophthalmology. 2^nd ed. Philadelphia: WB Saunders Co; 2000.
• Epstein DL, Allingham RR, Schuman JS. Chandler and Grant's Glaucoma. 4^th ed. Baltimore: Lippincott Williams & Wilkins; 1997.
• Newell FW. Ophthalmology, Principles and Concepts. 7^th ed. St. Louis: CV Mosby; 1991.
• Rouhiainen HJ, Terasvirta ME, Tuovinen EJ. Peripheral anterior synechiae formation after trabeculoplasty. Arch Ophthalmol. Feb 1988;106(2):189-91. [Medline].
• Roy FH. Ocular Differential Diagnosis. 6^th ed. Baltimore: Lippincott Williams & Wilkins; 1997.
• Schwartz AL, Whitten ME, Bleiman B. Argon laser trabecular surgery in uncontrolled phakic open angle glaucoma. Ophthalmology. Mar 1981;88(3):203-12. [Medline].

Article Last Updated: Apr 7, 2006