Peripheral Anterior Synechia

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Background

Peripheral anterior synechiae (PAS), which were first described by Barkan in 1938, are adhesions between the iris and trabecular meshwork. PAS may reduce outflow of aqueous humor and may lead to raised intraocular pressure.

PAS result from prolonged appositional contact between the iris and trabecular meshwork (as in primary angle closure) or from anterior chamber inflammation or neovascularization (secondary angle closures). PAS may also be associated with anterior segment dysgenesis or other forms of secondary angle closure such as iridocorneal endothelial (ICE) syndrome.

Pathophysiology

Peripheral anterior synechiae may form under the following 2 circumstances: a nonproliferative state or a proliferative state.

Apposition of the iris against the trabecular meshwork as a result of pupil block or a posterior pushing mechanism without any inflammation can result in continuous peripheral anterior synechiae. These continuous peripheral anterior synechiae 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 trabecular meshwork, creating the peripheral anterior synechiae. 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.

Epidemiology

Frequency

United States

Peripheral anterior synechiae occurs infrequently.

International

Peripheral anterior synechiae occurs infrequently.

Mortality/Morbidity

The morbidity of peripheral anterior synechiae lies in its ability to occlude the angle and result in a pathological increase in intraocular pressure.

Race

Asian persons have the highest propensity for primary angle-closure glaucoma and, thus, peripheral anterior synechiae formation.[1] This condition is not as common in blacks. Whites are least likely to develop primary angle-closure glaucoma.

Sex

Females have shallower anterior chambers; therefore, they may have a greater disposition to forming peripheral anterior synechiae.

Age

The risk of peripheral anterior synechiae formation increases with age because of a reduction in anterior chamber 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.

History

See the list below:

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.

Table 1. Description of PAS on gonioscopy



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See the list below:

Causes

Table 2. Summary of Important Mechanisms and Causes of Peripheral Anterior Synechiae



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See the list below:

Laboratory Studies

For peripheral anterior synechiae (PAS), perform an inflammatory and infectious workup as required.

Imaging Studies

See the list below:

Other Tests

See the list below:

Procedures

An anterior chamber paracentesis with subsequent injection of viscoelastic into the anterior chamber 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 peripheral anterior synechiae. 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.

Medical Care

No specific medical management exists pertaining to the treatment of peripheral anterior synechiae (PAS). In general, the treatment of the underlying etiology prevents the formation of peripheral anterior synechiae.

Surgical Care

General principles in the surgical treatment of peripheral anterior synechiae are as follows:

Consultations

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

Medication Summary

No specific medical management exists pertaining to the treatment of peripheral anterior synechiae (PAS). In general, the treatment of the underlying etiology prevents the formation of peripheral anterior synechiae.

Brimonidine (Alphagan)

Clinical Context:  Selective alpha2-receptor that reduces aqueous humor formation and increases uveoscleral outflow.

Apraclonidine (Iopidine)

Clinical Context:  Reduces elevated, as well as normal, IOP whether or not accompanied by glaucoma. A relatively selective alpha-adrenergic agonist that does not have significant local anesthetic activity. Has minimal cardiovascular effects.

Class Summary

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

Levobunolol (AKBeta, Betagan)

Clinical Context:  Nonselective beta-adrenergic blocking agent that lowers IOP by reducing aqueous humor production and possibly increases outflow of aqueous humor.

Betaxolol ophthalmic (Betoptic, Betoptic S)

Clinical Context:  Selectively blocks beta1-adrenergic receptors with little or no effect on beta2-receptors. Reduces IOP by reducing production of aqueous humor.

Timolol maleate (Timoptic, Timoptic XE, Blocadren)

Clinical Context:  May reduce elevated and normal IOP, with or without glaucoma, by reducing production of aqueous humor or by outflow.

Class Summary

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.

Pilocarpine (Akarpine, Adsorbocarpine, Ocusert Pilo-40, Pilagan, Pilocar)

Clinical Context:  Directly stimulates cholinergic receptors in the eye, decreasing resistance to aqueous humor outflow.

Instillation frequency and concentration are determined by patients' response. Individuals with heavily pigmented irides may require higher strengths.

If other glaucoma medications also are being used, at bedtime, use gtt at least 5 min before gel.

Patients may be maintained on pilocarpine as long as IOP is controlled and there is no deterioration in visual fields. May use alone or in combination with other miotics, beta-adrenergic blocking agents, epinephrine, carbonic anhydrase inhibitors, or hyperosmotic agents to decrease IOP.

Class Summary

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.

Latanoprost (Xalatan)

Clinical Context:  May decrease IOP by increasing outflow of aqueous humor.

Class Summary

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.

Epinephrine (Epifrin, Glaucon) or Dipivefrin (AKPro, Propine)

Clinical Context:  Epinephrine lowers IOP by increasing outflow and reducing production of aqueous humor. Used as adjunct to miotic or beta-blocker therapy. Combination of miotic and sympathomimetic has additive effects in lowering IOP.

Dipivefrin is converted to epinephrine in eye by enzymatic hydrolysis. Appears to act by decreasing aqueous production and enhancing outflow facility. Has same therapeutic effect as epinephrine with fewer local and systemic adverse effects. May be used as an initial therapy or as an adjunct with other antiglaucoma agents for the control of IOP.

Class Summary

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.

Atropine IV/IM (Atropisol, Atropair, Isopto)

Clinical Context:  Acts at parasympathetic sites in smooth muscle to block response of sphincter muscle of iris and muscle of ciliary body to acetylcholine, causing mydriasis and cycloplegia. Phenylephrine (2.5% or 10% solution) concurrently with atropine may prevent formation of synechiae by producing wide dilation of pupil.

Class Summary

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

Acetazolamide (Diamox, Diamox Sequels)

Clinical Context:  Inhibits enzyme carbonic anhydrase, reducing rate of aqueous humor formation, which, in turn, reduces IOP. Used for adjunctive treatment of chronic simple (open-angle) glaucoma and secondary glaucoma and preoperatively in acute angle-closure glaucoma when delay of surgery desired to lower IOP.

Methazolamide (Neptazane)

Clinical Context:  Reduces aqueous humor formation by inhibiting enzyme carbonic anhydrase, which results in decreased IOP.

Dorzolamide (Trusopt, Cosopt)

Clinical Context:  Used concomitantly with other topical ophthalmic drug products to lower IOP. If more than one ophthalmic drug is being used, administer the drugs at least 10 min apart. Reversibly inhibits carbonic anhydrase, reducing hydrogen ion secretion at renal tubule and increasing renal excretion of sodium, potassium bicarbonate, and water to decrease production of aqueous humor.

Brinzolamide (Azopt)

Clinical Context:  Catalyzes reversible reaction involving hydration of carbon dioxide and dehydration of carbonic acid. May use concomitantly with other topical ophthalmic drug products to lower IOP. If more than one topical ophthalmic drug is being used, administer drugs at least 10 min apart.

Dorzolamide HCl/ timolol maleate (Cosopt)

Clinical Context:  Carbonic anhydrase inhibitor that may decrease aqueous humor secretion, causing a decrease in IOP. Presumably slows bicarbonate ion formation with subsequent reduction in sodium and fluid transport.

Timolol is nonselective beta-adrenergic receptor blocker that decreases IOP by decreasing aqueous humor secretion and may slightly increase outflow facility. Both agents administered together bid may result in additional IOP reduction compared with either component administered alone, but reduction is not as much as when dorzolamide tid and timolol bid are administered concomitantly

Class Summary

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.

Prednisolone ophthalmic (Pred Forte)

Clinical Context:  Treats acute inflammations following eye surgery or other types of insults to eye. Decreases inflammation by suppressing migration of polymorphonuclear leukocytes and reversing increased capillary permeability. In cases of bacterial infections, concomitant use of anti-infective agents is mandatory; if signs and symptoms do not improve after 2 days, reevaluate patient. Dosing may be reduced, but advise patients not to discontinue therapy prematurely.

Class Summary

Reduces intraocular inflammation.

Further Outpatient Care

Further care depends on the disease process that leads to peripheral anterior synechiae (PAS) formation.

Deterrence/Prevention

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

Complications

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

Prognosis

See the list below:

Patient Education

Patient education depends on the disease process that leads to peripheral anterior synechiae formation.

Author

Andrew J Tatham, MBChB, FRCOphth, FRCSEd, FEBO, Consultant Ophthalmic Surgeon, Princess Alexandra Eye Pavilion; Honorary Senior Clinical Lecturer, University of Edinburgh; NHS Scotland Career Research Fellow

Disclosure: Serve(d) as a director, officer, partner, employee, advisor, consultant or trustee for: Allergan; Novartis <br/>Serve(d) as a speaker or a member of a speakers bureau for: Allergan; Heidelberg Engineering; Alcon; Santen.

Specialty Editors

Simon K Law, MD, PharmD, Clinical Professor of Health Sciences, Department of Ophthalmology, Jules Stein Eye Institute, University of California, Los Angeles, David Geffen School of Medicine

Disclosure: Nothing to disclose.

J James Rowsey, MD, Former Director of Corneal Services, St Luke's Cataract and Laser Institute

Disclosure: Nothing to disclose.

Chief Editor

Hampton Roy, Sr, MD, Associate Clinical Professor, Department of Ophthalmology, University of Arkansas for Medical Sciences

Disclosure: Nothing to disclose.

Additional Contributors

Baseer U Khan, MD,

Disclosure: Nothing to disclose.

Bradford Shingleton, MD, Assistant Clinical Professor of Ophthalmology, Harvard Medical School; Consulting Staff, Department of Ophthalmology, Massachusetts Eye and Ear Infirmary

Disclosure: Nothing to disclose.

Iqbal Ike K Ahmed, MD, FRCSC, Clinical Assistant Professor, Department of Ophthalmology, University of Utah

Disclosure: Nothing to disclose.

Khalid Hasanee, MD, Glaucoma and Anterior Segment Fellow, Department of Ophthalmology, University of Toronto

Disclosure: Nothing to disclose.

References

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  3. Fukuda R, Usui T, Tomidokoro A, Mishima K, Matagi N, Miyai T, et al. Noninvasive observations of peripheral angle in eyes after penetrating keratoplasty using anterior segment fourier-domain optical coherence tomography. Cornea. 2012 Mar. 31(3):259-63. [View Abstract]
  4. Lin Z, Liang Y, Wang N, Li S, Mou D, Fan S, et al. Peripheral anterior synechia reduce extent of angle widening after laser peripheral iridotomy in eyes with primary angle closure. J Glaucoma. 2013 Jun-Jul. 22(5):374-9. [View Abstract]
  5. Harasymowycz PJ, Papamatheakis DG, Ahmed I, Assalian A, Lesk M, Al-Zafiri Y, et al. Phacoemulsification and goniosynechialysis in the management of unresponsive primary angle closure. J Glaucoma. 2005 Jun. 14(3):186-9. [View Abstract]
  6. Teekhasaenee C, Ritch R. Combined phacoemulsification and goniosynechialysis for uncontrolled chronic angle-closure glaucoma after acute angle-closure glaucoma. Ophthalmology. 1999 Apr. 106(4):669-74; discussion 674-5. [View Abstract]
  7. Takanashi T, Masuda H, Tanito M, Nonoyama S, Katsube T, Ohira A. Scleral indentation optimizes visualization of anterior chamber angle during goniosynechialysis. J Glaucoma. 2005 Aug. 14(4):293-8. [View Abstract]
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  14. Roy FH. Ocular Differential Diagnosis. 6th ed. Baltimore: Lippincott Williams & Wilkins; 1997.
Description of PAS Associations Possible Conditions
Broad bands
 PAS to all levels but not to cornea No bridging usually presentAngle-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 sitesNeovascularization
Scattered, irregular
 PAS tent and form columns up to, but not on, the corneaIridocyclitis with keratic and trabecular precipitates
 Small PAS to scleral spurPost-argon laser trabeculoplasty (ALT)
Iris Pulled Forward Iris Pushed Forward
Neovascular membrane ICE membrane Posterior polymorphous dystrophy Epithelial/fibrous ingrowth



Uveitis



Pupil block
Trauma



Inflammatory syndromes



Infectious



Lens related



Primary angle-closure glaucoma



Posterior synechiae resulting in iris bombé



Pseudophakic or aphakic pupil block



Iridoschisis



Flat anterior chamberPlateau iris



Posterior pushing



Postsurgical



Trauma



Choroidal effusion



-Posterior uveitis



-CRVO



-Nanophthalmos



-Post-pan retinal photocoagulation (PRP) or cryotherapy



Suprachoroidal hemorrhage



Ciliary block (malignant) glaucoma (aqueous misdirection)



Posterior segment tumors



-Retinoblastoma



-Choroidal melanoma or metastasis



Iris cyst or tumor



Ciliary body cyst, tumor, or effusion



Contracting retrolental tissue



-Retinopathy of prematurity



-Persistent hyperplastic primary vitreous (PHPV)



Postscleral bucking surgery



Anterior lens subluxation (ectopia lentis)



Lens intumescence (phacomorphic)



Neurofibromatosis



Argon laser trabeculoplasty