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.
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.
United States
Peripheral anterior synechiae occurs infrequently.
International
Peripheral anterior synechiae occurs infrequently.
The morbidity of peripheral anterior synechiae lies in its ability to occlude the angle and result in a pathological increase in intraocular pressure.
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.
Females have shallower anterior chambers; therefore, they may have a greater disposition to forming peripheral anterior synechiae.
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.
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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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Table 2. Summary of Important Mechanisms and Causes of Peripheral Anterior Synechiae
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For peripheral anterior synechiae (PAS), perform an inflammatory and infectious workup as required.
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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 depend on the causative agent; they can be fibrovascular, epithelial endothelial, or inflammatory in nature.
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.
General principles in the surgical treatment of peripheral anterior synechiae are as follows:
A rheumatologic consultation should be considered in patients with a sterile uveitis of unknown origin.
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.
Clinical Context: Selective alpha2-receptor that reduces aqueous humor formation and increases uveoscleral outflow.
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.
Topical adrenergic agonists, or sympathomimetics, decrease aqueous production and reduce resistance to aqueous outflow. Adverse effects include dry mouth and allergenicity.
Clinical Context: Nonselective beta-adrenergic blocking agent that lowers IOP by reducing aqueous humor production and possibly increases outflow of aqueous humor.
Clinical Context: Selectively blocks beta1-adrenergic receptors with little or no effect on beta2-receptors. Reduces IOP by reducing production of aqueous humor.
Clinical Context: May reduce elevated and normal IOP, with or without glaucoma, by reducing production of aqueous humor or by outflow.
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.
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.
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.
Clinical Context: May decrease IOP by increasing outflow of aqueous humor.
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.
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.
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.
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.
Can relax any ciliary muscle spasm that can cause a deep aching pain and photophobia.
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.
Clinical Context: Reduces aqueous humor formation by inhibiting enzyme carbonic anhydrase, which results in decreased IOP.
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.
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.
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
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.
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.
Further care depends on the disease process that leads to peripheral anterior synechiae (PAS) formation.
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 include elevated intraocular pressure leading to ocular pain, decreased visual acuity, and glaucomatous optic neuropathy with visual loss.
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Patient education depends on the disease process that leads to peripheral anterior synechiae formation.
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 presentPosterior pushing mechanism, postoperatively shallow AC, or from iris bombé PAS with new vessels, multiple sites Neovascularization 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)
Iris Pulled Forward Iris Pushed Forward Neovascular membrane ICE membrane Posterior polymorphous dystrophy Epithelial/fibrous ingrowth
UveitisPupil block Trauma
Inflammatory syndromes
Infectious
Lens relatedPrimary angle-closure glaucoma
Posterior synechiae resulting in iris bombé
Pseudophakic or aphakic pupil block
IridoschisisFlat anterior chamber Plateau iris
Posterior pushingPostsurgical
TraumaChoroidal 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)
NeurofibromatosisArgon laser trabeculoplasty