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.
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.
Peripheral anterior synechiae 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 peripheral anterior synechiae formation. Specific inquiry should include the following:
History of ocular infection, surgery, or trauma
Family history of glaucoma or other eye disease
Medical history, specifically inquiring about rheumatological disease and inflammatory syndromes
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 peripheral anterior synechiae.
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 peripheral anterior synechiae 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 peripheral anterior synechiae to estimate the filtration capabilities of the eye.
The point of anterior attachment of peripheral anterior synechiae should be noted because peripheral anterior synechiae that obstruct the central third of the trabecular meshwork are more likely to result in increased intraocular pressure.
Table 1. Description of PAS on gonioscopy
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Prominent uveal meshwork (must be differentiated from peripheral anterior synechiae)
Can be confused for peripheral anterior synechiae
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 peripheral anterior synechiae.
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
Anterior chamber 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 anterior chamber.
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 iridocorneal endothelial 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 anterior chamber.
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.
Central retinal vein occlusion 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 intraocular pressure with optic nerve damage; if intraocular pressure 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 peripheral anterior synechiae (usually > two thirds).
Intraocular pressure may be normal even if a significant portion of the angle has been closed by peripheral anterior synechiae due to the phenomenon of bridging, ie, when the iris has attached anterior to the trabecular meshwork, leaving a space in front of the trabecular meshwork allowing it to function. This typically occurs in iridocorneal endothelial syndromes and congenital anomalies and is not seen in primary angle closure.
Postoperatively, low intraocular pressure in the presence of extensive peripheral anterior synechiae also warrants consideration for cyclodialysis.
Table 2. Summary of Important Mechanisms and Causes of Peripheral Anterior Synechiae
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Congenital
Anterior segment dysgenesis (ie, Peters anomaly, posterior embryotoxon, Axenfeld anomaly, Rieger anomaly) - Associated with prominent uveal meshwork. See Gonioscopy in Physical.
Iridocorneal endothelial 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 trabecular meshwork.
Persistent hyperplastic primary vitreous - Associated with microphthalmia and elongated ciliary processes. Contracture of retrolental mass and lens intumescence also can lead to peripheral anterior synechiae and angle closure.
Retinopathy of prematurity
Neurofibromatosis - Possible mechanisms of peripheral anterior synechiae 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 - Peripheral anterior synechiae can form while the iris is in contact with the trabecular meshwork or the cornea and can persist after an iridectomy. Peripheral anterior synechiae also may form during an acute attack in which there would be scattered peripheral anterior synechiae formation, or they may occur in a chronic state in which case peripheral anterior synechiae would form in a continuous, creeping, angle-closure manner. This is a diagnosis of exclusion (ie, there cannot be any other etiologies for peripheral anterior synechiae 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
Peripheral anterior synechiae is rarely caused by acute episodes of uveitis but rather in chronic inflammatory states. If peripheral anterior synechiae 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. Peripheral anterior synechiae is typically 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 anterior chamber can result after filtering surgery, leading to peripheral anterior synechiae due to early postoperative wound leaks or overfiltration. peripheral anterior synechiae usually occurs after 1 week of peripheral iris-cornea touch.
Argon laser trabeculoplasty[2] - Higher risk of inflammation and peripheral anterior synechiae 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 anterior chamber. 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 [C3 F8]) after vitrectomy and/or scleral buckling surgery can lead a shallow anterior chamber 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 peripheral anterior synechiae[3]
Cataract extraction/IOL insertion, including phacoemulsification
Surgical-related processes that can lead to peripheral anterior synechiae - Epithelial ingrowth; wound leak, leading to a shallow anterior chamber; persistent postoperative uveitis; residual lens cortex "fluffing"; and pushing the iris forward
Pseudophakic-related processes that can lead to peripheral anterior synechiae - Pseudophakic pupil block, the haptics of a posterior chamber lens can push the iris forward, leading to peripheral anterior synechiae 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 anterior chamber lenses
Neovascular glaucoma
See Glaucoma, Neovascular for causes.
Peripheral anterior synechiae preceded by rubeosis iridis and fibrovascular membrane - May have intraocular pressure elevation prior to obvious peripheral anterior synechiae formation
Contractile forces along new vessels lead to peripheral anterior synechiae.
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 peripheral anterior synechiae and should be evacuated.
Dialysis of the iris root can lead to peripheral anterior synechiae in the healing process.
Vitreous in the anterior chamber leads to inflammation that can cause peripheral anterior synechiae.
Wound healing after a corneal wound (eg, iatrogenic, traumatic) can lead to epithelial proliferation that results in peripheral anterior synechiae, particularly lacerations that cross the limbus.
Lens subluxation anteriorly
Physical - Posterior pushing mechanisms resulting in appositional closure, then synechial closure
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 anterior chamber 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)
Useful in evaluating the angle in angle-closure glaucoma
Can delineate peripheral anterior synechiae and determine their extent
May demonstrate a small space between peripheral anterior synechiae and the trabecular meshwork, suggesting that the trabecular meshwork may still be capable of normal function
May be useful in demonstrating supraciliary fluid
Corneal specular microscopy - Useful in identifying iridocorneal endothelial or posterior polymorphous dystrophy cells
Provocative testing - This test measures intraocular pressure 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 intraocular pressure with mydriasis implies pupil block
Pharmacologic mydriatic test - Increase in intraocular pressure 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 intraocular pressure implies miosis has reduced pupil block
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.
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.
The appropriate management of peripheral anterior synechiae depends on the disease process that leads to peripheral anterior synechiae 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 intraocular pressure (IOP) as necessary.
Topical alpha-agonists, beta-blockers, carbonic anhydrase inhibitors, and prostaglandin analogs may be useful in lowering intraocular pressure in eyes with peripheral anterior synechiae.
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° peripheral anterior synechiae exist.
General principles in the surgical treatment of peripheral anterior synechiae are as follows:
If peripheral anterior synechiae are to be successfully surgically treated to increase aqueous outflow, treatment should be undertaken within the first 612 months of formation according to conventional thinking. After this time, significant scarring has occurred in the trabecular meshwork and synechialysis will open the angle, but the trabecular meshwork will not be able to function normally. However, there has been more recent literature to suggest that peripheral anterior synechiae from an appositional etiology may be amenable to treatment even a few years after formation.
The intraocular pressure of the contralateral eye will play a role in modifying the threshold for these procedures, ie, if the intraocular pressure is elevated or on the high end of normal, this would lower the threshold because it suggests poor baseline function of the exposed trabecular meshwork. The converse also would be true; with a low intraocular pressure, the threshold would be increased.
Anterior chamber compression with Zeiss gonioprism may be successful, although unlikely, 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 peripheral anterior synechiae; consider even with nonelevated intraocular pressure.
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 anterior chamber intraocular lenses (IOLs) or who are aphakic.
Surgical iridectomy is performed in cases where a laser iridotomy is indicated but unable to be performed.
Argon laser peripheral iridoplasty
When peripheral anterior synechiae 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 trabecular meshwork.
Argon laser peripheral iridoplasty also may be useful in preventing peripheral anterior synechiae formation in a persistent narrow angle after iridotomy.[4]
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[5, 6, 7, 8]
Surgical lysis of synechiae has been shown to be an effective surgical modality when the etiology of the peripheral anterior synechiae formation has been secondary to primary angle closure.
Using a smooth-tipped irrigating cyclodialysis spatula, the iris can be separated from the TM, rupturing the peripheral anterior synechiae. This is not recommended unless there is 270° or more of synechial closure. This is performed under either direct or indirect visualization of the meshwork intraoperatively.
More recently, goniosynechialysis has been described using intraocular microforceps.
If significant glaucomatous cupping associated with visual field loss is present, a filtering operation would be performed in addition to goniosynechialysis.
Concurrent lens extraction (independent of the presence of a cataract) is strongly recommended when performing goniosynechialysis as removal of the lens helps to further widen the angle, which facilitates intraoperative access as well as removing an etiologic contribution to angle closure.
Glaucoma filtering procedures
Trabeculectomy,[9] while the criterion standard of glaucoma filtering procedure, has generally had lower success rates in angle closure patients in the case of primary angle closure with higher rates of choroidal effusions, aqueous misdirection, and flat anterior chambers. In secondary angle closures, the etiologic process further reduces the likelihood of success such as in neovascular glaucoma or iridocorneal endothelial (ICE) syndromes.[1]
Primary tube shunt surgery is certainly a consideration in primary angle closure patients, and is strongly advised for secondary etiologies.
The Mini Express Shunt is a potential alternative to trabeculectomy as well, given its preclusion to an iridectomy and relatively controlled outflow. More research in this area is required to fully evaluate this technology in this context.
Goniophotocoagulation/panretinal photocoagulation is used to treat neovascular glaucoma.
Choroidal tap is used to treat choroidal effusions or hemorrhage.
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:
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.
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.
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.
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.
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:
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.
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.
Peripheral anterior synechiae should be treated within 6 months of formation if the trabecular meshwork is to regain normal function. Beyond this, the trabecular meshwork will have incurred permanent damage.
Ultimately, prognosis depends on the adequacy of management of the etiologic process that leads to peripheral anterior synechiae formation.
Eyes with 360-degree peripheral anterior synechiae may not be treated adequately with medications and, thus, require a glaucoma filtering procedure.
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
