Peripheral anterior synechiae (PAS), which were first documented by Salzmann in 1914,[1] are adhesions between the iris and trabecular meshwork. PAS may reduce outflow of aqueous humor, which leads to elevated intraocular pressure.
Peripheral anterior synechiae result from prolonged appositional contact between the iris and trabecular meshwork (as in primary angle-closure glaucoma) or from anterior chamber inflammation or neovascularization (secondary angle-closure glaucoma). Peripheral anterior synechiae may also be associated with anterior segment dysgenesis or other forms of secondary angle-closure glaucoma such as iridocorneal endothelial syndrome.
Peripheral anterior synechiae (PAS) may form in either a nonproliferative 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 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 trabecular meshwork. This membrane contracts, resulting in PAS formation and angle-closure glaucoma caused by an anterior pulling mechanism. Examples of this process include the fibrovascular membrane formed in neovascular glaucoma, proliferating abnormal endothelial cells in iridocorneal endothelial syndromes, epithelialization of the angle due to epithelial ingrowth, and 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 (PAS) lies in the ability to occlude the anterior chamber angle, resulting in a pathologic increase in intraocular pressure.
Race
Asian individuals have the highest propensity for primary angle-closure glaucoma and, thus, PAS formation.[2] This condition is not as common in Black individuals. White individuals are least likely to develop primary angle-closure glaucoma.
Sex
Females have shallower anterior chambers; therefore, they may have a greater disposition to formation of PAS.
Age
The risk of PAS formation increases with age because of a reduction in anterior chamber depth. This is due to a combination of increased thickness of the lens and laxity of the zonules, resulting in forward displacement of the lens.
Both eyes should be examined. Examination of the unaffected eye in unilateral presentations can be extremely helpful in determining the etiology of PAS formation.
The following aspects of the clinical ophthalmic examination are relevant.
Refraction because hyperopia is a risk factor for angle closure
Gonioscopy
Areas where the angle abruptly changes from open to closed indicate the presence of PAS.
The entire circumference of the angle should be examined for an open, normal-looking portion of the angle that can be compared with the regions of PAS to estimate the filtration capacity of that eye.
The anterior point of attachment or the "height" of the PAS should be noted because PAS that obstruct the central third of the trabecular meshwork are more likely to result in increased intraocular pressure.
Indentation gonioscopy
Indentation gonioscopy (with a goniolens with a small contact surface such as the Zeiss lens) should be performed to distinguish appositional closure from synechial closure.
If not directly visible, the presence of synechiae may 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 absent, a displacement can be seen on indentation.
Table 1. Appearance of Peripheral Anterior Synechiae (PAS) on Gonioscopy
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See Table
The following aspects of the clinical ophthalmic examination are relevant.
Can be mistaken for PAS.
More common and extensive in brown irides compared with blue irides.
Has a lacy and porous appearance through which angle structures can be visualized; the view can be enhanced using transillumination.
Axenfeld-Rieger syndrome (anterior segment dysgenesis) may present with an anterior, prominent uveal meshwork with an anteriorly displaced Schwalbe line that is not believed to be true PAS.
Keratic precipitates indicate an inflammatory etiology.
Polymorphous opacities at the Descemet membrane level suggest posterior polymorphous dystrophy.
Corneal guttata and/or edema suggest Chandler syndrome or 1 of the iridocorneal endothelial syndromes.
Congenital corneal opacities or sclerocornea suggest a congenital corneal defect (anterior segment dysgenesis).
Posterior embryotoxon
If the peripheral depth in a particular region is one-fourth or less of the corneal thickness, the possibility of angle closure exists (Van Herick grading technique).
Distinction should be made between peripheral and central shallowing.
Pupil block commonly results in shallowing that is greater at the periphery than at the center.
Posterior pushing mechanisms result in an equal degree of peripheral and central shallowing.
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 in the anterior iris stroma and ectropion uveae indicate 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.
Glaukomflecken suggest 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.
An intumescent lens may cause shallowing of the anterior chamber.
Any cause of vascular compromise (eg, diabetic retinopathy, central retinal artery occlusion, central retinal vein occlusion) can precipitate neovascular glaucoma.
Central retinal vein occlusion can cause choroidal or supraciliary effusions.
Choroid: Choroidal masses, effusion, or hemorrhage may result in a posterior pushing mechanism.
Neuroretinal rim pallor suggests previous attacks of acute angle-closure glaucoma.
Cupping may be present or absent; cupping may be present if there is persistently increased intraocular pressure with optic nerve damage; if intraocular pressure is normal or nearly normal, the optic nerve may not show evidence of cupping on clinical examination.
Rises when a significant portion of the angle is occluded by PAS (usually more than two-thirds).
Intraocular pressure may be normal even if a significant portion of the angle appears to be closed by PAS as a result of bridging, wherein the iris is attached anterior to the trabecular meshwork while leaving a space in front of the trabecular meshwork, allowing it to function. This tends to occur in patients with iridocorneal endothelial syndromes and congenital anomalies and is not seen in patients with primary angle-closure glaucoma.
Low intraocular pressure in the presence of extensive PAS warrants consideration of ciliary body hyposecretion, cyclodialysis, or other causes of excessive aqueous outflow.
Table 2. Summary of Important Causes of Peripheral Anterior Synechiae by Mechanism
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The causes of peripheral anterior synechiae (PAS) are as follows:
Anterior segment dysgenesis (eg, Peters anomaly, posterior embryotoxon, Axenfeld-Rieger syndrome): This is associated with prominent uveal meshwork.
Iridocorneal endothelial syndromes (essential iris atrophy, Chandler syndrome, Cogan-Reese syndrome): Epithelial-like endothelial membrane forms over the angle.
Nanophthalmos (>10 diopters hyperopia or < 20 mm axial length): Pupil block or uveal effusion narrows the angle.
Posterior polymorphous dystrophy: Epithelial-like endothelial membrane forms over the angle.
Aniridia: Iris stumps may block the trabecular meshwork.
Persistent hyperplastic primary vitreous: This is associated with microphthalmia and elongated ciliary processes. Contracture of retrolental mass and lens intumescence can also lead to PAS formation and angle closure.
Retinopathy of prematurity: This may cause shallowing of the anterior chamber, which may be due to forward movement of the lens-iris diaphragm, pupil block, choroidal detachment due to excessive photocoagulation, and retrolental fibrosis. Neovascular glaucoma may also develop in patients with chronic retinal detachment.
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), which can lead to anterior displacement of the iris diaphragm and narrowing of the angle; and (3) Lisch nodules blocking the angle recess.
Primary angle-closure glaucoma: Peripheral anterior synechiae can form while the iris is in contact with the trabecular meshwork or the cornea and can persist despite a patent iridectomy. An episode of acute angle closure tends to produce scattered PAS, whereas in chronic angle-closure glaucoma, PAS may form in a continuous, creeping manner. This is a diagnosis of exclusion: no other causes of PAS should be present.
Posterior synechiae resulting in iris bombé
Pseudophakic or aphakic pupil block
Plateau iris-flat, anterior iris insertion and anteriorly rotated ciliary processes
See the list below:
: Mechanisms include the following:See the list below:
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 are rarely caused by acute episodes of uveitis; they are due to chronic inflammatory states. If PAS develop as a result of an acute episode, the condition is more likely to occur in eyes that have a concurrent narrow angle in which an edematous iris can easily come into contact with the cornea.
Inflammatory: Idiopathic etiology is the most common. Specific inflammatory syndromes include juvenile rheumatoid arthritis, interstitial keratitis, lens-related (eg, phacolytic, lens particle, phacoanaphylactic), sarcoidosis, pars planitis, and uveitis-glaucoma-hyphema syndrome. Peripheral anterior synechiae are NOT typically found in patients experiencing a glaucomatocyclitic crisis (Posner-Schlossman syndrome) or Fuchs heterochromic iridocyclitis.
Infectious: Infectious causes include herpes simplex, herpes zoster, toxoplasmosis, and syphilis.
Filtering surgery: A shallow anterior chamber can develop after filtering surgery and lead to PAS formation. PAS usually form after at least 1 week of peripheral iris-cornea contact.
Laser trabeculoplasty[3] : A higher risk of inflammation and PAS formation is associated with narrow angles, posterior burns, high-power burns, and brown irides. Formation of PAS has also been reported to occur after selective laser trabeculoplasty[4] .
Scleral buckling surgery: Anterior displacement of the vitreous can lead to a shallow anterior chamber. Compression of the vortex veins with reduced venous drainage from the ciliary body, leading to supraciliary effusion and anterior rotation of the ciliary body, can also occur.
Intravitreal expansile gas injection: intravitreal injection of an expansile gas (eg, sulfur hexafluoride [SF6] or octafluoropropane [C3 F8]) after vitrectomy and/or scleral buckling surgery can lead to a shallow anterior chamber due a posterior pushing mechanism.
Silicone oil: Can cause pupil block, especially in eyes without a peripheral iridectomy, particularly in aphakic eyes.
Cryotherapy or panretinal photocoagulation: Can result in choroidal/ciliary body effusion, leading to a posterior pushing mechanism.
Penetrating keratoplasty: Can result in loss of angle support postoperatively, resulting in formation of PAS[5] .
Cataract extraction/intraocular lens (IOL) insertion, including phacoemulsification.
Surgery-related factors that can lead to PAS: epithelial ingrowth, wound leakage causing anterior chamber shallowing, persistent postoperative uveitis, residual lens cortex expansion pushing the iris forward
Pseudophakia-related factors that can lead to PAS: pseudophakic pupil block, the iris pushed anteriorly by the haptics of a posterior chamber IOL (increased incidence [65%-85%] with anteriorly vaulted haptics), or irritation and uveitis caused by the haptics of a sulcus- or angle-supported IOL (uveitis-glaucoma-hyphema syndrome).
See Neovascular Glaucoma for causes.
Peripheral anterior synechiae are preceded by rubeosis iridis and a fibrovascular membrane over the angle; may present with intraocular pressure elevation before frank formation of PAS occurs
Contractile forces along new vessels lead to PAS formation.
Epithelial or fibrous ingrowth may occur as a result of an epithelial membrane growing over the angle after penetrating surgery or truama.
Hyphema: A total hyphema that has not cleared by the fifth day or a large hyphema persisting for more than 10 days can lead to PAS formation and should be evacuated.
Dialysis of the iris root can lead to PAS formation during the healing process.
Vitreous in the anterior chamber leads to inflammation that can cause PAS.
Wound healing after a corneal injury (eg, iatrogenic, traumatic) can lead to epithelial proliferation that results in PAS, particularly with lacerations that cross the limbus.
Lens subluxation can occur anteriorly.
Choroidal or supraciliary effusion
Suprachoroidal hemorrhage
Aqueous misdirection syndrome (also known as ciliary block glaucoma or malignant glaucoma)
Ectopia lentis - Marfan syndrome, homocystinuria, Weill-Marchesani syndrome, microspherophakia, Ehlers-Danlos syndrome, trauma, and pseudoexfoliation syndrome can cause anterior subluxation of the lens due to zonular laxity.
Miotics - cause a forward displacement of the lens-iris diaphragm
Anticholinergic agents (eg, topical cycloplegics or systemic atropine, antihistamines, antiparkinsonism drugs, antipsychotics, botulinum toxin) - cause pupillary dilation, which may result in increased pupil block in a predisposed eye
Adrenergics (eg, topical or systemic epinephrine, central nervous system stimulants, appetite suppressants, bronchodilators, hallucinogenic agents) - cause pupillary dilation, which may result in increased pupil block in a predisposed eye 0
Medications that can cause ciliary effusions (eg, sulfonamides, tetracycline)
Provocative testing - 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 glaucoma.
Dark room: Increase in intraocular pressure with mydriasis implies pupil block.
Pharmacologic mydriatic test: Increase in intraocular pressure with mydriasis implies pupil block.
Block iris dilator muscles, resulting in miosis with no effect on outflow facility.
Decrease intraocular pressure, which implies that miosis has reduced pupil block.
A paracentesis with injection of viscoelastic into the anterior chamber done in an attempt to deepen a narrow angle can be used to differentiate appositional closure from synechial closure. By deepening the angle, a better view of the angle can be obtained to determine the presence of PAS. Sometimes, this procedure can be both diagnostic and therapeutic.
The following drug categories may be considered, depending on the primary diagnosis: topical β-blockers, topical α-agonists, topical carbonic anhydrase inhibitors, oral carbonic anhydrase inhibitors, topical prostaglandin agonists, miotics, cycloplegics, and topical corticosteroids.
Treat elevated intraocular pressure, as necessary.
Topical α-agonists, β-blockers, carbonic anhydrase inhibitors, and prostaglandin agonists may be useful in lowering intraocular pressure in eyes with PAS.
Miotics are useful in the treatment of pupil block due to primary angle-closure but may exacerbate angle closure due to posterior pushing mechanisms.
Miotics or prostaglandin analogs are unlikely to be useful in cases in which the PAS extent is 360 degrees.
Treat inflammation, as necessary.
Topical steroids minimize inflammation and, therefore, PAS formation.
Cycloplegics should be used to prevent formation of posterior synechiae.
Miotics and epinephrine should be avoided because they can increase inflammation.
General principles in the surgical treatment of peripheral anterior synechiae (PAS) are as follows:
As much as possible, the pathologic process causing PAS formation should be addressed. Various laser and surgical procedures may be indicated, depending on the etiology.
If PAS have already formed, surgical treatment to restore aqueous outflow through the trabecular meshwork should be undertaken within the first 6 months of formation.[8] After this time, significant trabecular meshwork (TM) scarring has already occurred, and the TM may no longer function normally, despite an anatomically successful synechialysis.[9]
It is possible, although unlikely, to break a pupil block or early PAS by performing anterior chamber compression using a gonioprism such as a Zeiss goniolens.
Indicated when pupil block is the cause of or contributes to the formation of PAS. Consider performing this even when the intraocular pressure is not yet elevated.
Prophylactic treatment of the other eye should be considered in patients with primary angle-closure glaucoma.
The fellow eye's angle closure risk is 50% within 5 years without an iridotomy in patients with primary angle-closure glaucoma.
Prophylactic iridectomy is recommended for patients who receive anterior chamber intraocular lenses or who have aphakia.
Surgical iridectomy can be performed when a laser iridotomy is indicated but cannot be performed.
Indicated when PAS continue to form or the angle fails to widen after a patent iridotomy. Creating burns in the peripheral iris causes the iris to contract and pull away from the TM.
Useful when posterior pushing mechanisms, such as plateau iris and nanophthalmos, are involved. [RK1]
Has limited usefulness in anterior pulling mechanisms such as uveitis.
Argon laser pupilloplasty is used to expand or enlarge the pupil, which may break an acute angle-closure attack and/or posterior synechiae.
Lens extraction is needed if the lens size, shape, or position is significantly contributing to PAS formation.
See the list below:
[8, 10, 11, 12] is an effective surgical modality when the etiology of the PAS formation is primary angle closure. See the list below:
A spatula or microforceps can be used to pull the iris away from the TM to break the PAS. This is not recommended unless synechial closure is 270 degrees or greater. This can be performed under either direct or indirect visualization of the meshwork. Continuous irrigation or a viscoelastic is used to maintain the anterior chamber during the procedure.
If significant glaucomatous cupping and visual field loss are present, a filtering operation may be required in addition to goniosynechialysis.
Concurrent lens extraction (independent of the presence of a cataract) is strongly recommended when goniosynechialysis is performed because removal of the lens helps to further widen the angle, which facilitates intraoperative access and eliminates a potential contributing etiology of the angle closure.
Trabeculectomy,[13] despite being the gold standard glaucoma-filtering procedure, has a generally lower rat of success in patients with primary angle-closure glaucoma and higher rates of choroidal effusion, aqueous misdirection, and flat anterior chamber. In some patients with secondary angle-closure glaucoma, the pathologic process reduces the likelihood of trabeculectomy success; expamples include neovascular glaucoma and iridocorneal endothelial syndromes.[2]
Primary tube shunt surgery can be considered for patients with primary angle-closure glaucoma and is the first-choice procedure for certain secondary etiologies.
Insertion of the Ex-PRESS Mini Shunt is a potential alternative to trabeculectomy. More research in this area is required to fully evaluate this technology in this context.
Goniophotocoagulation can be used to treat the open stage of neovascular glaucoma.
Choroidal tap is used to treat choroidal effusions or hemorrhage.
No specific medication that can treat peripheral anterior synechiae (PAS) is available. Some medications may act on the underlying etiology to prevent the formation or progression of PAS. Most medications are only capable of treating the main sequela of PAS, which is elevation of intraocular pressure (IOP).
Clinical Context:
Reduces intraocular pressure. 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 allergic reactions.
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 monitored in patients receiving topical beta-blocker therapy, and punctal occlusion may need to 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.
Causes contraction of the ciliary muscle which tightens the trabecular meshwork and allows increased outflow of aqueous. Miosis results from action of these drugs on the pupillary sphincter. Adverse effects include brow ache, induced myopia, and decreased vision in low light.
Increase uveoscleral outflow of aqueous humor. One mechanism of action may be through induction of metalloproteinases in ciliary body, which breaks down extracellular matrix, thereby reducing resistance to outflow through the ciliary body.
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.
Causes pupil dilation which may help break or prevent posterior synechiae formation. Causes relaxation of the ciliary muscle which can deepen the anterior chamber.
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 there is a delay of the surgery intended to lower the 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.
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.
Appropriate and timely management of the disease process that can lead to PAS is necessary to prevent PAS from forming or progressing. This is the most important aspect of management because once PAS have formed treatment shifts to managing the sequela of PAS, intraocular pressure elevation, rather than the PAS itself.
Complications include elevated intraocular pressure leading to ocular pain, decreased visual acuity, and glaucomatous optic neuropathy with vision loss.
Peripheral anterior synechiae should be treated within 6 months of formation if the trabecular meshwork is to regain normal function[8] . Beyond this, the trabecular meshwork will have sustained permanent damage.
Ultimately, prognosis depends on the adequacy of management of the etiologic process that led to PAS formation.
Eyes with 360 degrees of PAS are unlikely to be treated adequately with medications and are likely to require a glaucoma filtering procedure.
Patient education depends on the disease process that led to PAS formation. Emphasis must be placed on the necessity of prompt treatment to prevent the progression of the condition.
What is peripheral anterior synechiae (PAS)?What is the pathophysiology of peripheral anterior synechiae (PAS)?What is the prevalence of peripheral anterior synechiae (PAS)?What is the morbidity and mortality associated with peripheral anterior synechiae (PAS)?What are the racial predilections for peripheral anterior synechiae (PAS)?Why are women at higher risk for peripheral anterior synechiae (PAS)?How does age impact the risk for peripheral anterior synechiae (PAS)?Which clinical history findings are characteristic of peripheral anterior synechiae (PAS)?What is the focus of the clinical history for the evaluation of peripheral anterior synechiae (PAS)?Which physical findings are characteristic of peripheral anterior synechiae (PAS)?What causes peripheral anterior synechiae (PAS)?What are the differential diagnoses for Peripheral Anterior Synechia?Which factors determine the treatment of peripheral anterior synechiae (PAS)?Which lab tests are performed in the workup of peripheral anterior synechiae (PAS)?What is the role of imaging studies in the workup of peripheral anterior synechiae (PAS)?What is the role of provocative testing in the workup of peripheral anterior synechiae (PAS)?What is the role of paracentesis in the workup of peripheral anterior synechiae (PAS)?Which histologic findings are characteristic of peripheral anterior synechiae (PAS)?How is peripheral anterior synechiae (PAS) staged?How is peripheral anterior synechiae (PAS) treated?What is the role of medications in the treatment of peripheral anterior synechiae (PAS)?What is the role of surgery in the treatment of peripheral anterior synechiae (PAS)?Which specialist consultations are beneficial to patients with peripheral anterior synechiae (PAS)?What is included in the long-term monitoring of peripheral anterior synechiae (PAS)?Which medications are used in the treatment of peripheral anterior synechiae (PAS)?Which medications in the drug class Ophthalmics, Other are used in the treatment of Peripheral Anterior Synechia?Which medications in the drug class Carbonic anhydrase inhibitors are used in the treatment of Peripheral Anterior Synechia?Which medications in the drug class Cycloplegics/mydriatics are used in the treatment of Peripheral Anterior Synechia?Which medications in the drug class Antiglaucoma, Prostaglandin Agonists are used in the treatment of Peripheral Anterior Synechia?Which medications in the drug class Miotic agents (parasympathomimetics) are used in the treatment of Peripheral Anterior Synechia?Which medications in the drug class Beta-blockers are used in the treatment of Peripheral Anterior Synechia?Which medications in the drug class Adrenergic agonists are used in the treatment of Peripheral Anterior Synechia?Which factors determine the long-term care for patients with peripheral anterior synechiae (PAS)?How is the progression of peripheral anterior synechiae (PAS) prevented?What are the possible complications of peripheral anterior synechiae (PAS)?What is the prognosis for peripheral anterior synechiae (PAS)?What is included in the patient education about peripheral anterior synechiae (PAS)?
Maria Hannah Pia U de Guzman, MD, DPBO, FPAO, Consultant, Department of Ophthalmology, Glaucoma Section, Asian Hospital and Medical Center; Consultant, Eye Institute, Glaucoma Service, St Luke’s Medical Center, Philippines
Disclosure: Nothing to disclose.
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
Andrew J Tatham, MD, MBA, FRCOphth, FEBO, FRCS(Ed), 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; Santen; Thea; Glaukos<br/>Serve(d) as a speaker or a member of a speakers bureau for: Allergan; Heidelberg Engineering; Alcon; Santen.
Baseer U Khan, MD, Associate Professor of Ophthalmology, University of Toronto Faculty of Medicine; Ophthalmologist, Clarity Eye Institute, Canada
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
