Peripheral Anterior Synechia Clinical Presentation

See the list below:

• 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

  • Ocular and systemic medications

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 (Open Table in a new window)

See the list below:

• 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 (Open Table in a new window)

See the list below:

• 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

  • Choroidal effusions

  • Suprachoroidal hemorrhage

  • Ciliary bock (malignant) glaucoma (aqueous misdirection)

  • Posterior segment tumors (eg, retinoblastoma, choroidal melanoma, metastasis)

  • Iris cysts or tumors

  • Ciliary body tumor, cysts, or effusions

  • Intumescent lens (phacomorphic glaucoma)

  • Ectopia lentis - Marfan, homocystinuria, Weill-Marchesani syndrome, microspherophakia, Ehlers-Danlos syndrome, trauma, and pseudoexfoliation syndromes can lead to the anterior subluxation of the lens, leading to a shallow 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)