Peripheral Anterior Synechia Clinical Presentation

Updated: Mar 19, 2021
  • Author: Maria Hannah Pia U de Guzman, MD, DPBO, FPAO; Chief Editor: Hampton Roy, Sr, MD  more...
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Presentation

History

Peripheral anterior synechiae (PAS) can present in the following ways:

  • Acute angle closure with the classic constellation of symptoms, including ocular pain, headaches, blurred vision, and haloes
  • Subacute history of multiple transient attacks of intraocular pressure elevation, which consist of mild ocular pain, reduced vision, and haloes
  • Chronic angle closure, which is often asymptomatic but may present with reduced vision due to corneal edema or end-stage glaucomatous optic neuropathy

The history can be valuable in identifying the process or processes that may have led to PAS 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 rheumatologic disease and inflammatory syndromes, diabetes mellitus, and hypertension
  • Use of ocular and systemic medications
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Physical

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
  • Anterior chamber angle
    • 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 (Open Table in a new window)

General Appearance

Detailed Appearance

Possible Causes

Broad bands

 

PAS to all levels but not to cornea.

Bridging usually not present.

Angle-closure glaucoma

 

PAS to all levels, sometimes to cornea.

Bridging may be present.

Posterior pushing mechanism, post-operative shallow anterior chamber, or 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 

The following aspects of the clinical ophthalmic examination are relevant. 

  • Prominent uveal meshwork (must be differentiated from PAS)
    • 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.
  • Cornea
    • 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
  • Anterior chamber depth
    • 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
    • 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.
  • Lens
    • 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.
  • Retina
    • 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.
  • Optic nerve
    • 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.
  • Intraocular pressure
    • 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.
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Causes

Table 2. Summary of Important Causes of Peripheral Anterior Synechiae by Mechanism (Open Table in a new window)

Iris Pulled Forward

Iris Pushed Forward

Neovascular membrane

Iridocorneal endothelial membrane

Posterior polymorphous dystrophy

Epithelial/fibrous ingrowth

Uveitis

Trauma

Inflammatory syndromes

Infection

Flat anterior chamber

Post-surgical

Trauma

Post-laser trabeculoplasty

Pupil block

Primary angle-closure glaucoma

Posterior synechiae resulting in iris bombé

Pseudophakic or aphakic pupil block

Iridoschisis

Plateau iris

Choroidal or supraciliary effusion

  - Posterior uveitis

  - Central retinal vein occlusion

  - Nanophthalmos

  - Post-panretinal photocoagulation or cryotherapy

Suprachoroidal hemorrhage

Aqueous misdirection syndrome

Posterior segment tumors

  - Retinoblastoma

  - Choroidal melanoma

  - Metastasis

Iris cyst or tumor

Ciliary body cyst or tumor

Contracting retrolental tissue

  - Retinopathy of prematurity

  - Persistent hyperplastic primary vitreous

Post-scleral bucking surgery

Anterior lens subluxation (ectopia lentis)

Lens intumescence (phacomorphic glaucoma)

Neurofibromatosis

   

The causes of peripheral anterior synechiae (PAS) are as follows:

  • Congenital
    • 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.
  • Relative pupil block and iris bombé
    • 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
  • Uveitis: 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.
  • Etiology
    • 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.
  • Postsurgical
    • 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).
  • Neovascular glaucoma
    • 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. 
  • Trauma
    • 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.
  • Physical: Posterior pushing mechanisms resulting in appositional closure followed by synechial closure:
    • Choroidal or supraciliary effusion
    • Suprachoroidal hemorrhage
    • Aqueous misdirection syndrome (also known as ciliary block glaucoma or malignant glaucoma)
    • Posterior segment tumors (eg, retinoblastoma, choroidal melanoma, metastasis)
    • Iris cysts or tumors
    • Ciliary body cysts or tumors
    • Intumescent lens (phacomorphic 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.
  • Medications
    • 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)
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