Iris Synechiae

Key points at a glance

Key Points at a Glance

• Iris synechiae is a condition in which the iris adheres to adjacent structures due to intraocular inflammation.
• It is broadly classified into posterior synechiae (adhesion between the iris and the anterior lens capsule) and peripheral anterior synechiae (PAS: adhesion between the iris and the angle).
• The most common cause is uveitis, but it can also occur after trauma or surgery.
• When posterior synechiae become circumferential, they can lead to pupil block, iris bombé, and eventually acute glaucoma attack.
• Extensive formation of peripheral anterior synechiae can obstruct aqueous outflow, leading to secondary angle-closure glaucoma.
• The basic treatment involves reducing inflammation of the underlying disease and preventing or releasing adhesions using mydriatic agents.
• If glaucoma is present, laser iridotomy or surgical intervention is required.

1. What is Iris Synechia?

Iris synechiae (Synechiae) is a general term for conditions in which the iris adheres to adjacent structures due to intraocular inflammation, etc. The term originates from the Greek word “synekhes” (to hold together).

Iris adhesion is broadly classified into two types based on the site of adhesion.

Posterior Synechia

Definition: Adhesion of the posterior surface of the iris to the anterior lens capsule.

Predilection: Commonly occurs at the pupillary margin associated with anterior chamber inflammation (uveitis).

Clinical significance: If circumferential, it can lead to pupillary block, iris bombé, and acute glaucoma attack.

Peripheral Anterior Synechia

Definition: Adhesion of the peripheral iris to the trabecular meshwork or Schwalbe’s line in the anterior chamber angle (PAS).

Shape: Various forms including tent-shaped, trapezoidal, and broad planar.

Clinical significance: It obstructs the aqueous humor outflow pathway and can cause secondary angle-closure glaucoma.

Posterior synechiae are common in uveitis. A study of pediatric uveitis (juvenile idiopathic arthritis-associated and idiopathic) reported that posterior synechiae were present in approximately 18.4% of eyes at the initial visit¹⁾.

Q What is the difference between posterior synechiae and peripheral anterior synechiae?

A

Posterior synechiae are adhesions between the posterior surface of the iris and the anterior lens capsule, causing pupil block. In contrast, peripheral anterior synechiae (PAS) are adhesions between the peripheral iris and angle structures (e.g., trabecular meshwork), directly obstructing the aqueous outflow pathway. Both are important complications of uveitis.

2. Main symptoms and clinical findings

Subjective symptoms

Symptoms directly caused by iris adhesion are often minimal. They are usually perceived as symptoms of the underlying uveitis.

• Eye pain/headache: Ciliary injection and eye pain associated with acute iridocyclitis.
• Blurred vision/decreased visual acuity: Opacification due to flare and inflammatory cells in the anterior chamber. Progression of complicated cataract.
• Photophobia: Light sensitivity due to inflammation.
• Redness: Primarily ciliary injection. Prominent in acute inflammation.
• Sudden severe eye pain/nausea: Acute glaucoma attack due to circumferential posterior synechiae, accompanied by severe eye pain, headache, and nausea.

Clinical Findings (Findings Confirmed by Physician Examination)

Findings of Posterior Synechiae

Confirmed by slit-lamp microscopy.

• Irregular pupil margin: The pupil is deformed at the adhesion site, resulting in poor dilation. It may not respond to mydriatics and become petal-shaped.
• Iris pigment deposition on the anterior lens capsule: Iris pigment remains on the anterior capsule even after the adhesion detaches. This serves as evidence of past uveitis.
• Iris bombé: Circumferential posterior synechiae block aqueous humor flow from the posterior chamber to the anterior chamber, causing the iris to bulge forward.

Findings of Peripheral Anterior Synechiae (PAS)

Confirmed by gonioscopy.

• Angle synechiae: The peripheral iris adheres at various heights from the scleral spur to Schwalbe’s line and corneal endothelium. Differentiation from normal iris processes is important.
• Tent-shaped peripheral anterior synechiae: In granulomatous uveitis (e.g., ocular sarcoidosis), tent-shaped peripheral anterior synechiae form after resolution of angle nodules.
• Indentation gonioscopy: Compress the cornea with the gonioscope to differentiate between synechial and appositional iris adhesion.

Clues to suspect posterior synechiae

If the pupil does not dilate sufficiently even after instilling mydriatic drops, posterior synechiae is suggested. A petal-shaped deformity in the miotic position is often seen in sarcoidosis and prolonged Harada disease. If arcuate deposits of iris pigment are observed on the anterior lens capsule after dilation, it provides evidence of a past history of uveitis.

Q Is the inability to dilate the pupil even with mydriatic drops due to iris synechiae?

A

One cause of poor mydriasis is posterior synechiae. If there is a history of uveitis, the likelihood of synechiae is high. However, other causes such as pseudoexfoliation syndrome or post-traumatic conditions also exist, so differentiation by slit-lamp microscopy is necessary.

3. Causes and Risk Factors

The most common cause of iris synechiae is uveitis (intraocular inflammation). Deposition of inflammatory cells, fibrin, and proteins promotes adhesion formation between structures.

Diseases Prone to Posterior Synechiae

• Acute anterior uveitis (e.g., HLA-B27-associated): Accompanied by severe anterior chamber inflammation and fibrin exudation, leading to a high rate of posterior synechiae.
• Sarcoidosis: Chronic granulomatous inflammation causes persistent synechiae formation.
• Vogt-Koyanagi-Harada disease: In the protracted phase, posterior synechiae in a miotic position are characteristic.
• Behçet’s disease and juvenile idiopathic arthritis-associated uveitis: Chronic inflammation predisposes to posterior synechiae.
• Diabetic iritis: Accompanied by strong fibrin exudation, may lead to posterior synechiae.
• After intraocular surgery: May form following inflammation after cataract surgery or laser iridotomy.

Conditions predisposing to peripheral anterior synechiae (PAS)

• Granulomatous uveitis: Tent-shaped peripheral anterior synechiae remain after resolution of angle nodules.
• Chronic iridocyclitis: Persistent inflammation leads to formation of peripheral anterior synechiae in the angle.
• Neovascular glaucoma: New vessels on the iris and angle form a fibrovascular membrane, progressing to peripheral anterior synechiae²⁾.
• ICE syndrome: Characterized by high peripheral anterior synechiae.
• Trauma: Blunt trauma can cause sheet-like peripheral anterior synechiae.

It is known that Fuchs heterochromic iridocyclitis does not cause posterior synechiae. This is a clue for differential diagnosis.

Prevention and Daily Care

• If diagnosed with uveitis, use eye drops as directed by your doctor. Discontinuing on your own may cause inflammation to recur and increase the risk of synechiae.
• If mydriatic eye drops are prescribed, be sure to use them. They are important for preventing synechiae.
• For recurrent uveitis, see an ophthalmologist as soon as you notice any symptoms.

4. Diagnosis and Examination Methods

Slit-lamp microscopy and gonioscopy are fundamental for diagnosing iris adhesions.

Slit-Lamp Microscopy

It is essential for detecting posterior synechiae. Pay attention to the pupillary margin and observe for adhesions between the iris and the anterior lens capsule. After instilling mydriatic drops, the extent and severity of adhesions can be assessed by evaluating the degree of mydriasis and pupil shape.

Flare and inflammatory cells in the anterior chamber are evaluated as follows:

Finding	Evaluation Method	Grade
Flare	Degree of turbidity	1+ to 4+
Cell count	Number of inflammatory cells	1+ to 4+

When accompanied by fibrin exudation or hypopyon, the inflammation is severe and the risk of posterior synechiae is high.

Gonioscopy

Gonioscopy is essential for detecting and evaluating peripheral anterior synechiae. Indirect gonioscopy using a Goldmann lens or Zeiss four-mirror lens is employed. The entire angle is observed, and the extent, height, and shape of synechiae are recorded.

• Static gonioscopy: Evaluates the presence and degree of synechiae.
• Compression (dynamic) gonioscopy: By compressing the cornea and pushing the iris root posteriorly, organic synechiae (PAS) are differentiated from functional apposition.

The height of peripheral anterior synechiae varies from slight involvement of the scleral spur to complete occlusion of the trabecular meshwork, and characteristic forms are seen depending on the underlying disease ³⁾.

Importance of Gonioscopy

Even if the anterior chamber appears normal, abnormal findings in the angle (such as nodules or PAS) may be found. Gonioscopy is essential in the examination of uveitis.

Q Which test detects posterior synechiae?

A

It is diagnosed by slit-lamp microscopy. Adhesions between the pupillary margin and the anterior lens capsule can be directly observed. If the pupil does not dilate sufficiently after instillation of mydriatic drops or if petaloid deformation is seen, posterior synechiae is strongly suggested. Gonioscopy is required to confirm peripheral anterior synechiae.

5. Standard Treatment

Treatment of iris adhesions is based on three pillars: control of inflammation of the underlying disease, prevention of adhesions, and management of lysis and complications.

Anti-inflammatory treatment (treatment of underlying disease)

Anti-inflammatory treatment for uveitis is most important.

• Steroid eye drops: Betamethasone or dexamethasone eye drops are basic. For severe inflammation, hourly instillation may be performed.
• Subconjunctival steroid injection: Decadron injection (3.3 mg/mL) 0.3 mL subconjunctivally, or Kenacort-A (40 mg/mL) subconjunctivally.
• Systemic steroid administration: Considered when the main site of inflammation is in the posterior segment of the eye.
• NSAIDs: After inflammation subsides, switch to fluorometholone or NSAIDs considering the risk of steroid-induced glaucoma.

Prevention and Release of Adhesions with Mydriatics

When anterior chamber inflammation is severe, posterior synechiae may occur. Therefore, mydriatics are used to dilate the pupil and prevent adhesions.

• Tropicamide/phenylephrine hydrochloride combination (Mydrin P): Instilled 3 times daily. Standard medication for adhesion prevention.
• Phenylephrine (Neosynesin Kowa 5%): Used in combination with Mydrin P.
• Atropine ophthalmic solution (1%): Used when there are strong adhesions.

Precautions When Using Mydriatics and Intraocular Pressure-Lowering Drugs

• In uveitis-related intraocular pressure elevation, avoid using prostaglandin-related drugs as they may paradoxically increase pressure.
• Avoid pilocarpine (miotic) as it may promote posterior synechiae.
• Indiscriminate use of steroids carries a risk of steroid-induced glaucoma. Taper or change according to inflammation severity.

Intraocular Pressure Management

For intraocular pressure elevation due to iris synechiae, use beta-blocker eye drops or carbonic anhydrase inhibitor eye drops/oral medication.

Laser Therapy

• Laser peripheral iridotomy (LPI): Performed for pupillary block and iris bombé due to circumferential posterior synechiae. It relieves pupillary block and corrects the pressure difference between the anterior and posterior chambers.
• Caution: Re-occlusion due to inflammation may occur; if repeated, consider surgical peripheral iridectomy.

Surgical Treatment

• Synechiolysis: Surgical separation of extensive adhesions.
• Peripheral iridectomy: Performed for pupillary block that cannot be managed with laser iridotomy.
• Goniosynechialysis: Performed for angle closure due to extensive peripheral anterior synechiae.
• Glaucoma surgery: If intraocular pressure cannot be controlled with medication or laser, consider trabeculectomy or tube shunt surgery.

Q What happens if iris adhesions are left untreated?

A

If posterior synechiae progress to involve the entire circumference, they can cause pupillary block, leading to iris bombé and acute glaucoma attack. Extensive formation of peripheral anterior synechiae can lead to chronic angle-closure glaucoma. Both can cause severe visual impairment, so early anti-inflammatory treatment and prevention of adhesions are important.

6. Pathophysiology and detailed pathogenesis

Mechanism of posterior synechia formation

Inflammation in the anterior chamber is the fundamental cause of posterior synechia formation. When inflammation occurs in the iris and ciliary body, vascular permeability increases, and plasma proteins and inflammatory cells leak into the anterior chamber. Fibrin deposits on the pupillary margin, bridging the iris and the anterior lens capsule. If inflammation persists, fibrous organization progresses, leading to irreversible adhesions.

Progression from posterior synechiae to secondary glaucoma

When posterior synechiae become circumferential, the following chain reaction occurs.

1. Pupillary block: Aqueous humor flow from the posterior chamber to the anterior chamber is obstructed.
2. Increased posterior chamber pressure: Aqueous humor accumulates in the posterior chamber, raising pressure.
3. Iris bombé: The iris bulges forward due to posterior chamber pressure.
4. Angle closure: The bulging iris compresses the angle structures, leading to peripheral anterior synechiae formation.
5. Acute glaucoma attack: Intraocular pressure rises rapidly.

The condition in which the entire 360-degree circumference of the pupillary margin is adherent is called seclusio pupillae.

Mechanisms of peripheral anterior synechia formation

There are multiple mechanisms for the formation of peripheral anterior synechiae.

• Inflammatory: In uveitis, inflammatory cells and proteins in the anterior chamber form adhesions between the iris and the angle wall ²⁾. After the angle nodules resolve, tent-shaped peripheral anterior synechiae remain.
• Pushing mechanism from behind: Ciliary body edema or lens bulging pushes the iris forward, causing it to contact and adhere to the trabecular meshwork.
• Neovascular: Fibrovascular membrane extends into the angle, and contraction pulls the iris, causing adhesion²⁾.

Diverse mechanisms of intraocular pressure elevation

Intraocular pressure elevation associated with uveitis occurs in about 20% of patients, and its mechanisms are diverse²⁾. Both open-angle and angle-closure mechanisms are involved.

Mechanism	Classification
Trabecular meshwork clogging	Open-angle
Trabeculitis	Open angle
Angle nodules	Open angle
Peripheral anterior synechiae	Angle closure
Posterior synechiae and pupillary block	Angle closure
Neovascularization	Angle closure
Steroid effects	Open angle

Since treatment strategies differ, it is important to thoroughly observe the angle and estimate the mechanism of intraocular pressure elevation.

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7. Latest Research and Future Prospects (Research Stage Reports)

For Patients: Please Read Carefully

The following content is currently in the research or clinical trial stage and is not standard treatment available at general hospitals. It is reference information for professionals regarding future medical developments.

Since iris adhesion is more of a complication of uveitis than an independent disease, research is mainly progressing in the context of anti-inflammatory treatment for uveitis and glaucoma treatment.

Long-term outcomes of tube shunt surgery (e.g., Ahmed valve) for uveitic glaucoma have been reported, and intraocular pressure control has been achieved with tube implantation even in the uveitis group ²⁾. However, it has been noted that the uveitis group has a significantly higher rate of tube removal due to exposure, necessitating careful postoperative follow-up.

Advances in anterior segment imaging devices such as anterior segment OCT and ultrasound biomicroscopy (UBM) are enabling quantitative assessment of peripheral anterior synechiae and objective diagnosis of pupillary block. Although these imaging techniques do not completely replace gonioscopy, they are expected to be useful as supplementary evaluation tools.

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8. References

1. Cann M, Ramanan AV, Crawford A, et al. Outcomes of non-infectious Paediatric uveitis in the era of biologic therapy. Pediatr Rheumatol Online J. 2018;16(1):51. doi:10.1186/s12969-018-0266-5. PMID:30081917; PMCID:PMC6080499.
2. Bodh SA, et al. Inflammatory glaucoma. Oman J Ophthalmol. 2011;4(1):3-9.
3. 日本緑内障学会. 緑内障診療ガイドライン（第5版）. 日眼会誌. 2022;126:85-177.