Vitreous wick syndrome is a condition in which a small wound dehiscence occurs after ophthalmic surgery or ocular trauma, and prolapsed vitreous becomes incarcerated in the wound, forming a “vitreous wick.” It is also called vitreous tug syndrome or vitreous touch syndrome, as reported by Iliff.
Initially, this syndrome was thought to be limited to anterior segment surgery. Later, it was also identified in cases of posterior fistula formation with vitreous incarceration after vitreoretinal surgery, and as a cause of endophthalmitis after intravitreal triamcinolone injection via the pars plana. With the widespread use of intravitreal injection devices, it can now occur in association with a wider range of procedures.
A representative complication is cystoid macular edema (CME), also known as Irvine-Gass syndrome. The presence or absence of CME greatly affects visual prognosis (see “Treatment” section for details).
This is a rare disease worldwide and in Japan, with no reported tendency for age, sex, or race.
It most commonly occurs when the posterior capsule is ruptured or the zonules are torn during cataract surgery, or when anterior vitrectomy is insufficient. It can also occur after sutureless small-incision vitrectomy, intravitreal injection of drugs, or repair of scleral or corneoscleral lacerations.
Examination involves evaluating both macroscopic and slit-lamp findings.
Macroscopic Findings
Mucous thread-like material from the wound: Vitreous strands protruding externally.
Corneal opacity: The cornea near the wound becomes opaque.
Ocular congestion and discharge: Appear depending on the degree of inflammation or infection.
Hypopyon: Seen in severe cases or when infection is present.
Slit-lamp microscopy findings
External vitreous exposure: Identification of vitreous at the wound and vitreous strands is key to diagnosis.
Pupillary distortion (pear-shaped pupil): The iris is pulled by vitreous strands, causing pupil deformation.
Cells and flare in the anterior chamber: Reflects the degree of intraocular inflammation.
Positive Seidel test: Confirms aqueous humor leakage from the wound.
Apply a fluorescein strip to the suspected leakage site and observe color changes under white light. If leakage is present, the dye changes from orange (concentrated) to green (diluted), showing a waterfall pattern. Fluid outflow is more clearly observed under blue light.
Under slit-lamp microscopy, the vitreous wick appears as a mucoid substance. Gently stimulate the wick with a cotton swab or cellulose sponge and check whether the iris and vitreous strands in the anterior chamber move synchronously. Pupillary distortion is also a finding strongly suggestive of vitreous strands in the anterior chamber.
Because vitreous strands incarcerated in the anterior chamber pull the iris toward the wound, the pupil becomes pear-shaped (peaked pupil). This finding is an important clinical sign suggesting the presence of vitreous strands and, when observed after cataract surgery, provides a basis for suspecting this syndrome.
Vitreous wick syndrome occurs in the setting of iatrogenic or non-iatrogenic trauma.
If vitreous prolapsed during cataract surgery due to posterior capsule rupture or zonular dialysis is not carefully removed, vitreous fibers may become incarcerated in the corneoscleral incision, leading to prolonged postoperative inflammation and cystoid macular edema.
Ruiz and Teeters pointed out that minute wound dehiscence is the “point of no return” in the development of this syndrome. Corneal wound healing is slower on the endothelial (inner) side, and improper suturing technique is a major cause of wound dehiscence. Overtightening sutures leads to tissue necrosis and wound communication, progressing to aqueous humor leakage and vitreous incarceration.
Important aspects of the medical history for diagnosis include the following:
Slit-lamp examination is central to diagnosis. Seidel test, pupillary deviation, and vitreous exposure at the wound site should be assessed (see “Clinical Findings” section for details).
Diseases to consider when vitreous wick syndrome is suspected are listed below.
| Differential Diagnosis | Key Differentiating Features |
|---|---|
| Postoperative bacterial endophthalmitis | Rapid progression of inflammation, positive culture |
| Intraocular foreign body (IOFB) | History of trauma, foreign body confirmed on imaging |
| Iris prolapse | Type of tissue (vitreous vs. iris tissue) |
If infection is suspected, specimens (swab, vitreous wick, or aqueous humor) should be collected from external and internal sites, and the following tests should be performed.
Optical coherence tomography (OCT) and fluorescein angiography (FA) are useful for diagnosing cystoid macular edema associated with vitreous wick syndrome. OCT can confirm edema with cystoid changes in the macula, and FA shows late-phase pooling of fluorescein dye corresponding to a petaloid pattern of cysts. When considering prophylactic vitrectomy, it is recommended to perform both tests as a baseline to document the macular status.
Treatment of vitreous wick syndrome is primarily surgical, but may be combined with pharmacotherapy as needed. Strenuous activities and contact sports should be restricted until recovery.
Laser treatment is the mainstay of surgical treatment for this syndrome.
If the vitreous strand passes through the pupil, instill 2% pilocarpine 3–4 drops every 10 minutes preoperatively to induce miosis. Miosis places tension on the vitreous strand, making it easier to identify and confirming release of tension upon cutting.
There are four approaches to the vitreous strand.
Approach 1 (Gonioscopy)
Cataract surgery wound: The most reliable indicator that the vitreous strand always terminates. Visualize and irradiate using a gonioscopy lens. Energy settings are typically 6–12 mJ (start with low energy).
Approach 2 (Direct Limbal)
Direct cutting near the limbus: When the cornea is clear and the strand is visible away from the iris stroma. Use no contact lens or an Abraham lens. Usually requires 4–8 mJ.
Successful treatment releases tension, and the strand-like vitreous changes into an amorphous gel. Cutting large strands may require hundreds of shots over multiple sessions.
Until visual improvement is achieved (usually 2–3 months), use the following medications.
If cystoid macular edema does not improve with YAG laser vitreolysis alone, consider sub-Tenon triamcinolone injection, intravitreal injection, or steroid implant.
This is selected when laser treatment is difficult or when there is extensive vitreous incarceration.
The exposed vitreous strand is held with a cotton swab or forceps and cut with Vannas scissors, or a suction-cutting device (cutter) is inserted into the anterior chamber. Vitrectomy is performed via an anterior limbal approach or a closed posterior approach.
Important point: It is essential not to leave vitreous strands anterior to the pupil plane. To confirm residual vitreous, insert a spatula through a paracentesis site 90 degrees away from the surgical wound and sweep the anterior chamber.
Injection of a miotic agent (e.g., carbachol) into the anterior chamber is effective in pulling back residual vitreous wick into the posterior segment. Also, intracameral injection of preservative-free triamcinolone acetonide is useful for visualizing vitreous strands.
If the pupil is round, centered, and reactive to light, it suggests that the vitreous in the anterior chamber has been removed. The wound is closed with 10-0 nylon sutures.
Even in the absence of cystoid macular edema, laser treatment of vitreous strands at the wound site may be performed to prevent future development. However, not all cases with vitreous strands develop cystoid macular edema, and large-scale randomized controlled trials are needed to confirm the usefulness of this approach.
Katzen et al. reported visual acuity improvement in all 14 cases. In contrast, in the series of 29 cases by Steinart and Wasson, visual acuity improvement of 2 lines or more was only 55%, and improvement was limited in some cases due to other macular diseases or severe glaucoma. Cases with extremely poor pre-treatment visual acuity tend to show poor improvement response.
The onset of vitreous wick syndrome begins with a small wound dehiscence. Corneal wound healing is slower on the endothelial (inner) side. Overtightening of sutures causes puckering, enlarging the suture tract and promoting tissue necrosis within the suture loop.
When the gap behind the wound and the defect in front communicate, aqueous humor leaks out and the vitreous moves forward. This displaced vitreous becomes incarcerated in the wound, forming a “vitreous wick.” In some cases, tissue strangulated within the suture loop may completely detach.
Since the vitreous is a connective tissue (a gel structure composed of collagen fibers and hyaluronic acid), the strand of vitreous incarcerated in the wound dries and degenerates, providing a continuous inflammatory stimulus.
Anterior traction by vitreous strands is transmitted to the posterior pole macula via the vitreous. This physical traction and release of inflammatory cytokines cause breakdown of the blood-retinal barrier, leading to cystoid macular edema. Cystoid macular edema causes cystoid changes in the outer plexiform layer (especially Henle fiber layer) and inner nuclear layer, with Müller cells and axonal fibers forming the cyst septa.
Cystoid macular edema occurring after cataract surgery is specifically called Irvine-Gass syndrome, and vitreous wick syndrome is one of the main causes.
This syndrome can also occur after microperforations from ocular trauma by sharp objects. Neetens et al. reported a case of an 8-year-old girl who sustained an injury from a sharp object penetrating the upper eyelid. Only eyelid wound repair was performed without referral to an ophthalmologist, and 2-3 weeks later, a microperforation of the conjunctiva and sclera with vitreous wick syndrome was discovered.
With the widespread use of intravitreal injections of anti-VEGF drugs and steroids, the occurrence of vitreous wick syndrome due to inadequate wound closure after injection has gained attention. Improving the reliability of sutureless post-injection port closure and standardizing postoperative management protocols are research challenges.
For cystoid macular edema associated with vitreous wick syndrome, evaluations are ongoing for the efficacy of prophylactic postoperative NSAID eye drops that suppress prostaglandin production, intravitreal VEGF inhibitors, and sustained-release steroid implants. In refractory cases with persistent cystoid macular edema, vitrectomy combined with internal limiting membrane peeling has also been reported.
Currently, since some patients with vitreous strands do not develop cystoid macular edema, the indications for prophylactic vitreous strand cutting have not been established. Large-scale randomized controlled trials to verify the cost-effectiveness and indications of preventive intervention are important future tasks.
