Vitreous Wick Syndrome (Vitreous Touch Syndrome)

In October 1970, Ruiz and Teeters first described vitreous wick syndrome when they reported 11 cases of late complications following uneventful cataract surgeries. ^[1] The syndrome consisted of microscopic wound breakdown, followed by a vitreous prolapse that developed into a vitreous wick seen externally. Cases were divided into 3 groups as follows:

• The first group included 5 patients in whom vitreous wicks developed without subsequent intraocular inflammation

• The second group included 4 patients in whom vitreous wicks and intraocular inflammation developed

• The third group included 2 patients who developed severe intraocular inflammation and subsequent vision loss

Since this initial description, vitreous wick syndrome has been reported to occur after penetrating keratoplasty, discission of the posterior capsule, and corneal-relaxing incisions.

At first, vitreous wick syndrome was limited to anterior-segment procedures. Subsequently, however, posterior fistulous tracts with vitreous entrapment were reported after vitreoretinal surgery. Vitreous wick syndrome has also been identified as a potential cause of endophthalmitis after intravitreal injection of triamcinolone through the pars plana. ^[2]  With the rise of intravitreal drug delivery devices currently available, vitreous wick syndrome may become more common.

Vitreous wick syndrome develops in the setting of trauma, either iatrogenic or non-iatrogenic. Vitreous wick syndrome of iatrogenic origin usually follows anterior-segment surgery, though it may also follow sub-Tenon injection and muscle surgery. Microscopic wound breakdown has been hypothesized as the “point of no return” for the development of vitreous wick syndrome—a point emphasized by Ruiz and Teeters in their initial description. ^[1]

Corneal wound healing has been documented to be slower on the endothelial side (inner layers). Poor suturing technique is implicated as a significant factor for wound breakdown. Tightly compressed corneal wound edges may demonstrate puckering and lead to enlargement of suture tracts, promoting tissue necrosis within the suture loop.

Once communication between the posterior wound gap and the anterior wound defect occurs (after tissue necrosis from tight sutures), the anterior aqueous fluid may egress; vitreous incarceration may also occur, producing the vitreous wick. Occasionally, complete sloughing of strangulated tissue within the suture loop may occur.

Noniatrogenic traumatic causes involve sharp injuries. Neetens et al reported an 8-year-old girl hit by a sharp object that perforated the upper lid and caused a black eye. ^[3] A surgeon repaired the palpebral wound, and the child was not referred to an ophthalmologist. The girl reported vision loss 2-3 weeks later. The injury resulted in a micro-perforation of the globe through the conjunctiva and sclera.

Vitreous wick syndrome is caused by trauma. Vitreous wick syndrome of iatrogenic origin is always related to poor surgical technique. Iatrogenic traumatic causes of vitreous wick syndrome include the following:

• Cataract surgery ^[4]

• Retinal surgery

• Muscle surgery

• Penetrating keratoplasty

• Discission of the posterior capsule

• Subtenon injection

• Corneal-relaxing incision

• Pars plana intravitreal injection

The main non-iatrogenic cause is injury from a sharp object.

Vitreous wick syndrome is rare in the United States and throughout the world. No age predisposition has been documented for this syndrome. No gender predisposition has been identified, and the condition has no apparent racial predilection.

Staphylococcus epidermidis has been reported as the etiologic agent in bacterial endophthalmitis associated with a vitreous wick after penetrating keratoplasty. Lindstrom and Doughman reported a case of alpha-streptococcal (not group D) and coagulase-negative staphylococcal endophthalmitis associated with a vitreous wick 26 days after uncomplicated intracapsular cataract extraction. ^[5]

Srinivasan et al reported a single case of Staphylococcus aureus endophthalmitis associated with a vitreous wick. ^[6]  Rice and Michels reported techniques for managing epithelial downgrowth associated with a vitreous wick, including excision of the tract and patch graft. ^[7]

Early identification and intervention lead to excellent results. The longer the vitreous wick is left unnoticed and unmanaged, the higher the risk for infection and inflammation. Unnoticed and unmanaged vitreous wick syndrome may result in sight-threatening complications, such as sterile and infectious endophthalmitis. Postoperative patients should report to their ophthalmologists if delayed-onset eye redness, blurring of vision, and pain are noted.

Visual prognosis depends on the severity of the vitreous wick and the delay before identification. A single vitreous wick incarcerated in a sutured wound without prolapse to the external eye surface may be managed medically and not cause any hypotony, macular edema, or endophthalmitis. Conversely, a large incarceration with significant prolapse may cause inflammation, infection, hypotony, and vision-threatening macular edema. Earlier detection leads to better visual prognosis. Delayed detection and management may lead to vision-threatening conditions.

Patients undergoing elective or emergency eye surgery should be seen postoperatively after 24-48 hours. It is important to avoid any activity that may lead to straining or result in direct eyeball pressure. Postoperative protective goggles should be worn at all times, especially at bedtime, for the first 1-2 weeks to prevent direct pressure or trauma to the eyeball. An immediate eye examination is recommended if any signs and symptoms listed above become present during the postoperative period.