Background: In October 1970, Ruiz and Teeters first described the vitreous wick syndrome when they reported 11 cases of late complications following uneventful cataract operations. The syndrome consisted of microscopic wound breakdown, followed by a vitreous prolapse that developed into a vitreous wick, which was seen externally. They divided their cases into 3 groups.

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 then, there have been reports of the vitreous wick syndrome occurring after penetrating keratoplasty, discission of the posterior capsule, and corneal-relaxing incisions.

Vitreous wick syndrome initially was limited to anterior segment surgeries. In the past decade, posterior fistulous tracts with vitreous entrapment also have been reported.

Pathophysiology: Vitreous wick syndrome is caused by trauma, either iatrogenic (eg intraocular surgery) or noniatrogenic. Iatrogenic causes always involve poor surgical technique. It usually follows anterior segment surgery, although it has been reported to follow sub-Tenon injection and muscle surgery. All other factors being present, microscopic wound breakdown has been hypothesized as the "point of no return" for the vitreous wick syndrome. Ruiz and Teeters emphasized this point in their initial description.

Corneal wound healing has been documented to be slower on the endothelial side (inner layers). Poor suture techniques are implicated as a major factor for wound breakdown. Tightly compressed corneal wound edges may demonstrate puckering and also may lead to enlargement of suture tracts promoting tissue necrosis within the suture loop. Once a communication between the posterior wound gap and anterior wound defect occurs (following tissue necrosis from tight sutures), anterior aqueous fluid may egress; vitreous incarceration may occur, producing the vitreous wick. Occasionally, complete sloughing of strangulated tissue within the suture loop may occur.

Noniatrogenic traumatic causes involve sharp injuries. Neetens, Rubbens, and Smets reported an 8-year-old girl who was hit by a sharp object, perforating the upper lid and causing a black eye. A surgeon repaired the palebral wound and the child was not referred to an ophthalmologist. The girl reported vision loss 2-3 weeks later. The injury resulted in a microperforation of the globe through the conjunctiva and sclera.

Frequency:

• In the US: Rare

• Internationally: Rare

Mortality/Morbidity:

• Staphylococcus epidermidis has been reported as the etiologic agent in a bacterial endophthalmitis that was associated with a vitreous wick after penetrating keratoplasty.

• Lindstrom and Doughman reported an alpha-streptococcal (not group D) and coagulase-negative staphylococcal endophthalmitis that was associated with vitreous wick 26 days after uncomplicated intracapsular cataract extraction.

• In 1987, Srinivasan et al reported a single case of Staphylococcus aureus endophthalmitis that was associated with vitreous wick.
   

• Epithelial downgrowth: Rice and Michels reported techniques on managing epithelial downgrowth that is associated with vitreous wick, including excision of the tract and patch graft.

Race: No racial predilection exists.

Sex: No gender predisposition exists.

Age: No age predisposition exists.