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Vitreous Wick Syndrome

  • Author: Manolette R Roque, MD, MBA, FPAO; Chief Editor: Hampton Roy, Sr, MD  more...
 
Updated: Oct 20, 2015
 

Practice Essentials

Vitreous wick syndrome occurs after eye surgery or trauma and consists of microscopic wound breakdown, followed by a vitreous prolapse that develops into a vitreous wick. Vitreous wick syndrome may result from the following:

  • Routine cataract surgery with unrecognized posterior capsular rupture or zonular dehiscence with vitreous prolapse
  • Complicated cataract surgery with posterior capsular rupture and inadequate anterior vitrectomy
  • Transconjunctival scleral intravitreal injection of pharmacologic agents
  • Sutureless small-gauge pars plana vitrectomy
  • Inadequate prolapsed vitreous removal during repair of scleral or sclerocorneal lacerations

Signs and symptoms

The history may reveal the following:

  • Pain
  • Blurring of vision
  • Itchiness or foreign body sensation
  • Gush of warm fluid
  • Recent eye surgery
  • Recent eye trauma

Gross physical findings may include the following:

  • Mucous threadlike substance protruding from a surgical site
  • Irregular pupil
  • Corneal haze
  • Hypopyon
  • Eye redness
  • Eye discharge

See Presentation for more detail.

Diagnosis

Specimens may be obtained from the external and internal eye for the following studies:

  • Gram stain or Giemsa stain
  • Cultures and sensitivities
  • Calcofluor white (suspected fungal infection)

Findings from slit-lamp examination may include the following:

  • Externalized vitreous at the wound site (see image below)
  • Necrotic area around the vitreous wick
  • Vitreous strand(s) in the anterior chamber
  • Peaked pupil
  • Displaced intraocular lens implant
  • Posterior capsular rupture
  • Anterior chamber cells and flare
  • Positive Seidel test result (A Seidel test is used to identify leakage of aqueous fluid from the anterior chamber. After applying topical anesthesia on the lower eyelid V-pocket, a drop of anesthetic is placed on a fluorescein sodium ophthalmic strip, which is administered on the same area. Examination using a slit lamp biomicroscope with cobalt blue filter is performed to identify pooling of dye and dilution of the dye. Dilution of the dye at the wound area signifies a positive Seidel test result.)
  • Corneal haze
  • Hypopyon
  • Posterior chamber cells and flare
  • Vitreous degeneration
  • Cystoid macular edema
  • Retinal tears or detachment
  • Endophthalmitis

See Workup for more detail.

Management

Principles of management for vitreous wick syndrome are as follows:

  • Treatment is primarily surgical but may also include medical therapy as appropriate
  • The surgical approach to the management depends on the presentation
  • The type of topical antibiotics used in treatment depends on the suspected infecting agent or the culture and sensitivity results
  • Postoperative medications may include topical antibiotics (broad-spectrum or targeted), nonsteroidal anti-inflammatory drug (NSAID)-containing ophthalmic drops, steroid drops, and pilocarpine ophthalmic drops
  • Patients should receive follow-up care 1-2 days after surgery
  • The use of an eye shield, especially at night, protects the globe from any untoward traumatic episodes

See Treatment and Medication for more detail.

Image library

Externalized vitreous with a peaked pupil. Image cExternalized vitreous with a peaked pupil. Image courtesy of Manolette Roque, MD, MBA, Roque Eye Clinic.
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Background

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, which was 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.

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Pathophysiology

Vitreous wick syndrome develops in the setting of trauma, either iatrogenic or noniatrogenic. Vitreous wick syndrome of iatrogenic origin usually follows anterior-segment surgery, though it may also follow subtenon 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 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 communication between the posterior wound gap and the anterior wound defect occurs (subsequent to tissue necrosis from tight sutures), 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 who was 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 microperforation of the globe through the conjunctiva and sclera.

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Etiology

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
  • Discission of the posterior capsule
  • Subtenon injection
  • Corneal-relaxing incision
  • Pars plana intravitreal injection

The main noniatrogenic cause is injury from a sharp object.

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Epidemiology

Both in the United States and throughout the world, vitreous wick syndrome is rare. 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 a bacterial endophthalmitis that was 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 that was associated with a vitreous wick 26 days after uncomplicated intracapsular cataract extraction.[5]

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

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Prognosis

With regard to prognosis, 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 prior to identification. A single vitreous wick that is incarcerated in a sutured wound without prolapse to the external eye surface may be managed medically and may not cause any hypotony, macular edema, or endophthalmitis. Conversely, a large incarceration with significant prolapse may cause considerable 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.

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Patient Education

Patients who have undergone 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 may result in direct pressure to the eyeball. 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. If any signs and symptoms listed above become present during the postoperative period, an immediate eye examination is recommended.

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Contributor Information and Disclosures
Author

Manolette R Roque, MD, MBA, FPAO Section Chief, Ocular Immunology and Uveitis, Department of Ophthalmology, Asian Hospital and Medical Center; Section Chief, Ocular Immunology and Uveitis, International Eye Institute, St Luke's Medical Center Global City; Senior Eye Surgeon, The LASIK Surgery Clinic; Director, AMC Eye Center, Alabang Medical Center

Manolette R Roque, MD, MBA, FPAO is a member of the following medical societies: American Academy of Ophthalmology, American Society of Cataract and Refractive Surgery, Philippine Medical Association, American Uveitis Society, International Ocular Inflammation Society, Philippine Ocular Inflammation Society, American Society of Ophthalmic Administrators, American Academy of Ophthalmic Executives, Philippine Society of Cataract and Refractive Surgery

Disclosure: Nothing to disclose.

Coauthor(s)

C Stephen Foster, MD, FACS, FACR, FAAO, FARVO Clinical Professor of Ophthalmology, Harvard Medical School; Consulting Staff, Department of Ophthalmology, Massachusetts Eye and Ear Infirmary; Founder and President, Ocular Immunology and Uveitis Foundation, Massachusetts Eye Research and Surgery Institution

C Stephen Foster, MD, FACS, FACR, FAAO, FARVO is a member of the following medical societies: Alpha Omega Alpha, American Academy of Ophthalmology, American Association of Immunologists, American College of Rheumatology, American College of Surgeons, American Federation for Clinical Research, American Medical Association, American Society for Microbiology, American Uveitis Society, Association for Research in Vision and Ophthalmology, Massachusetts Medical Society, Royal Society of Medicine, Sigma Xi

Disclosure: Nothing to disclose.

Barbara L Roque, MD, DPBO, FPAO Senior Partner, Roque Eye Clinic; Chief of Service, Pediatric Ophthalmology and Strabismus Section, Department of Ophthalmology, Asian Hospital and Medical Center; Active Consultant Staff, International Eye Institute, St Luke's Medical Center Global City

Barbara L Roque, MD, DPBO, FPAO is a member of the following medical societies: American Academy of Ophthalmology, American Association for Pediatric Ophthalmology and Strabismus, American Society of Cataract and Refractive Surgery, Philippine Society of Cataract and Refractive Surgery, Philippine Academy of Ophthalmology, Philippine Society of Pediatric Ophthalmolo

Disclosure: Nothing to disclose.

Chief Editor

Hampton Roy, Sr, MD Associate Clinical Professor, Department of Ophthalmology, University of Arkansas for Medical Sciences

Hampton Roy, Sr, MD is a member of the following medical societies: American Academy of Ophthalmology, American College of Surgeons, Pan-American Association of Ophthalmology

Disclosure: Nothing to disclose.

Acknowledgements

Jerre Freeman, MD Founder and Chairman, Memphis Eye and Cataract Associates; Clinical Professor, Department of Ophthalmology, University of Tennessee Health Science Center College of Medicine

Jerre Freeman, MD is a member of the following medical societies: American Academy of Ophthalmology, American Medical Association, American Society of Cataract and Refractive Surgery, and Tennessee Medical Association

Disclosure: Nothing to disclose.

Simon K Law, MD, PharmD Associate Professor of Ophthalmology, Jules Stein Eye Institute, University of California, Los Angeles, David Geffen School of Medicine

Simon K Law, MD, PharmD is a member of the following medical societies: American Academy of Ophthalmology, American Glaucoma Society, and Association for Research in Vision and Ophthalmology

Disclosure: Nothing to disclose.

J James Rowsey, MD Former Director of Corneal Services, St Luke's Cataract and Laser Institute

J James Rowsey, MD is a member of the following medical societies: American Academy of Ophthalmology, American Association for the Advancement of Science, American Medical Association, Association for Research in Vision and Ophthalmology, Florida Medical Association, Pan-American Association of Ophthalmology, Sigma Xi, and Southern Medical Association

Disclosure: Nothing to disclose.

References
  1. Ruiz RS, Teeters VW. The vitreous wick syndrome. A late complication following cataract extraction. Am J Ophthalmol. 1970 Oct. 70(4):483-90. [Medline].

  2. Chen SD, Mohammed Q, Bowling B, Patel CK. Vitreous wick syndrome--a potential cause of endophthalmitis after intravitreal injection of triamcinolone through the pars plana. Am J Ophthalmol. 2004 Jun. 137(6):1159-60; author reply 1160-1. [Medline].

  3. Neetens A, Rubbens MC, Smets RM. Vitreous wick syndrome. Bull Soc Belge Ophtalmol. 1987. 223 Pt 2:41-5. [Medline].

  4. Rouw J, Shaver JF. Vitreous wicking syndrome as a complication of extracapsular cataract extraction. Optometry. 2008 Apr. 79(4):193-6. [Medline].

  5. Lindstrom RL, Doughman DJ. Bacterial endophthalmitis associated with vitreous wick. Ann Ophthalmol. 1979 Nov. 11(11):1775-8. [Medline].

  6. Srinivasan BD, Hofeldt A, Coleman DJ, DeVoe AG. Vitreous wick syndrome. Am J Ophthalmol. 1979 May. 87(5):662-4. [Medline].

  7. Rice TA, Michels RG. Current surgical management of the vitreous wick syndrome. Am J Ophthalmol. 1978 May. 85(5 Pt 1):656-61. [Medline].

  8. Couch SM, Bakri SJ. Use of triamcinolone during vitrectomy surgery to visualize membranes and vitreous. Clin Ophthalmol. 2008 Dec. 2(4):891-6. [Medline]. [Full Text].

  9. Schmidt JC, Chofflet J, Hörle S, Mennel S, Meyer CH. Three simple approaches to visualize the transparent vitreous cortex during vitreoretinal surgery. Dev Ophthalmol. 2008. 42:35-42. [Medline].

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Externalized vitreous with a peaked pupil. Image courtesy of Manolette Roque, MD, MBA, Roque Eye Clinic.
Cellulose sponge teasing the vitreous wick. Image courtesy of Manolette Roque, MD, MBA, Roque Eye Clinic.
Castroviejo sweep performed with a cyclodialysis spatula. Image courtesy of Manolette Roque, MD, MBA, Roque Eye Clinic.
 
 
 
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