Vitreous wick syndrome, also known as vitreous touch syndrome, occurs after eye surgery or trauma and consists of microscopic wound breakdown accompanied by 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 and adhesion to the surgical wound
Complicated cataract surgery with posterior capsular rupture and inadequate anterior vitrectomy with adhesion to the surgical wound
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
Vitreous strands adherent to the internal aspect of the surgical wound
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
It is essential to determine whether the vitreous wick extends beyond the surgical wound or is merely adherent to the internal edge of the surgical wound. In the latter, the risk of infection is markedly reduced, but one must be aware of the potential long-term effects of ocular inflammation, vitreoretinal traction, and macular edema.
See Treatment and Medication for more detail.
Imagelibrary
View Image
Externalized vitreous with a peaked pupil. Image courtesy of Manolette Roque, MD, MBA, Roque Eye Clinic.
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.
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.
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 noniatrogenic cause is injury from a sharp object.
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]
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.
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.
Depending on the presentation of vitreous wick syndrome, also known as vitreous touch syndrome, specimens (eg, swab, vitreous wick, or aqueous) should be obtained from the external and internal eye for the following studies:
Gram stain or Giemsa stain
Cultures and sensitivities
Calcofluor white (if fungal infection is suspected)
In the Seidel test, a strip of fluorescein is placed on the area that is suspected of containing a leak, and the dye color is then observed in white light. If a leak is present, the dye changes from orange (concentrated) to green (diluted) and exhibits a waterfall-like effect at the leaking zone. The egress of fluid is noted best under blue light.
On slit-lamp biomicroscopy, the vitreous wick may have the appearance of a mucoid substance. The examiner may tease the wick with a cotton applicator or a cellulose sponge while taking note of synchronous movement of the iris or of the vitreous strand in the anterior chamber (see the image below). A peaked pupil may also indicate a vitreous strand in the anterior chamber.
View Image
Cellulose sponge teasing the vitreous wick. Image courtesy of Manolette Roque, MD, MBA, Roque Eye Clinic.
Treatment of vitreous wick syndrome, also known as vitreous touch syndrome, is primarily surgical but may also include medical therapy as appropriate. The surgical approach to the management of this syndrome depends on the presentation. No restrictions on diet are indicated. Participation in strenuous activities and contact sports is restricted until recovery is complete.
The type of topical antibiotics used in the treatment of vitreous wick syndrome depends on the suspected infecting agent or the culture and sensitivity results.
In cases of endophthalmitis, medical therapy is initiated that is known to be effective against the suspected or confirmed (via culture and sensitivity results) infecting agents. Subconjunctival and intravitreal antibiotics have been given. (See Bacterial Endophthalmitis and Postoperative Endophthalmitis.)
The precise surgical treatment varies with the circumstances. The following is a generalized procedural description.
Initially, the vitreous wick is excised or severed with Vannas-type scissors by lifting the exposed vitreous strand with a cotton-tipped applicator or fine nontoothed forceps. Alternatively, a suction-cutting instrument inserted into the anterior chamber may be used.
Vitrectomy may be performed via an anterior limbal approach or a closed posterior approach. It is imperative that no vitreous strand is left above the pupillary plane. To detect any remaining vitreous, sweep the anterior chamber with a spatula from a paracentesis site 90° away from the surgical wound (see the image below).
View Image
Castroviejo sweep performed with a cyclodialysis spatula. Image courtesy of Manolette Roque, MD, MBA, Roque Eye Clinic.
Intracameral injection of pupil constrictors (carbachol intraocular solution) may help pull any remaining anterior-chamber vitreous wick back into the posterior segment. Intracameral preservative-free triamcinolone acetonide may help visualize vitreous strands.[8, 9] An immobile round pupil suggests clearance from any vitreous that is invading the anterior chamber. Adequate surgical closure is accomplished with nylon 10-0 sutures.
The patient is discharged on a regimen of topical antibiotics, either broad-spectrum or targeted on the basis of culture and sensitivity results. Nonsteroidal anti-inflammatory drug (NSAID)-containing ophthalmic drops are given to decrease cystoid macular edema. Steroid drops are given to decrease inflammation. Pilocarpine ophthalmic drops are given to maintain pupillary constriction and prevent anterior segment migration of posterior vitreous during the acute healing phase.
Patients should receive follow-up care 1-2 days after surgery. If this initial follow-up examination identifies no problems, regular checkups should be scheduled for uneventful anterior segment surgeries. The use of an eye shield, especially at night, protects the globe from any untoward traumatic episodes.
Meticulous surgical technique is essential for all ophthalmic surgery. Fundamental surgical principles must be adhered to. All incisions must be closed securely.
In cases of broken capsules with vitreous presentation in the anterior segment, it is vital to ensure that all vitreous has been removed from the anterior segment by means of appropriate anterior vitrectomy technique. If this is not possible, consideration should be given to trans pars plana vitrectomy at a later date in consultation with a vitreoretinal surgeon.
Definitive management of vitreous wick syndrome, also known as vitreous touch syndrome, is primarily surgical. Medical therapy is limited to broad-spectrum topical antibiotics for uncomplicated cases.
Clinical Context:
Vancomycin is used as empiric therapy for gram-positive organisms. It has excellent gram-positive coverage and possesses the added advantage of providing better coverage against resistant organisms. It is bactericidal against most organisms and bacteriostatic for enterococci. Inhibits cell wall biosynthesis, interfering with cell membrane permeability and RNA synthesis.
Vancomycin is the drug of choice for intravitreal and systemic administration. After systemic administration, it penetrates most tissues, including vitreous, especially if the blood-ocular barrier is compromised. In patients with renal impairment, the dosage is adjusted on the basis of creatine clearance.
Clinical Context:
Moxifloxacin is indicated for treating bacterial conjunctivitis. It inhibits topoisomerase II (DNA gyrase) and IV enzymes. DNA gyrase is essential in bacterial DNA replication, transcription, and repair. Topoisomerase IV plays a key role in chromosomal DNA portioning during bacterial cell division.
Clinical Context:
Ofloxacin is a pyridine carboxylic acid derivative with broad-spectrum bactericidal effect. It inhibits bacterial growth by inhibiting DNA gyrase. It is indicated for superficial ocular infections of conjunctiva or cornea due to susceptible microorganisms.
Clinical Context:
This combination is used for ocular infection of the cornea or conjunctiva caused by susceptible microorganisms. It is available as a solution (polymyxin/trimethoprim) and as an ointment (polymyxin/bacitracin).
Clinical Context:
Ciprofloxacin has activity against Pseudomonas and Streptococcus species, methicillin-resistant Staphylococcus aureus (MRSA), S epidermidis, and most gram-negative organisms; it has no activity against anaerobes.
Clinical Context:
Norfloxacin has activity against susceptible gram-negative and gram-positive bacteria. Antibiotics in this class inhibit bacterial DNA synthesis and thus growth by inhibiting DNA gyrase.
Clinical Context:
Erythromycin is indicated for infections caused by susceptible strains of microorganisms and for prevention of corneal and conjunctival infections.
Clinical Context:
This agent interferes with bacterial growth by inhibiting bacterial folic acid synthesis by competitively antagonizing para-aminobenzoic acid. It is available in solution, ointment, and lotion form.
Clinical Context:
Tobramycin is an aminoglycoside that interferes with bacterial protein synthesis by binding to 30S and 50S ribosomal subunits, causing a defective bacterial cell membrane. It is available in solution, ointment, and lotion form.
Clinical Context:
Ketorolac ophthalmic inhibits prostaglandin synthesis by decreasing the activity of the enzyme cyclooxygenase. This results in decreased formation of prostaglandin precursors, which, in turn, results in reduced inflammation.
Clinical Context:
Diclofenac ophthalmic is one of a series of phenylacetic acids that has demonstrated anti-inflammatory and analgesic properties in pharmacological studies. It is believed to inhibit the enzyme cyclooxygenase, which is essential in the biosynthesis of prostaglandins. It may facilitate outflow of aqueous humor and decrease vascular permeability. Any equivalent topical NSAID also can be used.
Clinical Context:
Flurbiprofen ophthalmic facilitates outflow of aqueous humor by inhibiting prostaglandin synthesis, causing a subsequent decrease in vascular permeability.
Clinical Context:
Nepafenac is a pro-drug of amfenac, a potent NSAID. Nepafenac undergoes amide hydrolysis by intraocular hydrolases to form the pharmacologically active amfenac. Amfenac inhibits both cyclooxygenase COX-1 and COX-2 activity.Therefore, its effects are intraocular (CME) and have less effect (or side-effect) on the ocular surface.
The inhibition of prostaglandin synthesis results in vasoconstriction, a decrease in vascular permeability, leukocytosis, and a decrease on intraocular pressure (IOP). However, these agents have no significant effect on IOP.
Clinical Context:
Prednisolone is used to treat acute inflammation following eye surgery or other insults to the eye. It decreases inflammation and corneal neovascularization, suppresses migration of polymorphonuclear leukocytes, and reverses increased capillary permeability.
In cases of bacterial infection, concomitant use of anti-infective agents is mandatory. If signs and symptoms do not improve after 2 days, the patient should be reevaluated. Dosing may be reduced, but patients should be advised not to discontinue therapy prematurely.
Clinical Context:
Dexamethasone is used for various allergic and inflammatory diseases. It decreases inflammation by suppressing migration of polymorphonuclear leukocytes and reducing capillary permeability.
Clinical Context:
Rimexolone decreases inflammation by suppressing the migration of polymorphonuclear leukocytes and reversing increased capillary permeability.
Clinical Context:
This agent decreases inflammation by suppressing migration of polymorphonuclear leukocytes and reversing increased capillary permeability. It is a topical ester steroid eye drop that poses a decreased risk of glaucoma. It is available in 0.2% and 0.5% concentrations.
Corticosteroids are used for pseudomembranes and decreased vision and/or glare due to subepithelial infiltrates. They have anti-inflammatory properties and cause profound and varied metabolic effects. In addition, these agents modify the body's immune response to diverse stimuli.
Clinical Context:
Pilocarpine for ophthalmic administration is a sterile solution containing a direct-acting cholinergic parasympathomimetic agent that acts through direct stimulation of muscarinic neuroreceptors and smooth muscle (eg, in the iris and secretory glands). Pilocarpine produces miosis through contraction of the iris sphincter, causing increased tension on the scleral spur and opening of the trabecular meshwork spaces to facilitate outflow of aqueous. Outflow resistance is thereby reduced, lowering intraocular pressure.
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
Disclosure: Nothing to disclose.
Coauthor(s)
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
Disclosure: Nothing to disclose.
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
Disclosure: Serve(d) as a director, officer, partner, employee, advisor, consultant or trustee for: Aldeyra Therapeutics (Lexington, MA); Bausch & Lomb Surgical, Inc (Rancho Cucamonga, CA); Eyegate Pharma (Waltham, MA); Novartis (Cambridge, MA); pSivida (Watertown, MA); Xoma (Berkeley, CA); Allakos (Redwood City, CA)<br/>Serve(d) as a speaker or a member of a speakers bureau for: Alcon (Geneva, Switzerland); Allergan (Dublin, Ireland); Mallinckrodt (Staines-upon-Thames, United Kingdom)<br/>Received research grant from: Alcon; Aldeyra Therapeutics; Allakos Pharmaceuticals; Allergan; Bausch & Lomb; Clearside Biomedical; Dompé pharmaceutical; Eyegate Pharma; Mallinckrodt pharmaceuticals; Novartis; pSivida; Santen; Aciont.
Chief Editor
Andrew A Dahl, MD, FACS, Assistant Professor of Surgery (Ophthalmology), New York College of Medicine (NYCOM); Director of Residency Ophthalmology Training, The Institute for Family Health and Mid-Hudson Family Practice Residency Program; Staff Ophthalmologist, Telluride Medical Center
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
){kind=link}
){kind=link}
){kind=link}