- •Preface
- •Contributors
- •Dedication
- •INFECTIOUS DISEASES
- •ACINETOBACTER
- •BACILLUS SPECIES INFECTIONS
- •ESCHERICHIA COLI
- •GONOCOCCAL OCULAR DISEASE
- •INFECTIOUS MONONUCLEOSIS
- •MICROSPORIDIAL INFECTION
- •MOLLUSCUM CONTAGIOSUM
- •MORAXELLA
- •PROPIONIBACTERIUM ACNES
- •PROTEUS
- •PSEUDOMONAS AERUGINOSA
- •STREPTOCOCCUS
- •VARICELLA AND HERPES ZOSTER
- •PARASITIC DISEASES
- •PEDICULOSIS AND PHTHIRIASIS
- •NUTRITIONAL DISORDERS
- •INFLAMMATORY BOWEL DISEASE
- •DISORDERS OF CARBOHYDRATE METABOLISM
- •MUCOPOLYSACCHARIDOSIS IH
- •MUCOPOLYSACCHARIDOSIS IH/S
- •MUCOPOLYSACCHARIDOSIS II
- •MUCOPOLYSACCHARIDOSIS III
- •MUCOPOLYSACCHARIDOSIS IV
- •MUCOPOLYSACCHARIDOSIS VI
- •MUCOPOLYSACCHARIDOSIS VII
- •DISORDERS OF LIPID METABOLISM
- •HEMATOLOGIC AND CARDIOVASCULAR DISORDERS
- •CAROTID CAVERNOUS FISTULA
- •DERMATOLOGIC DISORDERS
- •ERYTHEMA MULTIFORME MAJOR
- •CONNECTIVE TISSUE DISORDERS
- •PSEUDOXANTHOMA ELASTICUM
- •RELAPSING POLYCHONDRITIS
- •UVEITIS ASSOCIATED WITH JUVENILE IDIOPATHIC ARTHRITIS
- •WEGENER GRANULOMATOSIS
- •WEILL–MARCHESANI SYNDROME
- •SKELETAL DISORDERS
- •PHAKOMATOSES
- •NEUROFIBROMATOSIS TYPE 1
- •STURGE–WEBER SYNDROME
- •NEUROLOGIC DISORDERS
- •ACQUIRED INFLAMMATORY DEMYELINATING NEUROPATHIES
- •CREUTZFELDT–JAKOB DISEASE
- •NEOPLASMS
- •JUVENILE XANTHOGRANULOMA
- •LEIOMYOMA
- •ORBITAL RHABDOMYOSARCOMA
- •SEBACEOUS GLAND CARCINOMA
- •SQUAMOUS CELL CARCINOMA
- •MANAGEMENT OF SCLERAL RUPTURES 871.4 AND LACERATIONS 871.2
- •IRIS LACERATIONS 364.74, IRIS HOLES 364.74, AND IRIDODIALYSIS 369.76
- •ORBITAL IMPLANT EXTRUSION
- •SHAKEN BABY SYNDROME
- •PAPILLORENAL SYNDROME
- •ANTERIOR CHAMBER
- •CHOROID
- •ANGIOID STREAKS
- •CHOROIDAL DETACHMENT
- •SYMPATHETIC OPHTHALMIA
- •CONJUNCTIVA
- •ALLERGIC CONJUNCTIVITIS
- •BACTERIAL CONJUNCTIVITIS
- •LIGNEOUS CONJUNCTIVITIS
- •OPHTHALMIA NEONATORUM
- •CORNEA
- •BACTERIAL CORNEAL ULCERS
- •CORNEAL MUCOUS PLAQUES
- •CORNEAL NEOVASCULARIZATION
- •FUCHS’ CORNEAL DYSTROPHY
- •KERATOCONJUNCTIVITIS SICCA AND SJÖGREN’S SYNDROME
- •LATTICE CORNEAL DYSTROPHY
- •NEUROPARALYTIC KERATITIS
- •PELLUCID MARGINAL DEGENERATION
- •EXTRAOCULAR MUSCLES
- •ACCOMMODATIVE ESOTROPIA
- •CONVERGENCE INSUFFICIENCY
- •MONOFIXATION SYNDROME
- •NYSTAGMUS
- •EYELIDS
- •BLEPHAROCHALASIS
- •BLEPHAROCONJUNCTIVITIS
- •EPICANTHUS
- •FACIAL MOVEMENT DISORDERS
- •FLOPPY EYELID SYNDROME
- •MARCUS GUNN SYNDROME
- •SEBORRHEIC BLEPHARITIS
- •XANTHELASMA
- •GLOBE
- •BACTERIAL ENDOPHTHALMITIS
- •FUNGAL ENDOPHTHALMITIS
- •INTRAOCULAR PRESSURE
- •ANGLE RECESSION GLAUCOMA
- •GLAUCOMA ASSOCIATED WITH ELEVATED VENOUS PRESSURE
- •GLAUCOMATOCYCLITIC CRISIS
- •NORMAL-TENSION GLAUCOMA (LOW-TENSION GLAUCOMA)
- •IRIS AND CILIARY BODY
- •ACCOMMODATIVE SPASM
- •LACRIMAL SYSTEM
- •LACRIMAL HYPOSECRETION
- •DISLOCATION OF THE LENS
- •LENTICONUS AND LENTIGLOBUS
- •MICROSPHEROPHAKIA
- •MACULA
- •CYSTOID MACULAR EDEMA
- •EPIMACULAR PROLIFERATION
- •OPTIC NERVE
- •ISCHEMIC OPTIC NEUROPATHIES
- •TRAUMATIC OPTIC NEUROPATHY
- •ORBIT
- •EXTERNAL ORBITAL FRACTURES
- •INTERNAL ORBITAL FRACTURES
- •OPTIC FORAMEN FRACTURES
- •RETINA
- •ACQUIRED RETINOSCHISIS
- •ACUTE RETINAL NECROSIS
- •DIFFUSE UNILATERAL SUBACUTE NEURORETINITIS
- •RETINOPATHY OF PREMATURITY
- •SCLERA
- •SCLEROMALACIA PERFORANS
- •VITREOUS
- •VITREOUS WICK SYNDROME
- •Index
somewhat less urgency because of slower progression of neovascular and fibrovascular proliferation; however, generally these eyes are operated on within two to three months if the hemorrhage is severe. It is of great importance to remove fibrovascular membranes with the vitreous cutter or scissors. In most diabetic eyes without traction detachments of the macula, vitreous surgery can usually restore useful vision including macular function. However, in these cases the visual outcome is always limited by the extent of retinal vascular damage from diabetes.
Dense vitreous hemorrhages can develop in eyes with agerelated macular degeneration, and most of these have significant, disciform scars. Nevertheless vitrectomy may be helpful in restoring useful peripheral vision in many cases.
There is no currently available medical or ocular treatment for vitreous hemorrhages. However, research using various enzymes, such as hyaluronidase, injected into the vitreous has shown promise in clearing vitreous hemorrhages. Current studies are beginning to evaluate the use of vascular endothelial growth factor inhibitors, such as pegaptanib (Macugen) and bevacizumab, injected into the vitreous to stimulate regression of neovascularization.
Complications of vitreous surgery include cataract development, glaucoma, and retinal detachment. These problems can usually be managed medically or with additional surgery.
Neovascular glaucoma can complicate eyes with ischemic retinopathy before or after a vitrectomy. In addition, depending upon the underlying pathology, there is at least a small risk of recurrent bleeding following a vitrectomy despite removal of or cautery applied to posterior segment neovascularization.
REFERENCES
Coats DK, Miller AM, McCreery KMB, et al: Involution of threshold retinopathy of prematurity after diode laser photocoagulation. Ophthalmology 111:1894–1898, 2004.
Eller AW: Diagnosis and management of vitreous hemorrhage: American Academy of Ophthalmology Focal Points 18:1–8, 2000.
Ibarra MS, Hermel M, Premer JL, Hassan TS: Longer-term outcomes of transconjunctival sutureless 25-gauge vitrectomy. Am J Ophthalmol 139:831–836, 2005.
Kupperman BD, Thomas EL, de Smet MD, Grillone LR, for the Vitrase for Vitreous Hemorrhage Study Groups: Pooled efficacy results from two multinational randomized controlled clinical trials of a single intravitreal injection of highly purified ovine hyaluronidase (Vitrase®) for the management of vitreous hemorrhage. Am J Ophthalmol 140:573–584, 2005.
Sarrafizadeh RH, Hassan TS, Ruby AJ, et al: Incidence of retinal detachment and visual outcome in eyes presenting with posterior vitreous separation and dense fundus-obscuring vitreous hemorrhage. Ophthalmology 108:2273–2278, 2001.
353 VITREOUS WICK SYNDROME
379.26
James P. Bolling, MD
Jacksonville, Florida
ETIOLOGY
The vitreous wick syndrome occurs when vitreous is incarcerated in a corneal or corneoscleral incision; this creates a ‘wick’
to the external ocular surface. Vitreous wick may be more common in the age of intravitreal injections and no-stitch vitrectomy. Vitreous loss or incarceration (wick) usually occurs:
●In the setting of unrecognized rupture in the posterior capsule; or
●After inadequate vitrectomy following recognized posterior capsule rupture;
●After intravitreal injection of steroids or other pharmacologic agents;
●After a laceration of the sclera when the edges of the wound are not completely cleaned of vitreous.
A vitreous wick can produce a noninfectious ocular inflammation with entrapment of vitreous, distortion of the pupil and release of mediators of inflammation. This in turn may result in cystoid macular edema. The anterior traction may extend to the vitreous base, causing retinal breaks or detachment. The vitreous incarcerated in the wound may serve as a stent and delay would closure increasing the risk of endophthalmitis.
DIAGNOSIS
Clinical signs and symptoms
●Anterior chamber cells and flare.
●Hypopyon.
●Strand(s) of vitreous in anterior chamber.
●Distorted pupil.
●Dilated iris vessels.
●Cells in vitreous.
●Degenerative vitreous changes and membranes.
●Cystoid macular edema.
●Retinal tears or detachment.
●Endophthalmitis.
TREATMENT
Ocular
Treatment varies, depending on the complications of the vitreous wick. Sometimes the vitreous incarceration in the wound may not be apparent until after completion of the surgery; if this is the case and no wound leak is present, no therapy need be given, although the patient should be followed closely in the immediate postoperative period.
If cystoid macular edema develops and abnormal inflammation is present, medical therapy should first be attempted.
●Topical prednisolone acetate drops can be tried for 2 weeks.
If no improvement is seen:
●Sub-Tenon’s injections of triamcinolone acetate may be used;
●Topical nonsteroidal anti-inflammatory drugs may also be tried;
●Oral acetazolamide also has been shown to be effective in reducing cystoid macular edema.
Surgical
If the primary situation involves wound leak, this may be recognized at the conclusion of surgery. It can then be repaired by:
●‘Sponge vitrectomy,’ lifting the vitreous strand at the wound with a small cellulose surgical sponge and cutting it with scissors; or
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●Using the vitreous cutter to aspirate over the wound with the cutter on.
If these methods are not effective in releasing all of the vitreous from the wound, it may be necessary to:
●Reopen the incision and clean the vitreous from the wound edges;
●Make a second incision away from the site of incarceration, permitting the vitreous strand(s) to be severed with an iris sweep or vitreous cutter.
Occasionally, the wound leak is the primary problem, carrying prolapsed vitreous forward to lodge in the wound. If this is the case, securely suturing the wound closed should prevent recurrent prolapse. If all these measures are not adequate, it may be necessary to perform:
●An anterior vitrectomy.
All cataract surgeons should be prepared to perform an anterior vitrectomy at the time of routine cataract surgery.
Sometimes the vitreous entrapped in the wound is not recognized until well after surgery; if symptoms of endophthalmitis are present (sudden onset of pain, vision loss, hypopyon, and vitreous inflammation):
●Immediate vitreous tap should be performed; and
●Systemic (oral, intravenous, or both) antibiotics should be started as soon as possible.
If endophthalmitis has compromised the patient’s vision to the level of light perception:
●A vitrectomy is indicated.
During a posterior vitrectomy, the wick can sometimes be released by aspirating immediately behind the implant.
Depending on the lapse of time since the original surgery:
●An anterior chamber incision may be necessary to pull a fibrin plaque off the surface of the implant, using a bent needle; sometimes the vitreous can also be engaged in this manner.
If manipulation of the wound and anterior chamber is not completely successful in removing the vitreous from the anterior structures:
●A pars plana vitrectomy may be necessary.
In fact, this is usually the situation because in most cases, the vitreous is adherent not only to the wound but also to the back of the iris, the capsule and the implant.
COMMENTS
In many cases, cataract surgery is now performed without any sutures to close the wound; vitrectomy surgery is also being performed without sutures. This may result in more patient comfort and less astigmatism postoperatively. Unfortunately, if the unsutured wound is leaking, vitreous may readily become lodged in the wound and endophthalmitis may be more common. It is important to check the wound carefully for leaks and securely close them when necessary.
REFERENCES
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 137(6):1159–1160, 2004.
Endophthalmitis Vitrectomy Study Group: Results of the Endophthalmitis Vitrectomy Study: a randomized trial of immediate vitrectomy and of intravenous antibiotics for the treatment of postoperative bacterial endophthalmitis. Arch Ophthalmol 113:1479–1496, 1995.
Nelson DB, Donnenfeld ED, Perry HD: Sterile endophthalmitis after sutureless cataract surgery. Ophthalmology 99:1655–1657, 1992.
Ruiz RS, Teeters VS: The vitreous wick syndrome: a late complication following cataract extraction. Am J Ophthalmol 70:483–490, 1970.
Turkalj JW, Carlson AN, Manos JP, Apple DJ: Is the sutureless cataract incision a valve for bacterial inoculation? J Cataract Refract Surg 21:472–476, 1995.
Venkatesh P, Verma L, Tewari H: Posterior vitreous wick syndrome: a potential cause of endophthalmitis following vitreo-retinal surgery. Medical Hyothesis 58(6):513–515, 2002.
Whitcup SM, Csaky KG, Podgor MJ, et al: A randomized, masked crossover trial of acetazolamide for cystoid macular edema in patients with uveitis. Ophthalmology 103:1054–1062, 1996.
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