Anterior Segment Complications of Vitreoretinal Surgery

Commentary from an expert on which ones can be avoided - and which cannot

Anterior Segment Complications of Vitreoretinal Surgery

Commentary from an expert on which ones can be avoided — and which cannot.


Vitreoretinal surgery has made remarkable progress in the almost 4 decades since the first patient was operated on in 1970. Outcomes have markedly improved; many diseases formerly untreatable are managed with high success rates: epimacular membranes, macular holes, diabetic traction, retinal detachments, giant retinal breaks, and many others.

Vitreoretinal surgery utilized in combination with anti-VEGF therapy and laser photocoagulation has significantly improved outcomes in the management of diabetic retinopathy. Some disease processes that seem ideal for a biologic solution — proliferative vitreoretinopathy and excessive repair after trauma — have not yet benefited from biotechnology developments. Although tremendous progress has been made in the vitreoretinal technique and technology arena, complications are ever-present, some technique-driven and others a consequence of biology.


Conjunctival damage from using various instruments to stabilize the eye during 23-gauge trocar insertion is preventable by using a constant relative orientation insertion technique (Figure 1), changing the insertion path as the eye compresses orbital fat instead of stabilizing the eye.1 Poor closure technique with overlapping margins and irritating Vicryl suture material remains a problem when using largely outdated sutured surgery.2 The author utilizes 25-gauge, sutureless, transconjunctival surgery for all cases.

Figure 1. Conjunctival damage can be avoided by using a constant relative orientation insertion technique.

Steve Charles, MD, is clinical professor of ophthalmology at the University of Tennessee, College of Medicine, Memphis. Dr. Charles reports significant financial interest in Alcon. He can be reached via e-mail at


Corneal epithelial defects are largely technique driven; Gelfoam, excessive use of topical anesthetics,3 inappropriate fundus contact lens coupling fluids, excessive exposure to povidone iodine,4 and inattention to corneal irrigation result in iatrogenic damage to the corneal epithelium. Removal of the corneal epithelium is required in less than 1% of the author's cases.

Corneal endothelial failure is also largely preventable; cell loss is caused by poor quality infusion fluid (lactated Ringers, BSS instead of BSS Plus, etc.),5 prolonged operating times with excessive fluid throughout (more frequent with 20-gauge surgery), and inappropriate use of various additives (dextrose, bicarbonate, epinephrine, antibiotics).6 Since vitreoretinal surgery is rarely elective, patients with low cell counts must still be operated on. Careful attention to technique and avoiding anterior-chamber intervention will minimize further cell loss.


Cataract (Figure 2) is not an inevitable consequence of vitrectomy;7 patients with clear lenses preoperatively will usually retain clear lenses if the optimal infusion fluid without additive is used (BSS Plus), fluid throughput is minimized, and intensive patient education is used to prevent gas bubble contact with the lens. Progression of pre-existing nuclear sclerosis is thought to be due to depletion of ascorbate associated with hyaluronan gel and vitreous collagen fiber matrix. Ascorbate absorbs oxygen; the partial pressure of oxygen permanently increases by 7 to 12 mm Hg after vitrectomy. Development of posterior capsular cataract is related to the factors described above, long term use of intravitreal steroids (not intraoperative), diabetes management, and disease-based factors.8

Figure 2. Cataract.


Glaucoma remains the most common and significant anterior-segment complication of posterior vitrectomy.9 Steroid glaucoma was once thought to affect only 6% of the population; this notion was based on studies utilizing 1% topical prednisolone. In-office use of intravitreal triamcinolone acetonide produces a roughly 30% incidence of glaucoma and the fluocinolone acetonide intravitreal implant Retisert (Bausch & Lomb) results in a ~90% incidence, with over 30% of patients requiring a glaucoma filtration procedure.10 Many surgeons, including the author, used subconjunctival triamcinolone in all patients undergoing vitrectomy not thought to be steroid responders. The author abandoned this practice in recent years and now uses subconjunctival Decadron because of the shorter duration of action.

Prior to the use of intravitreal and subconjunctival triamcinolone, it was thought that steroid glaucoma was reversible when the drug was gone, but this has not proved to be the case. Neovascular glaucoma is VEGF-driven and occurs after vitrectomy mostly in patients with diabetic retinopathy or retinal vein occlusions.11 Vitreous, lens, IOL, and trabecular meshwork are all diffusion barriers for VEGF, as well as substrates for neovascularization. Posterior vitrectomy in the presence of ischemic retina results in anterior vitreous cortex fibrovascular proliferation, unless the eye is aphakic and trabecular meshwork and iris neovascularization occurs because of anterior diffusion of VEGF.

Panretinal photocoagulation results in permanent decrease in VEGF production and is very effective in combination with anti-VEGF agents (eg, Avastin).12 Retinal detachment in the context of diabetic retinopathy increases VEGF production; retinal reattachment is effective in reducing VEGF release from the retina. The author has coined the term "particulate glaucoma" for increased IOP secondary to hemolyzed blood, erythroclasts (ghost cells), lens particles and associated inflammatory cells, micelles due to silicone oil emulsification, inflammatory cells, pigment due to pigment dispersion syndrome, and liquid perfluorocarbon droplets. In general, the treatment of particulate glaucoma is to remove the particulate materials and treat the inflammation.

Intraoperative lens dislocation (Figure 3) and decentration can result from gas bubble-pupillary block, iris retractors, and iris manipulation. For unknown reasons, low intraocular pressure causes severe miosis; careful attention to IOP control reduces the need for iris retractors. The Alcon Constellation Vision System with pressurized infusion and IOP compensation can reduce the incidence of intraoperative low IOP and secondary miosis.13 Synechia (Figure 4) between the IOL, capsule, and iris can result from gas-pupillary block combined with inflammation.

Figure 3. IOL dislocation.

Figure 4. Synechia.


Refractive changes from encircling buckles and silicone oil remain a significant issue in vitreoretinal surgery. Encircling buckles are, in the author's opinion, significantly overutilized in conjunction with vitrectomy. Vit-buckles have not been shown to produce better outcomes than so-called primary vitrectomy in the treatment of rhegmatogenous retinal detachment.14 The term "primary" vitrectomy implies that a buckle is first-line therapy for retinal detachment and a vitrectomy should only be used if the buckle fails or for special circumstances, such as PVR, vitreous hemorrhage, or obvious severe vitreous traction. Encircling buckles result in approximately 3 D of axial myopia, which is unacceptable in the broader context of emmetropic cataract surgery, LASIK, refractive lens exchange, toric IOLs, LRIs, etc.

In addition, encircling buckles cause strabismus (50% of patients have increased tropias and phorias). Encircling buckles also cause ptosis because of damage to the levator aponeurosis and Mueller's muscle, as well as longer operating time and substantially more pain. Silicone oil results in refractive change because the index of refraction of silicone oil differs from aqueous and vitreous. Preoperative determination of whether it is likely that the oil will ultimately be removed or retained behind an IOL can help determine required IOL power. It is a misconception that oil impairs vision; a normal retina will produce perfect vision through oil if an appropriate refraction is in place. It is also a mistake to think silicone oil is toxic and must be removed; emulsification glaucoma and corneal endothelial damage occur in about 3% of cases and virtually never if high quality oil (Alcon 1000 centistoke) is contained behind an IOL.


Iris damage from iris retractors, sphinc terotomies, iris sutures, and phaco probe contact results in cosmetic problems and patient complaints but rarely have functional implications. Contact-base wide-angle viewing systems (Volk, AVI), while not suitable for vitreomacular surgery because they decrease both axial and lateral resolution, are essential for viewing peripheral retinal pathology and often obviate the need for iris surgery or retractors.


Many anterior-segment complications of vitreoretinal surgery can be prevented by performing fast, efficient surgery and paying strict attention to technical details. Other complications, such as progression of pre-existing nuclear sclerosis, are physiologic and cannot be prevented but must be taken into account. Still others are based on complex disease processes such as PVR or are related to healing (eg, keloid) and cannot be prevented or treated by biologicals at this time. RP


  1. Arevalo JF, Sanchez JG, Freeman WR. 25-gauge transconjunctival sutureless vitrectomy for vitreous and retinal/choroidal biopsy. In: Rizzo S, Patelli F, Chow DR, eds. Vitreo-retinal Surgery. Berlin, Germany: Springer Verlag. 2008;147-156.
  2. Batman C, Ozdamar Y, Mutevelli S, Sonmez K, Zilelioglu G, Karakaya J. A comparative study of tissue glue and vicryl suture for conjunctival and scleral closure in conventional 20-gauge vitrectomy. Eye. 2008 Sep 5. [Epub ahead of print]
  3. Rizzo S, Genovesi-Ebert F, Patelli F. Small gauge vitrectomy: anesthesia, incision technique and cannula removal. In: Rizzo S, Patelli F, Chow DR, eds. Vitreo-retinal Surgery. Berlin, Germany: Springer Verlag. 2008;49-56.
  4. Freitas D, Santos N, Sousa L, Riguero M, Scarpi M. Corneal toxicity of povidone-iodine eye drops. Invest Ophthalmol Vis Sci. 2002;43:E-Abstract 4218.
  5. Charles S. Complications of vitreoretinal surgery. Retinal Physician. 2007;4(6):45-49.
  6. Liu L, Hartwig D, Harloff S, et al. Corneal epitheliotrophic capacity of three different blood-derived preparations. Invest Ophthalmol Vis Sci. 2006;47:2438-2444.
  7. Holekamp NM, Shui YB, Beebe DC. Vitrectomy surgery increases oxygen exposure to the lens: a possible mechanism for nuclear cataract formation. Am J Ophthalmol. 2005;139:302-310.
  8. Bhatnagar P, Schiff WM, Barile GR. Diabetic vitrectomy: the influence of lens status upon surgical outcomes. Curr Opin Ophthalmol. 2008;19:243-247.
  9. Campbell DG, Simmons RI, Tolentino FL, McMeel JW. Glaucoma occurring after closed vitrectomy. Am J Ophthalmol. 1977;83:63.
  10. Jaffe GJ, Martin D, Callanan D, Pearson PA, Levy B, Constock T; Fluocinolone Acetonide Uveitis Study Group. Fluocinolone acetonide implant (Retisert) for noninfectious posterior uveitis; thirty-four-week results of a multicenter randomized clinical study. Ophthalmology. 2006;113:10-27.
  11. Aiello LP, Avery RL, Arrigg PG, et al. Vascular endothelial growth factor in ocular fluid of patients with diabetic retinopathy and other retinal disorders. N Engl J Med. 1994;331:1480-1487.
  12. Ehlers JP, Spirn MJ, Lam A, Sivalingam A et al. Combination intravitreal bevacizumab/ panretinal photocoagulation versus panretinal photocoagulation alone in the treatment of neovascular glaucoma. Retina. 2008;28:696-702.
  13. Bonfiglio V, Bucolo C, Camillieri G, Drago F. Possible involvement of nitric oxide in morphine-induced miosis and reduction of intraocular pressure in rabbits. Eur J Pharmacol. 2006;534:227-232.
  14. Brazitikos PD. The expanding role of primary pars plana vitrectomy in the treatment of rhegmatogenous noncomplicated retinal detachment. Semin Ophthalmol. 2000;15:65-77.