Poor epithelial adherence can persist for weeks if the epithelium is removed at the time of vitrectomy (1, 2, 3, 4). Care during the prep, frequent irrigation of the cornea with balanced salt solution (BSS), and shorter operating times dramatically reduce the need to remove the epithelium. The authors remove the epithelium in less than 2% of cases. When necessary, the epithelium should be mobilized rather than scraped. The rounded blade used for mobilization should never touch Bowman’s membrane. The defect should be made the same size as the pupil, avoiding the peripheral cornea. Some surgeons use Gelfoam, tear substitutes, or viscoelastics during surgery, but the authors have not found these to be necessary or efficacious. Bandage contact lenses or pressure patches are not necessary in the typical postoperative management. In the rare cases requiring epithelial removal, the epithelium is healed within several days postvitrectomy and is always healed on the 2-week office visit. If the patient develops a recurrent epithelial defect, cessation of topical medications and taping the lid closed for 12 to 24 hours will usually be sufficient. A rare patient will require a therapeutic soft contact lens. Infection of the corneal epithelial defect may occur in conjunction with soft lens usage.

Endothelial cell damage is rare after vitrectomy with decreased turbulence three-port and 25-gauge systems, less fluid throughput, better lens removal techniques, and better irrigating fluids (BSS Plus). If those patients with previous surgical trauma, glaucoma, or inherited endothelial dystrophies are excluded, postoperative corneal edema should not happen. Prolonged contact of a gas bubble or a silicone bubble totally filling the anterior chamber can damage the corneal endothelium and must be avoided by proper postoperative positioning. Epithelial edema can be managed by topical hyperosmotic medications, although this is largely symptomatic treatment. Fortunately, sliding of endothelial cells and the regaining of function of the remaining cells cause clearing of corneal edema in most cases. If corneal edema persists and the eye is required for the patient’s visual function, Descemet’s Stripping Endokeratoplasty (DSEK) or penetrating keratoplasty should be performed.

Precipitates on the endothelium are frequently interpreted as evidence of inflammation, while in many cases, they represent pigment released from iris and retinal pigment epithelium or erythroclasts.

Most cells in the anterior chamber are erythroclasts released either from the vitreous lamella or as a result of intraoperative or postoperative bleeding. If no retinopexy is performed, vitrectomy results in little inflammation. Iris trauma in conjunction with vitreous surgery results in inflammation and should be avoided. Retained nucleus appears to play a greater role in postoperative inflammation than does persistent cortex. All cases of iris neovascularization and most cases of retinal detachment have protein release in the anterior chamber, which is visible as “flare.” Treatment of the basic disease process by reattachment of the retina or
panretinal photocoagulation (PRP) is more effective than topical steroids in reducing the flare due to neovascularization. Anti-vascular endothelial growth factor (VEGF) compounds have proven to be effective in these cases. Topical and intraoperative subconjunctival, long-acting steroids are used in all patients who are not steroid glaucoma responders (5). This is primarily because any severe inflammation can result in the development of a cyclitic membrane, periretinal membranes, and, ultimately, phthisis bulbi. Steroids do not appear to significantly retard the healing of any of the ocular structures and should be used to reduce inflammation. The authors rarely prescribe systemic steroids for primary ocular conditions. Inflammation not responsive to frequent topical steroids is treated with repeated subconjunctival triamcinolone.

The cause and treatment of iris neovascularization have been extensively discussed in Chapter 6. Occasionally, iris neovascularization will appear when retinal detachments with severe periretinal proliferation are operated on unsuccessfully. Intravitreal bevacizumab can be used to cause regression of the neovascularization postoperatively, followed by PRP (6). If anti-VEGF therapy and PRP cause regression of iris neovascularization, the large vessels will not disappear because of rheologic considerations. The examiner must concentrate on the presence of capillary activity and endothelial budding on the iris surface rather than the more impressive large vessels. Peripheral anterior synechiae and ectropion uveae are late changes and never disappear, even when capillary involution occurs. Although some clinicians have emphasized the difficulty in differentiating iris neovascularization from dilation of preexisting stromal vessels, as a rule, this is not a difficult problem.

Increased intraocular pressure (IOP) from varied mechanisms is an all too frequent complication of vitreous surgery. A high incidence of suspicion and frequent follow-up is a necessity for recognizing and managing this dreaded complication (7).