Postoperative Corneal Edema Clinical Presentation

Updated: Jan 18, 2023
  • Author: Michael Taravella, MD; Chief Editor: John D Sheppard, Jr, MD, MMSc  more...
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Presentation

History

Symptoms of bullous keratopathy and corneal edema include the following:

  • Poor vision
  • Vision is worst first thing in the morning and improves as the day progresses
  • Haloes around point sources of light
  • Pain
  • Foreign body sensation
  • Photophobia
  • Tenderness, particularly in the presence of an anterior-chamber intraocular lens (IOL)

Stromal edema affects vision much less and causes less light scatter than epithelial edema; epithelial edema involves the corneal surface and disrupts the normally smooth and regular tear film. The development and subsequent rupture of corneal bullae on the densely innervated corneal surface cause pain and photophobia. [18]

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Physical

Vision will be decreased in proportion to the development of central corneal edema. Slit lamp examination invariably reveals folds in the Descemet membrane and obvious overall thickening of the central and peripheral cornea.

In the more advanced stages of PBK, vesicles and bullae can be seen on the corneal surface.

In patients with predisposing corneal problems (eg, Fuchs dystrophy), cornea guttata may be seen. On slit lamp examination, guttate excrescences may appear as diffuse fine brownish pigment granules or, in more advanced cases, dense golden-brown confluent endothelial lesions and give the posterior corneal surface a characteristic beaten-metal appearance.

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Causes

Causes of corneal edema include the following:

  • Congenital hereditary endothelial syndrome [19]
  • Posterior polymorphous dystrophy [20]
  • Chandler syndrome, iridocorneal endothelialization (ICE) syndrome, Cogan-Reese syndrome
  • Herpetic disciform keratitis
  • Herpes zoster ophthalmicus, endotheliitis, uveitis, and keratitis
  • Epstein-Barr virus keratitis
  • Corneal transplant rejection
  • Surgical trauma at the time of cataract, glaucoma, or other intraocular surgical procedures
  • Severe blunt trauma
  • Chronic uveitis with keratic precipitates
  • Faulty anterior IOL design with anterior vaulting and endothelial trauma
  • Myopic intraocular contact lens (ICL) complications
  • Toxic anterior segment syndrome (TASS)
  • Anterior-chamber prolapsed vitreous touch
  • Silicone oil migration into the anterior chamber
  • Flat anterior chamber and iris touch

Surgical trauma at the time of cataract surgery

Surgical trauma at the time of cataract surgery can be associated with a marked reduction in endothelial cell counts. [21, 22, 23, 24, 25]

With modern techniques of cataract extraction (eg, phacoemulsification) using ophthalmic viscosurgical devices, the rate of endothelial cell loss is reported to be about 2-7%. It varies greatly and is significantly associated with the cataract grade and anterior chamber depth. Diabetes also is a risk factor for endothelial damage.  [26]  

Endothelial cell loss has been correlated with cataract incision size and location, density of nucleus, total ultrasound energy used, and volume of fluid irrigated into the eye at the time of surgery. Individual surgeon techniques and skill vary widely, and, correspondingly, endothelial cell loss will vary. [27, 28, 29]  

Directly touching the endothelium during cataract surgery with instruments, nuclear fragments, or the intraocular lens should be avoided. Routine use of viscoelastic agents has resulted in a dramatic decrease in endothelial cell loss and offers a practical and effective means of protecting the cornea from inadvertent trauma during cataract surgery. [30] Dispersive viscoelastics may offer more protection to the endothelium than cohesive viscoelastics, especially if the surgeon's technique is such that nuclear fragments are removed with phacoemulsification more anteriorly, above the iris plane. Minimization of excess fluid currents, limitation of total surgical time and irrigation time, maintenance of tight primary and secondary wound openings without external reflux, and overall reduction of total balanced salt solution (BSS) use per case all are tactics to reduce endothelial trauma through surgical technique. 

Retained lens fragments after phacoemulsification surgery also commonly present with focal corneal edema and rarely can evolve to corneal decompensation requiring transplantation if not removed in time. [31, 32]

Intraocular lenses

Older-style intraocular lenses have been associated with accelerated endothelial cell loss following cataract surgery.

In particular, closed-loop anterior chamber intraocular lenses (ie, Leiske, Hessburg, Azar 91Z style) have been implicated with this problem. The haptics with these lenses tended to be stiff and erode through uveal tissue, causing chronic low-grade inflammation and continued endothelial cell loss. In addition, anterior flexion of the IOL due to the stiff haptics brings the optic into close approximation of the endothelium, with augmented irritation during eye rubbing. Inappropriately large anterior-chamber IOL diameters for a given white-to-white diameter exacerbate both problems.

These IOL designs are thought to be partly responsible for the epidemic of PBK of the mid-1980s. These lenses no longer are implanted. Modern flexible open-loop anterior and posterior chamber intraocular lenses have proven to be much safer alternatives. Biocompatible materials (eg, polymethylmethacrylate, acrylic, silicone), excellent finish, and good flexibility characterize these lenses.

Corneal dystrophies

Corneal dystrophies (eg, Fuchs endothelial dystrophy) sometimes are overlooked on the preoperative examination, where the finding of cornea guttata may be subtle, particularly when there is minimal endothelial pigmentation. [33]  

Fuchs endothelial dystrophy. The apparently empty Fuchs endothelial dystrophy. The apparently empty spaces are occupied by guttate.

Fuchs dystrophy is more common in women than in men and usually presents in older patients. The pattern of inheritance is not known with certainty, but it is thought to be autosomal dominant. Characteristics of this dystrophy include cornea guttata, which are droplike excrescences produced by the endothelium, a thicker than normal Descemet membrane, and a decreased number of endothelial pump sites. [34]

An increased frequency of cornea guttata in the opposite unoperated eye in patients developing PBK has been noted. In one study, 67% of corneal buttons removed at the time of keratoplasty for bullous keratopathy from eyes with posterior chamber lenses (suggesting an intact posterior capsule and uncomplicated cataract surgery) were noted to have evidence of an endothelial dystrophy. Predictive modeling using pachymetry and elevation maps detecting Fuch’s dystrophy features such as loss of regular isopachs, displacement of the thinnest point, and posterior surface depression has shown that the risk of requiring EK after phacoemulsification can be as high as 76.5% in eyes with all of these 3 features. [35]  

This highlights the need for a careful preoperative slit lamp examination to help identify patients at risk for the development of postoperative corneal edema. If cornea guttata are noted on slit lamp examination, specular microscopy and ultrasound pachymetry should be performed to help quantify endothelial reserve and to aid in risk assessment. In such patients, the intraoperative use of balanced salt solution plus glutathione, bicarbonate, and adenosine (BSS plus) and dispersive viscoelastic agents may limit endothelial damage.

Patient counseling is essential to manage expectations, including the decision of whether to perform combined endothelial keratoplasty (eg, Descemet membrane endothelial keratoplasty [DMEK] or Descemet stripping endothelial keratoplasty [DSEK]) or to defer the decision on whether to perform the transplant until after the cataract surgery has been performed.

Recently, combined procedures have been found to not differ significantly from staged procedures in complication rates, endothelial cell loss, graft success, or visual improvement. Moreover, combined procedures are easier for the patient, more cost-effective, and do not increase the risk for complications. [36]

Intraocular irrigating fluid

The choice of intraocular irrigating fluid can have an effect on postoperative corneal edema.

Under experimental conditions, normal saline induces more corneal swelling than Ringer's lactate solution, whereas BSS causes the least amount of swelling. BSS contains an electrolyte balance very similar to aqueous humor. BSS plus probably is the best solution for use in compromised corneas and when long case times are anticipated (eg, synechiolysis, iris retractors, vitrectomies). [37, 38]

Glutathione is a free radical scavenger and antioxidant, and its use with BSS has been shown to result in the least amount of corneal edema compared with any other intraocular irrigating solution.

The use of intraocular solutions for specific purposes generally has proven to be safe in terms of endothelial cell loss and toxicity. [39]  These solutions include intracameral lidocaine for topical cataract anesthesia, Miochol and Miostat for pupillary miosis, epinephrine or phenylephrine combined with BSS and lidocaine to induce mydriasis at the beginning of cataract surgery, or Omidria (Omeros) to maintain mydriasis throughout cataract surgery, or intracameral antibiotics such as cefuroxime and moxifloxacin. However, the use of such solutions should be intelligently conserved, and the principal of the least amount of solution irrigated into the eye to accomplish the stated purpose should be followed. [40]

Episodes of toxic anterior segment syndrome (TASS) have brought the issue of the safety of irrigating solutions used in the eye to the forefront. An excellent review of toxic anterior segment syndrome can be found in References. [41]

Inflammation

Inflammation, specifically iritis and uveitis, can profoundly affect endothelial function. [42]

Classic examples include corneal transplant rejection and herpetic disciform keratitis. In both of these examples, the endothelial cells are the targets of the inflammatory response. However, even nonspecific inflammation, such as that occurring in postoperative and traumatic iritis and other causes of uveitis, can be associated with compromised endothelial function.

If a patient with previous corneal transplant and a history of herpetic keratitis in the operated eye presents with corneal edema and keratic precipitates, noting the location and boundary of the inflammatory process can help distinguish between the two. Inflammation that respects the corneal transplant graft-host wound margin is more likely to be a rejection reaction. If the host cornea and graft host interface are involved, this is more likely to be a recurrence of herpetic infection or stromal keratitis.

Judicious use of topical steroids (eg, prednisolone acetate, loteprednol etabonate, difluprednate, dexamethasone) can have a beneficial effect on corneal edema. This beneficial effect always must be balanced against the possible adverse effects of glaucoma, cataractogenesis, herpetic reactivation, delayed wound healing, and local immunosuppression.

High intraocular pressure

Intraocular pressure has an important effect on the state of corneal hydration.

High intraocular pressure, such as that occurring in attacks of narrow-angle glaucoma, drives fluid into the cornea and is associated with the acute onset of corneal edema, even when the corneal endothelium is otherwise healthy. Conversely, prephthisical eyes with low intraocular pressure may have clear corneas, regardless of endothelial cell count and function.

Lowering intraocular pressure can decrease corneal edema and thickness in the postoperative setting, even if the intraocular pressure is normal or only mildly elevated. Beta-blockers (eg, Timoptic, Betagan) and alpha-agonists (eg, Iopidine, Alphagan) are the first line of therapy for this purpose. Prostaglandin analogs (eg, Xalatan) and miotics (eg, pilocarpine) may adversely affect intraocular inflammation and are recommended to be used with caution. Articles have suggested that topical carbonic anhydrase inhibitors should be avoided in this instance owing to the question of endothelial toxicity in compromised corneas. A newer medication class such as Rho kinase inhibitor (eg, Rhopressa) also has been reported to be associated with reticular epithelial corneal edema. [43, 44, 45]

Vitreous touch and flat anterior chamber with intraocular lens touch

Postoperative factors that can be associated with endothelial cell loss include vitreous touch and flat anterior chamber with intraocular lens touch.

If the posterior capsule is ruptured at the time of cataract surgery, vitreous may bulge forward into the anterior chamber. Careful vitrectomy at the time of surgery usually prevents prolonged contact of vitreous with the endothelial surface. [46] However, if vitreous is noted to be in contact with the posterior cornea in the early postoperative period, serial pachymetry and specular microscopy can aid in determining if a vitrectomy is necessary.

Removal of the vitreous via a pars plana approach may be beneficial in preventing progressive endothelial cell loss. Similarly, a flat anterior chamber in which the intraocular lens shifts forward and touches the endothelium should be addressed by reforming the anterior chamber as soon as practical. Such a situation may arise if a wound leak or choroidal effusion is present.

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Complications

Factors limiting vision include a high association of this condition with cystoid macular edema, postoperative astigmatism, uveitis, and glaucoma.

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