Postoperative Corneal Edema Clinical Presentation

  • Author: Michael Taravella, MD; Chief Editor: Hampton Roy Sr, MD   more...
 
Updated: Feb 14, 2012
 

History

  • Symptoms of bullous keratopathy include the following:
    • Poor vision
    • Haloes around point sources of light
    • Pain
    • Foreign body sensation
    • Photophobia
  • Poor vision and haloes are symptoms of corneal edema.
  • 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.[13]
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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 appear as 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:
  • Surgical trauma at the time of cataract surgery can be associated with a marked reduction in endothelial cell counts.[16, 17, 18, 19, 20]
    • Modern techniques of cataract extraction (eg, phacoemulsification) are associated with endothelial cell loss of about 4-10%; however, on any individual patient, wide variations in cell loss can occur. Diabetes is a risk factor for endothelial damage as well.[21]
    • 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.[22, 23]
    • 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.[24] 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.
  • 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 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.
    • This style of lens is thought to be partly responsible for the epidemic of PBK of the mid 1980s. These lenses are no longer 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 (eg, Fuchs endothelial dystrophy) sometimes are overlooked on the preoperative exam, where the finding of cornea guttata may be subtle.[25] See the image below. 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.[26]
    • 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. 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.
  • The choice of intraocular irrigating fluid can have a profound affect on postoperative corneal edema.
    • Under experimental conditions, normal saline induces more corneal swelling than Ringer's lactate solution, while BSS causes the least amount of swelling. BSS contains an electrolyte balance very similar to aqueous humor. BSS plus is probably the best solution for use in compromised corneas and when long case times are anticipated (vitrectomies).[27, 28]
    • 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 to any other intraocular irrigating solution.
    • The use of intraocular solutions for specific purposes (eg, intracameral lidocaine for topical cataract anesthesia, Miochol and Miostat for pupillary miosis, epinephrine combined with BSS to maintain mydriasis during cataract surgery) has generally proven to be safe in terms of endothelial cell loss and toxicity.[29] However, the use of such solutions should be limited, and the principal of the least amount of solution irrigated into the eye to accomplish the stated purpose should be followed.
    • A recent outbreak of toxic anterior segment syndrome (TASS) 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 also be found in References.[30]
  • Inflammation, specifically iritis and uveitis, can profoundly affect endothelial function.[31]
    • 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.
    • Judicious use of topical steroids (eg, prednisolone acetate) can have a beneficial effect on corneal edema. This beneficial effect must always be balanced against the possible adverse effects of glaucoma and local immunosuppression.
  • 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 often 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) should be avoided because both drugs may adversely affect intraocular inflammation. Articles have suggested that topical carbonic anhydrase inhibitors should be avoided in this instance because some question as to their endothelial toxicity in compromised corneas exists.
  • 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.[32] 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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Contributor Information and Disclosures
Author

Michael Taravella, MD  Director of Cornea and Refractive Surgery, Rocky Mountain Lions Eye Institute; Professor, Department of Ophthalmology, University of Colorado School of Medicine

Michael Taravella, MD is a member of the following medical societies: American Academy of Ophthalmology, American Medical Association, American Society of Cataract and Refractive Surgery, Contact Lens Association of Ophthalmologists, and Eye Bank Association of America

Disclosure: Nothing to disclose.

Coauthor(s)

Mark Walker, MD  Medical Director, Laser Eye Connection

Mark Walker, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Ophthalmology, American Society of Cataract and Refractive Surgery, and Contact Lens Association of Ophthalmologists

Disclosure: Nothing to disclose.

Specialty Editor Board

Richard W Allinson, MD  Associate Professor, Department of Ophthalmology, Texas A&M University Health Science Center; Senior Staff Ophthalmologist, Scott and White Clinic

Richard W Allinson, MD, is a member of the following medical societies: American Academy of Ophthalmology, American Medical Association, and Texas 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.

Christopher J Rapuano, MD  Professor, Department of Ophthalmology, Jefferson Medical College of Thomas Jefferson University; Director of the Cornea Service, Co-Director of Refractive Surgery Department, Wills Eye Institute

Christopher J Rapuano, MD is a member of the following medical societies: American Academy of Ophthalmology, American Society of Cataract and Refractive Surgery, Contact Lens Association of Ophthalmologists, Cornea Society, Eye Bank Association of America, International Society of Refractive Surgery, and Pan-American Association of Ophthalmology

Disclosure: Allergan Honoraria Speaking and teaching; Allergan Consulting fee Consulting; Alcon Honoraria Speaking and teaching; RPS Ownership interest Other; EyeGate Pharma Consulting fee Consulting; Bausch & Lomb Honoraria Speaking and teaching; Bausch & Lomb Consulting; Merck Honoraria Speaking and teaching

Lance L Brown, OD, MD  Ophthalmologist, Affiliated With Freeman Hospital and St John's Hospital, Regional Eye Center, Joplin, Missouri

Disclosure: Nothing to disclose.

Chief Editor

Hampton Roy Sr, MD  Associate Clinical Professor, Department of Ophthalmology, University of Arkansas for Medical Sciences

Hampton Roy Sr, MD is a member of the following medical societies: American Academy of Ophthalmology, American College of Surgeons, and Pan-American Association of Ophthalmology

Disclosure: Nothing to disclose.

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Pseudophakic bullous keratopathy. Large multiple bullae, such as depicted here, are associated with moderate to severe pain and discomfort.
Pseudophakic bullous keratopathy in a patient with a Binkhorst style iris-fixated lens.
Pseudophakic bullous keratopathy. This patient has a closed-loop anterior chamber intraocular lens (Leiske model).
Specular microscopy of a normal cornea. Note the compact, uniform hexagonal appearance of the endothelial cells.
Specular microscopy illustrating moderate polymegathism and polymorphism. This is thought to be evidence of endothelial physiologic stress.
Fuchs endothelial dystrophy. The apparently empty spaces are occupied by guttate.
 
 
 
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