AUTHOR AND EDITOR INFORMATION

Section 1 of 11  

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• Introduction
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• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

INTRODUCTION

Section 2 of 11  

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• Introduction
• Clinical
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• Treatment
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• Follow-up
• Miscellaneous
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Background

Pseudophakic bullous keratopathy (PBK) and aphakic bullous keratopathy (ABK) refer to the development of irreversible corneal edema as a complication of cataract surgery. As corneal edema progresses and worsens, first stromal and then intercellular epithelial edema develops. Epithelial edema is associated with the development of bullae; hence, the name bullous keratopathy. The history of PBK parallels the history of the development of the intraocular lens. As surgical techniques and lens design have improved, the incidence of this complication has decreased dramatically. However, it still represents an important cause of visual disability following routine and complicated cataract surgery.

Pathophysiology

Corneal transparency is, in a large part, dependent on the ability of the cornea to remain in a dehydrated state. It is affected by several interdependent factors. The epithelium and the endothelium are both semipermeable membranes that create a barrier to the flow of water and other electrolytes into the cornea. Evaporation from the corneal tear film results in slightly hypertonic tears that tend to draw fluid out of the cornea. Intraocular pressure tends to drive fluid into the cornea. Osmotic forces and the electrolyte balance within the corneal stroma also tend to draw water into the cornea. However, the most important influence on corneal deturgescence is the presence of an active metabolic pump in the endothelium.

The endothelium is a single layer of cells present on the back of the cornea. The site of the metabolic pump is within the lateral cell membrane; it is temperature dependent, associated with the enzyme Na⁺/K⁺ ATPase, and it is inhibited by ouabain. Endothelial cells produce a basement membrane (Descemet membrane), and they are of neuroectodermal origin. Cell density at birth can be as high as 7500 cells/mm², decreasing to an average of about 2500-2700 cells/mm² in older adults.

Endothelial cells are not capable of significant mitotic activity. The normal rate of endothelial loss after age 20 is approximately 0.5% per year. Surgical trauma, inflammation, and corneal dystrophies can accelerate this normal aging loss. The final common pathway in the development of bullous keratopathy is damage to the corneal endothelium; when the cell density reaches a critically low level of about 300-500 cells/mm², corneal edema develops.

Frequency

United States

Exact incidence of PBK is unknown; however, it currently is estimated that 0.1% of patients undergoing cataract surgery will develop this problem. Food and Drug Administration premarket approval studies for intraocular lenses performed from 1978-1982 found an incidence of postoperative corneal edema of 0.06% for posterior chamber lenses, 1.2% for anterior chamber lenses, and 1.5% for iris fixated lenses. Certain styles of intraocular lenses introduced in the mid 1980s were reported to have an incidence as high as 5% (Leiske and Hessburg closed loop anterior chamber intraocular lenses, ORC Stableflex, and Azar model 91Z).

From 1984-1989, ABK and PBK accounted for the majority of corneal transplants performed in the US (about 33%). Since then, the number of cases has decreased, despite an increase in the number of overall cataract surgeries performed. Keratoconus surpassed PBK in 1990 as the leading indication for corneal transplantation in some studies in the US. This overall drop in the incidence of PBK reflects the rapid development and improvement of both intraocular lens design and cataract surgical technique.

International

Trends similar to the US have been noted in Canada, United Kingdom, Australia, and Scandinavia.

Race

No known association of PBK with sex exists. Patients of Northern European descent do have an increased incidence of Fuchs corneal dystrophy. This dystrophy does predispose to the development of corneal edema (see Pathophysiology, Causes, Histologic Findings).

Sex

No known association of PBK with race exists. Fuchs corneal dystrophy, a known predisposing factor in the development of postoperative corneal edema, occurs approximately 3 times more frequently in women.

Age

Older patients who have less endothelial reserve are more prone to develop this problem.

CLINICAL

Section 3 of 11  

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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.

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.

Causes

• Other causes of corneal edema include the following:
  • Congenital hereditary endothelial syndrome
  • Posterior polymorphous dystrophy
  • Chandler syndrome
  • Acute narrow-angle glaucoma
  • Herpetic disciform keratitis
  • Corneal transplant rejection
• Surgical trauma at the time of cataract surgery can be associated with a marked reduction in endothelial cell counts.
• • 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.
  • 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.
  • 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. 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.
• Fuchs dystrophy is more common in women 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.
• 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.
• 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).
• 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.
• 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) generally have proven to be safe in terms of endothelial cell loss and toxicity. 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.
• Inflammation, specifically iritis and uveitis, can profoundly affect endothelial function.
• 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. Recent 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. 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.

DIFFERENTIALS

Section 4 of 11  

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Other Problems to be Considered

Fuchs corneal dystrophy
Posterior polymorphous dystrophy
Iridocorneal endothelial syndrome
Brown-McLean syndrome

WORKUP

Section 5 of 11  

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Imaging Studies

• Specular microscopy
• • Specular microscopy represents a photographic method of assessing the endothelium in vivo. Light is projected onto the cornea, and reflected images from an optical interface (eg, endothelium, aqueous humor) can be visualized.
  • High magnification photographs are taken of the endothelial layer, allowing quantification of cell density. Normal cell density varies from 3000-3500 cells/mm² in young adults to 2000-2500 cells/mm² in older individuals. Corneas with cell densities less than 1000 cells/mm² are at moderate-to-high risk of developing corneal edema following intraocular surgery.
  • Current instruments digitize and analyze these photographs, assessing such parameters as the coefficient of variation and the percent of hexagonal cells present. Both of these numbers represent a way of measuring polymorphism and polymegethism (ie, variation in cell size and shape) in the endothelial layer. Endothelial cells that show a great variability in size and shape are considered to be under physiologic stress and abnormal.
  • Besides evaluating the risk for the development of postoperative corneal edema, specular photomicrographs can be useful as a diagnostic aid to assess corneal disease states (eg, Fuchs corneal dystrophy, posterior polymorphous dystrophy). The former is associated with characteristic guttate excrescences, while the latter may show patchy areas of normal endothelium adjacent to abnormal endothelium, as well as vesicles and plaques. Serial specular photomicrographs can be used to follow patients at risk for progressive endothelial loss, such as that occurring with vitreous prolapse into the anterior chamber with corneal touch and corneal transplant rejection episodes.

Other Tests

• Ultrasound pachymetry and optical pachymetry
• • Both ultrasound and optical pachymetry are methods of measuring corneal thickness. Normal corneal thickness measures about 0.55 mm centrally, increasing to about 0.8 mm in the corneal periphery. Disease states resulting in corneal edema are associated with central corneal thickening as the cornea begins to swell. Corneal thicknesses above 0.6 mm centrally are suspect for corneal edema (although a small number of normal subjects may have this thickness).
  • Serial measurements are helpful in gauging the progression of a disease process (eg, Fuchs dystrophy), as well as in assessing therapeutic regimens (eg, topical steroid use in corneal graft rejection).
  • Ultrasonic pachymetry is more reproducible and requires less skill than optical pachymetry; optical pachymetry is especially helpful in measuring the depth of cornea pathology (eg, scars, other lesions) when the full thickness of the corneal stroma is not involved and it is necessary for therapeutic reasons to estimate the depth of this pathology (preoperative for excimer laser phototherapeutic keratectomy).

Histologic Findings

Pathologic findings noted on corneas removed and replaced for PBK include attenuation and absence of normal endothelial cells. Occasionally, evidence of preexisting endothelial dystrophy (eg, Fuchs dystrophy) may be seen. This dystrophy sometimes is missed during the preoperative exam and, as such, is associated with the development of postoperative corneal edema. The hallmark of this dystrophy is the finding of corneal guttate (Latin for drop) excrescences and a thickened Descemet membrane. Cornea guttata appear as excrescences extending from the Descemet membrane toward the anterior chamber.

TREATMENT

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Medical Care

Medical therapy of PBK consists of attempting to minimize corneal edema and the associated symptoms of discomfort and poor vision. Patients with early mild corneal edema may benefit from the use of hypertonic agents, such as sodium chloride 2% and 5% solution and ointment. These agents work by creating a hypertonic tear film, drawing water out of the cornea. Because evaporation from the tear film is minimal at night with the eyes closed (therefore, the tears are less hypertonic), corneal edema tends to be worse in the morning. Use of hypertonic sodium chloride 5% ointment at night applied to the conjunctival cul-de-sac limits this build-up of edema. Use of hypertonic solutions in the morning also helps eliminate some of this nightly fluid accumulation.

A typical regimen is Muro 128 2-5% drops used hourly in the affected eye until noon (4-5 times). As the day progresses, evaporation from the tear film begins to create relative hypertonicity of the tears, drawing fluid from the cornea. This accounts for the typical history of improving vision toward the end of the day.

Other practical methods of limiting corneal edema in eyes with borderline endothelial function include treatment of both ocular inflammation and elevated intraocular pressure (see Pathophysiology, Causes) if present.

• Bandage contact lenses may be useful as an adjunct to medical treatment for the temporary relief of corneal pain and discomfort. They act to shield the cornea and epithelium from the eyelid. In general, thin, high- water content lenses are tolerated best because they are more oxygen permeable. However, contact lens wear, especially overnight wear, can be associated with increased corneal edema due to improper fit (tight lens) and an increased risk of infection in an already compromised cornea. Patients for whom a bandage lens is prescribed should be treated with a broad-spectrum antibiotic (eg, Polytrim) or an aminoglycoside 2-4 times a day. These patients require close follow-up care. Long-term use of a bandage lens for the treatment of this condition is not advised.
• Patients who have poor visual potential and severe pain sometimes can benefit from anterior stromal puncture. A 25- gauge needle is used to place multiple small superficial punctures in the affected area of the cornea. The depth of the puncture site is just at or below the Bowman layer. The epithelium subsequently scars firmly over the treated area. This often results in resolution of bullae and pain relief. A bandage lens should be placed over the cornea for 1-2 weeks to allow the epithelium to adhere to the underlying cornea. Excimer laser phototherapeutic keratectomy also has been used to achieve this effect.

Surgical Care

Definitive treatment of PBK and ABK is a corneal transplant. Corneal transplantation is indicated when vision is decreased significantly by corneal edema or when pain becomes intractable. Although a complete discussion of corneal transplantation is beyond the scope of this chapter, certain unique aspects of corneal transplantation in this setting should be emphasized. First, the size of the graft should be as large as practical without increasing the risk of placing the graft too close to the limbus, thereby increasing the risk of graft rejection. This generally means a donor graft size of 8.00-8.50 mm. Increasing the donor graft size means that more of the healthy endothelium is transplanted. In addition, grafts with higher initial cell counts, 2500-3000 cells/mm², are desirable for the same reason.

• Another important consideration is management of a preexisting intraocular lens.
• • Closed-loop anterior chamber intraocular lenses and iris clip style lenses should be removed because of their high association with continued endothelial cell loss and the potential harm to the donor cornea. Special techniques have been devised to remove the often scarred and embedded haptics of closed-loop anterior chamber intraocular lenses with the goal of minimizing iris and angle trauma and associated bleeding.
  • In general, well-positioned and appropriately sized flexible haptic anterior and modern posterior chamber intraocular lenses can be safely left in the eye. If replacement is anticipated, 4 options are currently available to the surgeon. These options include the following: (1) using a modern flexible loop anterior chamber intraocular lens, (2) placing a posterior chamber lens in the ciliary sulcus, (3) suturing a posterior chamber lens to the iris, or (4) suturing a posterior chamber lens in the sulcus. Often, the presence of anterior and posterior synechiae and glaucoma helps to determine the choice. Implantation techniques begin with careful removal of any anterior displaced vitreous and an equally careful lysis of iris synechiae.
  • Flexible haptic anterior chamber lenses should be reserved for those eyes with minimal anterior segment pathology, less than 90° of angle synechiae, and well-controlled intraocular pressure. Determining the correct width to implant is essential in preventing complications, such as iris tuck and ovaling (too large), as well as spinning or displacement of the lens (too small). Generally, the width chosen should correspond to a measurement of the horizontal white-to-white corneal diameter plus 1 mm. If inspection of the ciliary sulcus through gentle retraction of the iris reveals an intact and adequate capsular rim, then a posterior chamber intraocular lens can be inserted in the sulcus without suturing the lens in place.
• Sutured-in intraocular lenses generally should be reserved for eyes with extensive anterior segment pathology, lack of iris support for an anterior chamber lens, or glaucoma in which any further compromise of the angle may be anticipated to worsen the control of intraocular pressure.
• These 2 techniques are comparable in terms of results. Suturing a lens to the iris is technically easier than suturing a lens in the sulcus and has the added advantage of putting the iris on stretch, which may help to limit synechiae formation. However, once sutured, the iris no longer can be dilated and the retina easily examined. Suturing a lens in the ciliary sulcus places the haptics and lens optic in the most physiologic position; however, this technique is associated with a risk of lens tilt, bleeding from the ciliary body and uvea, and increased surgical time.
• Many different variations of this technique have evolved, and special intraocular lenses with eyelets placed on the haptics to aid suture placement are available. It is up to the individual practitioner to determine which of these lens implant options is most appropriate for a given patient; however, it is important to note that no study to date has clearly pointed to an advantage of one technique or style of intraocular lens replacement in terms of graft survival, vision, or development of secondary complications (eg, glaucoma).

MEDICATION

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The goal of pharmacotherapy is to reduce morbidity and to prevent complications.

Drug Category: Hypertonic solutions and ointments

Create an osmotic gradient, and draw fluid from the cornea.

Drug Category: Antibiotics

Empiric antimicrobial therapy must be comprehensive, covering all likely pathogens in the context of the clinical setting.

Drug Category: Corticosteroids

Have anti-inflammatory properties and cause profound and varied metabolic effects. Corticosteroids modify the body's immune response to diverse stimuli.

Drug Category: Alpha 2-adrenergic agonists

Can decrease IOP.

Drug Category: Beta-adrenergic blockers

These agents reduce elevated and normal IOP, with or without glaucoma.

FOLLOW-UP

Section 8 of 11  

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Further Outpatient Care

• Patients should receive follow-up care, as needed.

Complications

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

Prognosis

• Prognosis for visual recovery following penetrating keratoplasty for PBK generally is good. Approximately 90% of patients undergoing this procedure maintain a clear corneal graft. However, only about 50% of patients regain driving and reading vision, about 20/40.

MISCELLANEOUS

Section 9 of 11  

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Medical/Legal Pitfalls

• It is very important to identify and counsel patients at risk for developing corneal edema at the time of cataract or other intraocular surgery. This process begins with a careful slit lamp exam of the cornea. If microfolds or guttata are detected, an endothelial cell count, ultrasonic pachymetry, and specular microscopy should be performed. Patients found to have a low cell count, thicker than normal cornea, or guttata should be informed of the possible need for a corneal transplant; this should be documented clearly in the medical record and on the written informed consent form.

MULTIMEDIA

Section 10 of 11  

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Media file 1:  Pseudophakic bullous keratopathy. Large multiple bullae, such as depicted here, are associated with moderate to severe pain and discomfort.
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Media file 2:  Pseudophakic bullous keratopathy in a patient with a Binkhorst style iris-fixated lens.
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Media file 3:  Pseudophakic bullous keratopathy. This patient has a closed-loop anterior chamber intraocular lens (Leiske model).
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Media file 4:  Specular microscopy of a normal cornea. Note the compact, uniform hexagonal appearance of the endothelial cells.
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Media file 5:  Specular microscopy illustrating moderate polymegathism and polymorphism. This is thought to be evidence of endothelial physiologic stress.
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Media file 6:  Fuchs endothelial dystrophy. The apparently empty spaces are occupied by guttate.
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REFERENCES

Section 11 of 11

• Authors and Editors
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• References

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Article Last Updated: Mar 16, 2006