Pseudophakic bullous keratopathy (PBK) and aphakic bullous keratopathy (ABK) refer to the development of irreversible corneal edema as a complication of cataract surgery.[1] 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. See the image below.
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Pseudophakic bullous keratopathy. Large multiple bullae, such as depicted here, are associated with moderate to severe pain and discomfort.
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.
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, it is associated with the enzyme Na+/K+ ATPase, and it is inhibited by ouabain. Endothelial cells produce a basement membrane (the 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 years 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.[2]
The exact incidence of PBK is unknown; however, it is estimated that 0.1% of patients undergoing cataract surgery will develop this problem.
The US Food and Drug Administration (FDA) 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.[3, 4, 5] Certain styles of intraocular lenses introduced in the mid 1980s were reported to have an incidence as high as 5% (eg, Leiske and Hessburg closed loop anterior chamber intraocular lenses, ORC Stableflex, Azar model 91Z).[6, 7] See the image below.
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Pseudophakic bullous keratopathy. This patient has a closed-loop anterior chamber intraocular lens (Leiske model).
From 1984-1989, ABK and PBK accounted for most corneal transplants (about 33%) performed in the United States. 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 United States.[8, 9] 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 that in the United States have been noted in Canada, United Kingdom, Australia, and Scandinavia.[10, 11, 12, 13]
Race
No known association of PBK with race 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 sex exists.
Fuchs corneal dystrophy, a known predisposing factor in the development of postoperative corneal edema, occurs approximately 3 times more frequently in women than in men.
Age
Older patients who have less endothelial reserve are more prone to develop this problem.
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. There are often associated conditions (eg, cystoid macular edema) that may limit vision.
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.[14]
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.
Surgical trauma at the time of cataract surgery can be associated with a marked reduction in endothelial cell counts.[17, 18, 19, 20, 21]
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.[22]
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.[23, 24, 25] Significant reductions in total ultrasound energy can be obtained with the use of femtosecond laser-assisted cataract surgery (FLACS) by virtue of laser sectioning and partitioning of the nucleus prior to insertion of the phacoemulsification handpiece.[26]
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.[27] 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 are all tactics to reduce endothelial trauma through superior surgical technique.
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 exacerbates both problems.
These IOL designs are 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
Corneal dystrophies (eg, Fuchs endothelial dystrophy) are sometimes overlooked on the preoperative examination, where the finding of cornea guttata may be subtle, particularly when there is minimal endothelial pigmentation.[28] See the image below.
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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.[29]
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.
Patient counseling is essential to manage expectations, including the decision of whether to perform concomitant endothelial keratoplasty (eg, Descemet stripping endothelial keratoplasty [DSEK] or Descemet membrane endothelial keratoplasty [DMEK]) or to defer the transplant until after the cataract surgery has clearly declared a dysfunctional endothelial recovery.
Intraocular irrigating fluid
The choice of intraocular irrigating fluid can have a profound effect 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 (eg, synechiolysis, iris retractors, vitrectomies).[30, 31]
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 has generally proven to be safe in terms of endothelial cell loss and toxicity.[32] These solutions include intracameral lidocaine for topical cataract anesthesia, Miochol and Miostat for pupillary miosis, epinephrine combined with BSS and lidocaine to induce mydriasis at the beginning of cataract surgery, or Omidria (Omeros) to maintain mydriasis throughout cataract surgery. 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.
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 also be found in References.[33]
Inflammation
Inflammation, specifically iritis and uveitis, can profoundly affect endothelial function.[34]
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 must always 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 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 drug classes may adversely affect intraocular inflammation. Articles have suggested that topical carbonic anhydrase inhibitors should be avoided in this instance owing to the question of endothelial toxicity in compromised corneas.
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.[35] 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.
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.
Instruments digitize and analyze these photographs, assessing such parameters as the coefficient of variation and the percentage of normal 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. Fuchs dystrophy is characteristically most severe centrally with decreasing guttata density and gradually improving cell counts peripherally. 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. See the images below.
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Specular microscopy of a normal cornea. Note the compact, uniform hexagonal appearance of the endothelial cells.
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Specular microscopy illustrating moderate polymegathism and polymorphism. This is thought to be evidence of endothelial physiologic stress.
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 a given therapeutic regimen (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).
Pathologic findings noted on corneas removed and replaced for PBK include attenuation and absence of normal endothelial cells.[36] 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 unexpected and uncounseled postoperative corneal edema. The hallmark of this dystrophy is the finding of corneal guttate (Latin for drop) excrescences and a thickened Descemet membrane. Cornea guttate appear as excrescences extending from the Descemet membrane toward the anterior chamber.
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, thereby 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. Some clinicians even recommend a gentle hair dryer to the cornea in the morning to accelerate corneal deturgescence and therefore improved vision.
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, Azasite) 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.[37] 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 has also been used to achieve this effect, as has epithelial debridement or lamellar keratectomy.
Finally, amniotic membrane in the form of a free graft protected by a bandage CTL or a ring-mounted contact lens (ProKera, BioTissue) can provide adjunctive benefits through intrinsic wound healing and growth factors, as well as anticollagenolytic and antimicrobial properties.
Definitive treatment of PBK and ABK is a corneal transplant.[38, 39] 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 article, 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 the management of a preexisting intraocular lens.[40, 41, 42, 43]
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, 5 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. A fifth option is externalizing the haptics of a posterior chamber intraocular lens, inserting them under scleral flap into and scleral tunnel, and gluing the flap over the haptic as described by Argawal et al.[44] Often, the presence of anterior and posterior synechiae, iridodialysis, large peripheral or sector iridectomies, 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.[45, 46] 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.[47]
Sutured-in intraocular lenses generally should be reserved for eyes with extensive anterior segment pathology, lack of iris support for an anterior chamber lens, lack of anterior capsular support for a sulcus lens, or glaucoma in which any further compromise of the angle may be anticipated to worsen the control of intraocular pressure.[48]
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 open sky surgical time with its inherent increased risk of a choroidal effusion or hemorrhage. Externalizing the haptics of a 3-piece intraocular lens has gained popularity; however, this can be a time-consuming and difficult technique to master for novice surgeons.
Many different variations of these techniques 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 corneal transplant survival, vision, or development of secondary complications (eg, glaucoma).
A relatively new development in cornea transplantation has been the advent of DSAEK (Descemet Stripping Automated Endothelial Keratoplasty) and endothelial keratoplasty. Melles, Terry, Price, and Gorovoy have all been significant contributors to the development and refinement of this technique of endothelial replacement.[49, 50, 51, 52, 53]
The surgery begins by stripping off and removing a sheet of the patient's central endothelium (Descemet stripping). A posterior lamellar disc is prepared by placing a donor cornea in an artificial anterior chamber and cutting it with a microkeratome (the automated part). The donor disc is folded and inserted into the eye, where it is subsequently deployed and elevated up against the patient's cornea with an air bubble. The bubble is then partially removed after a few minutes, leaving the donor disc in place.[54]
A newer variation of endothelial keratoplasty is called Descemet membrane endothelial keratoplasty (DMEK). In this procedure, only Descemet membrane and endothelium from a donor is used to replace the recipient endothelium. DMEK offers quicker visual recovery, better best-corrected vision, and a decreased risk of rejection as opposed to Descemet stripping (automated) endothelial keratoplasty (DSAEK). DMEK has gained acceptance as a primary technique of endothelial keratoplasty but is associated with a steep learning curve as it pertains to manipulating and unfolding donor Descemet membrane.[55, 56]
Advantages of endothelial keratoplasty techniques over traditional keratoplasty include quicker visual recovery, preservation of the natural topography and prolate corneal contour, and a much smaller incision, with improved wound strength, comparable to that seen with small-incision cataract surgery. The patient's own corneal curvature is preserved, with less induction of astigmatism. Disadvantages include the potential for dislocation of the donor disc, a problem more frequently encountered during the surgeon's learning curve. Visual acuity can be reduced by hazing or opacification of the lamellar interface between the donor disc and the patient's posterior corneal stroma. It is also more difficult to deploy the donor cornea disc in the presence of a preexisting anterior chamber lens, since there is less room for the disc to unfold. Finally, the method of insertion can significantly damage the donor corneal endothelium, and the best technique for insertion remains a point of contention among surgeons.[57]
Clinical Context:
Used for ocular infections involving cornea or conjunctiva resulting from strains of microorganisms susceptible to this antibiotic combination.
Clinical Context:
Bacitracin prevents transfer of mucopeptides into the growing cell wall, which causes inhibition of bacterial cell wall synthesis. Polymyxin B damages bacterial cytoplasmic membrane and alters permeability, causing intracellular constituents to leak.
Clinical Context:
This ophthalmic macrolide antibiotic is indicated for bacterial conjunctivitis caused by susceptible strains of microorganisms and for prevention of corneal and conjunctival infections.
Have anti-inflammatory properties and cause profound and varied metabolic effects. Corticosteroids modify the body's immune response to diverse stimuli.
Michael Taravella, MD, Director of Cornea and Refractive Surgery, Rocky Mountain Lions Eye Institute; Professor, Department of Ophthalmology, University of Colorado School of Medicine
Disclosure: Received income in an amount equal to or greater than $250 from: J&J Vision (Consultant)/Proctor<br/> for: Coronet Surgical (Consultant), no income received.
Coauthor(s)
Mark Walker, MD, Medical Director, Laser Eye Connection
Disclosure: Nothing to disclose.
Specialty Editors
Francisco Talavera, PharmD, PhD, Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference
Disclosure: Received salary from Medscape for employment. for: Medscape.
Christopher J Rapuano, MD, Professor, Department of Ophthalmology, Sidney Kimmel Medical College of Thomas Jefferson University; Director of the Cornea Service, Co-Director of Refractive Surgery Department, Wills Eye Hospital
Disclosure: Serve(d) as a director, officer, partner, employee, advisor, consultant or trustee for: Cornea Society, AAO, OMIC, Avedro; Bio-Tissue; GSK, Kala, Novartis; Shire; Sun Ophthalmics; TearLab<br/>Serve(d) as a speaker or a member of a speakers bureau for: Avedro; Bio-Tissue; Shire<br/>Received income in an amount equal to or greater than $250 from: AAO, OMIC, Avedro; Bio-Tissue; GSK, Kala, Novartis; Shire; Sun Ophthalmics; TearLab.
Chief Editor
John D Sheppard, Jr, MD, MMSc, Professor of Ophthalmology, Microbiology and Molecular Biology, Clinical Director, Thomas R Lee Center for Ocular Pharmacology, Ophthalmology Residency Research Program Director, Eastern Virginia Medical School; President, Virginia Eye Consultants
Disclosure: Serve(d) as a director, officer, partner, employee, advisor, consultant or trustee for: 1-800-DOCTORS; AbbVie; Alcon; Aldeyra; Allergan; Alphaeon; ArcScan; Baush+Lomb; Bio-Tissue; Clearside; EyeGate; Hovione; Mededicus; NovaBay; Omeros; Pentavision; Portage; Santen; Science Based Health; Senju; Shire; Sun Pharma; TearLab;TearScience;Topivert<br/>Serve(d) as a speaker or a member of a speakers bureau for: AbbVie; Alcon; Allergan; Bausch+Lomb; Bio-tissue; EyeGate;Hovione;LayerBio; NovaBay;Omeros;Portage; Santen; Shire; Stemnion; Sun Pharma;TearLab;TearScience; Topivert <br/>Received research grant from: Alcon; Aldeyra; allergan; Baush+ Lomb; EyeGate; Hovione; Kala; Ocular Therapeutix;Pfizer; RPS; Santen;Senju;Shire;Topcon; Xoma.
Additional Contributors
Richard W Allinson, MD, Associate Professor, Department of Ophthalmology, Texas A&M University Health Science Center; Senior Staff Ophthalmologist, Scott and White Clinic
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