- •Contents
- •General Introduction
- •Objectives
- •Anatomy
- •Eyelids
- •Conjunctiva
- •Lacrimal Functional Unit
- •The Tear Film
- •Cornea
- •Sclera
- •2 Examination Techniques for the External Eye and Cornea
- •Evaluation of Vision in the Patient With an Abnormal Cornea
- •External Examination
- •Slit-Lamp Biomicroscopy
- •Direct Illumination Methods
- •Indirect Illumination Methods
- •Clinical Use
- •Stains
- •Fluorescein
- •Rose Bengal and Lissamine Green
- •Evaluation of the Tear Film and Tests of Tear Production
- •Tear Composition Assays
- •Imaging Technologies
- •Impression Cytology
- •Corneal Pachymetry
- •Measurement of Corneal Biomechanics
- •Measurement of Corneal Curvature
- •Zones of the Cornea
- •Shape, Curvature, and Power
- •Keratometry
- •Computerized Corneal Topography
- •Corneal Tomography
- •Indications
- •Ultrasound Biomicroscopy
- •Anterior Segment Optical Coherence Tomography
- •Confocal Microscopy
- •External and Slit-Lamp Photography
- •Specular Microscopy
- •Anterior Segment Fluorescein Angiography
- •Esthesiometry
- •Retinoscopy
- •3 Clinical Approach to Ocular Surface Disorders
- •Common Clinical Findings
- •Conjunctival Signs
- •Corneal Signs
- •Clinical Approach to Dry Eye
- •Mechanisms of Dry Eye
- •Aqueous Tear Deficiency
- •Evaporative Dry Eye
- •Treatment of Dry Eye
- •Rosacea
- •Seborrheic Blepharitis
- •Staphylococcal Blepharitis
- •Hordeola and Chalazia
- •Exposure Keratopathy
- •Floppy Eyelid Syndrome
- •Superior Limbic Keratoconjunctivitis
- •Recurrent Corneal Erosion
- •Neurotrophic Keratopathy and Persistent Corneal Epithelial Defects
- •Trichiasis and Distichiasis
- •Factitious Ocular Surface Disorders
- •Dellen
- •Limbal Stem Cell Deficiency
- •Sjögren Syndrome
- •Ichthyosis
- •Ectodermal Dysplasia
- •Xeroderma Pigmentosum
- •Vitamin A Deficiency
- •4 Infectious Diseases of the External Eye: Basic Concepts and Viral Infections
- •Defense Mechanisms of the External Eye
- •Normal Ocular Flora
- •Pathogenesis of Ocular Infections
- •Virulence
- •Inoculum
- •Host Defense
- •Ocular Microbiology
- •Diagnostic Laboratory Techniques
- •Specimen Collection
- •Staining Methods
- •Virology and Viral Infections
- •DNA Viruses: Herpesviruses
- •Herpes Simplex Eye Diseases
- •Varicella-Zoster Virus Dermatoblepharitis, Conjunctivitis, and Keratitis
- •Epstein-Barr Virus Dacryoadenitis, Conjunctivitis, and Keratitis
- •Cytomegalovirus Keratitis and Anterior Uveitis
- •DNA Viruses: Adenoviruses
- •DNA Viruses: Poxviruses
- •Molluscum Contagiosum
- •Vaccinia
- •DNA Viruses: Papovaviruses
- •RNA Viruses
- •Bacteriology
- •Gram-positive Cocci
- •Gram-negative Cocci
- •Gram-positive Rods
- •Gram-negative Rods
- •Gram-positive Filaments
- •Chlamydia Species
- •Spirochetes
- •Mycology
- •Yeasts
- •Septate Filamentous Fungi
- •Nonseptate Filamentous Fungi
- •Parasitology
- •Protozoa
- •Helminths
- •Arthropods
- •Prions
- •Staphylococcal Blepharitis
- •Fungal and Parasitic Infections of the Eyelid Margin
- •Bacterial Conjunctivitis in Children and Adults
- •Parinaud Oculoglandular Syndrome
- •Microbial and Parasitic Infections of the Cornea and Sclera
- •Contact Lens–Related Infectious Keratitis
- •Bacterial Keratitis
- •Atypical Mycobacteria
- •Fungal Keratitis
- •Acanthamoeba Keratitis
- •Corneal Stromal Inflammation Associated With Systemic Infections
- •Microsporidiosis
- •Loiasis
- •Microbial Scleritis
- •6 Ocular Immunology
- •Overview of the Ocular Surface Immune Response
- •Tear Film
- •Immunoregulation of the Ocular Surface
- •Angiogenesis and Lymphangiogenesis in the Cornea
- •Tissue-Specific Patterns of Immune-Mediated Ocular Disease
- •Conjunctiva
- •Cornea
- •Sclera
- •Diagnostic Approach to Immune-Mediated Ocular Disorders
- •Immune-Mediated Diseases of the Eyelid
- •Contact Dermatoblepharitis
- •Atopic Dermatitis
- •Immune-Mediated Disorders of the Conjunctiva
- •Hay Fever Conjunctivitis and Perennial Allergic Conjunctivitis
- •Vernal Keratoconjunctivitis
- •Atopic Keratoconjunctivitis
- •Ligneous Conjunctivitis
- •Stevens-Johnson Syndrome and Toxic Epidermal Necrolysis
- •Mucous Membrane Pemphigoid
- •Ocular Graft-vs-Host Disease
- •Other Immune-Mediated Diseases of the Skin and Mucous Membranes
- •Immune-Mediated Diseases of the Cornea
- •Thygeson Superficial Punctate Keratitis
- •Interstitial Keratitis Associated With Infectious Diseases
- •Reactive Arthritis
- •Cogan Syndrome
- •Marginal Corneal Infiltrates Associated With Blepharoconjunctivitis
- •Peripheral Ulcerative Keratitis Associated With Systemic Immune-Mediated Diseases
- •Mooren Ulcer
- •Corneal Transplant Rejection
- •Immune-Mediated Diseases of the Episclera and Sclera
- •Episcleritis
- •Scleritis
- •8 Clinical Approach to Neoplastic Disorders of the Conjunctiva and Cornea
- •Approach to the Patient With a Neoplastic Conjunctival Lesion
- •Management of Patients With Conjunctival Tumors
- •Surgical Treatment
- •Topical Chemotherapy
- •Tumors of Epithelial Origin
- •Benign Epithelial Tumors
- •Preinvasive Epithelial Lesions
- •Malignant Epithelial Lesions
- •Management of Atypical Epithelial Tumors
- •Other Malignant Epithelial Lesions
- •Glandular Tumors of the Conjunctiva
- •Oncocytoma
- •Sebaceous Gland Carcinoma
- •Tumors of Neuroectodermal Origin
- •Benign Pigmented Lesions
- •Preinvasive Pigmented Lesions
- •Malignant Pigmented Lesions
- •Neurogenic and Smooth-Muscle Tumors
- •Vascular and Mesenchymal Tumors
- •Benign Tumors
- •Malignant Tumors
- •Lymphatic and Lymphocytic Tumors
- •Lymphangiectasia and Lymphangioma
- •Lymphoid Hyperplasia
- •Lymphoma
- •Metastatic Tumors
- •9 Basic and Clinical Concepts of Congenital Anomalies of the Cornea, Sclera, and Globe
- •Developmental Anomalies of the Globe and Sclera
- •Cryptophthalmos
- •Microphthalmos
- •Nanophthalmos
- •Blue Sclera
- •Developmental Anomalies of the Anterior Segment
- •Anomalies of Size and Shape of the Cornea
- •Abnormalities of Corneal Structure and/or Clarity
- •Secondary Abnormalities Affecting the Fetal Cornea
- •Intrauterine Keratitis: Bacterial and Syphilitic
- •Congenital Corneal Keloid
- •Congenital Corneal Anesthesia
- •Congenital Glaucoma
- •Birth Trauma
- •Arcus Juvenilis
- •10 Corneal Dystrophies and Ectasias
- •Corneal Dystrophies
- •Epithelial and Subepithelial Dystrophies
- •Bowman Layer Corneal Dystrophies
- •Stromal Corneal Dystrophies: TGFBI Dystrophies
- •Stromal Dystrophies: Non-TGFBI Dystrophies
- •Endothelial Dystrophies
- •Ectatic Disorders
- •Keratoconus
- •Pellucid Marginal Degeneration
- •Keratoglobus
- •11 Systemic Disorders With Corneal Changes
- •Disorders of Carbohydrate Metabolism
- •Mucopolysaccharidoses
- •Diabetes Mellitus
- •Disorders of Lipid Metabolism and Storage
- •Hyperlipoproteinemias
- •Hypolipoproteinemias
- •Sphingolipidoses
- •Mucolipidoses
- •Disorders of Amino Acid Metabolism
- •Cystinosis
- •Tyrosinemia
- •Alkaptonuria
- •Disorders of Protein Metabolism
- •Amyloidosis
- •Disorders of Immunoglobulin Synthesis
- •Noninflammatory Disorders of Connective Tissue
- •Ehlers-Danlos Syndrome
- •Marfan Syndrome
- •Disorders of Nucleotide Metabolism
- •Gout
- •Porphyria
- •Disorders of Mineral Metabolism
- •Wilson Disease
- •Hypercalcemia
- •Hemochromatosis
- •Corneal and External Disease Signs of Systemic Neoplasia
- •Enlarged Corneal Nerves
- •Appendix
- •12 Clinical Approach to Depositions and Degenerations of the Conjunctiva, Cornea, and Sclera
- •Degenerative Changes of the Conjunctiva
- •Age-Related (Involutional) Changes
- •Pinguecula
- •Pterygium
- •Conjunctival Concretions
- •Conjunctival Inclusion Cysts
- •Conjunctivochalasis
- •Conjunctival Vascular Tortuosity and Hyperemia
- •Degenerative Changes in the Cornea
- •Age-Related (Involutional) Changes
- •Epithelial and Subepithelial Degenerations
- •Stromal Degenerations
- •Endothelial Degenerations
- •Scleral Degenerations
- •Drug-Induced Deposition and Pigmentation
- •Corneal Epithelial Deposits
- •Stromal and Descemet Membrane Pigmentation
- •Endothelial Manifestations
- •13 Clinical Aspects of Toxic and Traumatic Injuries of the Anterior Segment
- •Injuries Caused by Temperature and Radiation
- •Thermal Burns
- •Ultraviolet Radiation
- •Ionizing Radiation
- •Chemical Injuries
- •Alkali Burns
- •Acid Burns
- •Management of Chemical Injuries
- •Toxic Keratoconjunctivitis From Medications
- •Pathogenesis
- •Clinical Presentation
- •Management
- •Animal and Plant Substances
- •Insect Injuries
- •Vegetation Injuries
- •Concussive Trauma
- •Subconjunctival Hemorrhage
- •Corneal Changes
- •Traumatic Mydriasis and Miosis
- •Traumatic Iritis
- •Iridodialysis and Cyclodialysis
- •Traumatic Hyphema
- •Nonperforating Mechanical Trauma
- •Conjunctival Laceration
- •Conjunctival Foreign Body
- •Corneal Foreign Body
- •Corneal Abrasion
- •Perforating Trauma
- •Evaluation
- •Management
- •Surgical Trauma
- •Corneal Epithelial Changes From Intraocular Surgery
- •Descemet Membrane Changes During Intraocular Surgery
- •Corneal Endothelial Changes From Intraocular Surgery
- •Conjunctival and Corneal Changes From Extraocular Surgery
- •14 Treatment of Ocular Surface Disorders
- •Surgical Procedures of the Ocular Surface
- •Limbal Transplantation
- •Autologous Conjunctival Transplantation
- •Pterygium Excision
- •Mucous Membrane Grafting
- •Conjunctival Flap
- •Conjunctival Biopsy
- •Conjunctivochalasis Excision
- •Therapeutic Interventions for Corneal Disease
- •Superficial Keratectomy and Corneal Biopsy
- •Management of Descemetocele, Corneal Perforation, and Corneal Edema
- •Corneal Tattoo
- •Tarsorrhaphy
- •15 Clinical Approach to Corneal Transplantation
- •Corneal Transplantation
- •Eye Banking and Donor Selection
- •Criteria Contraindicating Donor Cornea Use
- •Surgical Approach to Corneal Disease
- •Preoperative Evaluation and Preparation
- •Penetrating Keratoplasty
- •Surgical Technique for Penetrating Keratoplasty
- •Combined Procedures
- •Intraoperative Complications
- •Postoperative Care and Complications
- •Control of Postoperative Corneal Astigmatism and Refractive Error
- •Diagnosis and Management of Graft Rejection
- •Pediatric Corneal Transplantation
- •Corneal Autograft Procedures
- •Keratoprosthesis
- •Lamellar Keratoplasty
- •Anterior Lamellar Transplantation
- •Surgical Technique
- •Postoperative Care and Complications
- •Endothelial Keratoplasty
- •DSEK Surgical Technique and Complications
- •Descemet Membrane Endothelial Keratoplasty
- •Basic Texts
- •Related Academy Materials
- •Requesting Continuing Medical Education Credit
of Descemet membrane can reduce vision or prolong vision rehabilitation.
Allograft rejection
DALK has been reported to significantly reduce the incidence of graft rejection and graft failure compared with full-thickness transplantation. Because the endothelium is not transplanted, endothelial rejection cannot take place. However, epithelial rejection, subepithelial infiltrates, and stromal rejection can occur, but these usually respond to corticosteroid therapy. Stromal rejection characterized by significant haze and deep vascularization can lead to corneal opacification (Fig 1514). If graft edema occurs, another cause for endothelial dysfunction must be sought.
Figure 15-14 Stromal haze (A) and deep vascularization (B) following deep anterior lamellar keratoplasty. (Courtesy of Robert W.
Weisenthal, MD.)
Inflammatory necrosis of the graft
Although inflammatory necrosis of the graft has previously been described as an allograft reaction, no immunohistopathologic evidence has confirmed this, and recent series have not shown this phenomenon. The mechanism probably relates to the preexisting corneal disease. Prognosis following retention of a clear graft is poor despite corticosteroid therapy.
Anwar M, Teichmann KD. Big-bubble technique to bare Descemet’s membrane in anterior lamellar keratoplasty. J Cataract Refract Surg. 2002;28(3):398–403.
Ardjomand N, Hau S, McAlister JC, et al. Quality of vision and graft thickness in deep anterior lamellar and penetrating corneal allografts. Am J Ophthalmol. 2007;143(2):228–235.
Borderie VM, Sandali O, Bullet J, Gaujoux T, Touzeau O, Laroche L. Long-term results of deep anterior lamellar versus penetrating keratoplasty. Ophthalmology. 2012;119(2):249–255. Epub 2011 Nov 4.
Gorovoy MS. Advances in lamellar corneal surgery. Focal Points: Clinical Modules for Ophthalmologists. San Francisco: American Academy of Ophthalmology; 2008, module 4.
John T, ed. Surgical Techniques in Anterior and Posterior Lamellar Keratoplasty. New Delhi, India: Jaypee Brothers Medical Publishers; 2006:L1–L687.
Reinhart WJ, Musch DC, Jacobs DS, Lee WB, Kaufman SC, Shtein RM. Deep anterior lamellar keratoplasty as an alternative to penetrating keratoplasty: a report by the American Academy of Ophthalmology. Ophthalmology. 2011;118(1):209–218.
Endothelial Keratoplasty
Gerrit Melles introduced the technique of posterior endothelial lamellar keratoplasty in 1998. As surgical techniques have evolved, DSEK (or Descemet stripping automated endothelial keratoplasty [DSAEK]) has become the most commonly performed procedure for the treatment of endothelial
dysfunction. It is used to treat Fuchs corneal dystrophy, PBK, failed corneal grafts, iridocorneal endothelial (ICE) syndrome, and posterior polymorphous dystrophy. Recently, DSEK has been used in pediatric populations to treat CHED. DSEK has the following advantages over PK:
enhanced globe integrity with a scleral or clear corneal incision, compared with a full-thickness central corneal incision (This reduces the risk of a devastating injury with trauma; Fig 15-15.) elimination of corneal suture–related problems
increased accuracy in IOL power calculations when combined with cataract extraction, although the shape of the lenticule in DSEK may produce hyperopic shift
less induced corneal astigmatism postoperatively
more rapid vision rehabilitation with less concern regarding ocular surface disorders
Figure 15-15 Iris prolapse following blunt trauma after Descemet stripping endothelial keratoplasty (DSEK). (Courtesy of Robert
W. Weisenthal, MD.)
Lee WB, Jacobs DS, Musch DC, Kaufman SC, Reinhart WJ, Shtein RM. Descemet’s stripping endothelial keratoplasty: safety and outcomes: a report by the American Academy of Ophthalmology. Ophthalmology. 2009;116(9):1818–1830.
Melles GR, Eggink FA, Lander F, et al. A surgical technique for posterior lamellar keratoplasty. Cornea. 1998;17(6):618–626.
DSEK Surgical Technique and Complications
Preparation of donor tissue
Cornea surgeons have the option of obtaining precut tissue from an eye bank or preparing the tissue
in the operating room using an automated microkeratome on an artificial anterior chamber. Recent studies have shown that there is no clinical difference in outcomes between tissue obtained from the eye banks and tissue prepared in the operating room.
The donor tissue is placed in a concave well. The tissue is marked to outline the microkeratome incision and assure proper centration of the cut to avoid thick edges and the possibility of including peripheral donor epithelium. A trephine is used to create a disk-shaped lamella of donor tissue from 8 to 9 mm in diameter.
Surgical technique for recipient eye
Some surgeons perform DSEK with the patient under topical anesthesia; however, many prefer a retrobulbar block. A limbal, clear corneal, or scleral incision may be used. The length of the incision varies from 3 to 6 mm. Several studies using vital dye staining of the endothelium after insertion of the donor corneal tissue have shown that placing tissue through a 3-mm incision causes more damage to the endothelium than using a 5-mm incision, regardless of the technique used to place the tissue.
Descemet membrane is then stripped in a circular fashion (descemetorrhexis), leaving a smooth posterior stromal bed (Fig 15-16A). This maneuver can be performed with a variety of instruments, including a hook, a specially designed Descemet stripper, or an irrigation/aspiration handpiece. The stripping can be performed under viscoelastic, air, or irrigation with balanced salt solution. Some surgeons feel that it is not necessary to strip Descemet membrane in patients with failed PK or PBK. Whether the retention of Descemet membrane in these cases may predispose to dislocation of the graft is controversial.
Figure 15-16 A, Stripping of Descemet membrane. B, Glide insertion of donor tissue (left); Busin glide insertion of donor tissue (right). C, Air is tamponaded to appose the donor graft to the host stromal bed. (Illustration by Christine Gralapp.)
There are many techniques to place the donor tissue within the eye. The goal is to minimize trauma to the donor endothelium during the insertion and positioning of the tissue in the anterior chamber. In one technique, the tissue can be placed on a sheet glide or the conjunctiva over a bed of viscoelastic and then pushed or pulled into the anterior chamber using forceps or a bent 27-gauge needle. Another popular technique is to fold the tissue using specially designed forceps to minimize tissue compression. Many special instruments have been designed to insert the tissue, including a shovel, glides, and injectors (Fig 15-16B). Retrospective series comparing endothelial cell loss with different techniques and devices are now being reported; however, at this time, there is no clear consensus on which technique is best.
After the tissue is placed in the anterior chamber, air is injected to float the donor graft against the host stromal bed (Fig 15-16C). It is not clear what factors are responsible for tissue adherence, but it is probably due to a combination of physical and physiologic factors. Intraoperative maneuvers to facilitate adhesion include scraping the peripheral recipient bed, draining fluid from the interface through vertical, midperipheral vent incisions, and sweeping the surface of the cornea with a roller. The air fill duration and pressure necessary to ensure tissue adherence are uncertain. Methods vary; they include a full air fill in the operating room for 10 minutes, followed by release and replacement with a partial air fill; a full air fill for up to 1 hour, with subsequent partial release at a slit lamp; and a complete air fill overnight, combined with an inferior iridectomy or use of acetazolamide.
Mehta JS, Por YM, Poh R, Beuerman RW, Tan D. Comparison of donor insertion techniques for Descemet stripping automated endothelial keratoplasty. Arch Ophthalmol. 2008;126(10):1383–1388.
Terry MA, Saad HA, Shamie N, et al. Endothelial keratoplasty: the influence of insertion techniques and incision size on donor endothelial survival. Cornea. 2009;28(1):24–31.
Intraoperative complications
Complications that can occur during DSEK include the following:
poor microkeratome dissection, precluding use of the donor tissue incomplete removal of Descemet membrane and endothelium
poor centration of the donor tissue during trephination, leading to a thick edge and possibly retention of epithelial cells, which could be implanted into the anterior chamber intraocular hyphema and blood in the interface (Fig 15-17)
excessive manipulation of the donor tissue, risking endothelial cell loss posterior dislocation of the donor tissue
disorientation during placement of the donor tissue, leading to placement of the endothelium against the host stromal cornea
Figure 15-17 Hemorrhage in the interface after DSEK. (Courtesy of Robert W. Weisenthal, MD.)
Postoperative care and complications
Originally, patients were advised to lie on their back for the first 24 hours to tamponade the donor graft against the posterior stroma with the retained air bubble; however, some surgeons have now relaxed the positioning requirements. On the first postoperative day, the lenticule should be well centered, without fluid in the interface. Typically, there is a 25%–40% air bubble (Fig 15-18). Over a 3- to 4-day period, the air bubble absorbs and the cornea begins to clear. After 6 months, it is difficult to visualize the interface centrally (Fig 15-19).
Figure 15-18 Residual air bubble on DSEK postoperative day 1. (Courtesy of Robert W. Weisenthal, MD.)
Figure 15-19 Slit-lamp picture of healed DSEK. (Courtesy of Robert W. Weisenthal, MD.)
The postoperative medication regimen is similar to that for PK. Some surgeons discontinue the topical corticosteroids after 1 year to reduce the incidence of steroid-induced ocular hypertension or cataract formation; however, in one recent report, graft rejection increased at 12–18 months after cessation of the steroid drops. Other clinicians use the topical corticosteroids indefinitely, particularly in pseudophakic patients.
Pupillary block If release of the intraoperative air fill is inadequate, or if the patient inadvertently leans his or her head forward, pupillary block may occur due to migration of the air behind the iris, thus closing the angle (Fig 15-20). The acute rise in pressure produces pain and can exacerbate underlying glaucoma. An inferior iridectomy may prevent pupillary block.
Figure 15-20 Pupillary block following DSEK. (Courtesy of Robert W. Weisenthal, MD.)
Dislocation of the donor graft The rate of dislocation of the donor graft (Fig 15-21) varies greatly in reported case series, from 4% with experienced surgeons up to 35%–40% with novice surgeons (those who have had fewer than 10 cases). Dislocation of the donor graft occurs primarily within the first 24 hours, but occasionally, inadvertent trauma from eye rubbing or a sudden blow to the eye has caused the donor disk to be displaced at a later time. The dislocation is managed with reinjection of air, which can be performed in the office or in the operating room, scheduled when convenient. Spontaneous reattachment of both partial and fully dislocated lenticules has been reported.
Figure 15-21 Dislocated lenticule after DSEK. (Courtesy of Robert W. Weisenthal, MD.)
Epithelial ingrowth Epithelial ingrowth (Fig 15-22) may be seen first as a white deposit within the interface; it may be relatively stable and asymptomatic. In rare cases, epithelial ingrowth may lead to graft failure that is missed on clinical examination but recognized on histologic examination of the tissue after removal. The source of the ingrowth may be host surface epithelial cells implanted within the eye during placement of the donor tissue or donor epithelial cells inadvertently left in place and implanted following eccentric trephination beyond the microkeratome dissection. In most reports, the
prognosis with epithelial ingrowth is benign and the condition can simply be observed without further intervention. In the atypical cases that lead to graft failure, a second DSEK or PK leads to a good prognosis without recurrent ingrowth. This is in contrast to the progressive and devastating course of intraocular epithelial downgrowth associated with intracapsular cataract extraction or full-thickness PK.
Suh LH, Shousha MA, Ventura RU, et al. Epithelial ingrowth after Descemet stripping automated endothelial keratoplasty: description of cases and assessment with anterior segment optical coherence tomography. Cornea. 2011;30(5):528–534.
Figure 15-22 Epithelial ingrowth (arrow) in the interface after DSEK. (Courtesy of Robert W. Weisenthal, MD.)
Interface problems Infections can occur in the interface as pathogens pass through vent incisions, due to contamination of the donor tissue, or are dragged in from the ocular surface during insertion. Interface opacification may occur because of retention of fibers, incomplete removal of Descemet membrane, calcareous deposition, and persistent interface fluid. Recently, a new condition called textural interface opacity has been described. It has 2 forms: an elongated type (a lacy honeycomb
pattern of deposits with intervening clear zones) (Fig 15-23) and a punctate type (small discrete deposits). In most patients, the textural interface opacity improves or disappears completely over time with improvement in visual acuity. The underlying cause is believed to be either retained viscoelastic or shearing of the stromal fibrils due to an irregular lamellar microkeratome cut of the donor tissue.
Figure 15-23 Textural interface opacity after DSEK. (Courtesy of Robert W. Weisenthal, MD.)
Decreased postoperative visual acuity After DSEK, the best-corrected spectacle acuity often ranges from 20/25 to 20/40. The cause of the decreased vision varies. Preexisting basement membrane changes may cause superficial irregularity or subepithelial fibrosis. In these cases, corneal debridement or superficial keratectomy may be necessary. Another potential factor is light scattering due to preexisting long-standing corneal edema. Evaluation of DSEK patients with Fuchs corneal dystrophy revealed that the corneal light scattering associated with anterior stromal haze improved significantly postoperatively but was still increased compared to that in a normal cornea 24 months after the procedure. Another possible cause for decreased vision is alteration of the posterior corneal curvature due to the unevenness and thickness of the donor tissue on the host posterior stroma.
The visual outcome following DMEK may be better than that following DSEK. Evaluation of the higher-order aberrations of the anterior central 4.0-mm zone showed no differences between DSEK and DMEK. However, compared with DSEK, DMEK produced a statistically significant overall reduction in total corneal aberrations, particularly posterior aberrations. The thin tissue transplanted in DMEK does not disturb the relationship between the anterior and posterior corneal curvature to the same degree as the thicker tissue transplanted in DSEK. As a result, some clinicians advocate the use of ultrathin DSEK (donor tissue <100 μm) to improve visual outcomes.
Baratz KH, McLaren JW, Maguire LJ, Patel SV. Corneal haze determined by confocal microscopy 2 years after Descemet stripping with endothelial keratoplasty for Fuchs corneal dystrophy. Arch Ophthalmol. 2012;130(7):868–874.
Rudolph M, Laaser K, Bachmann BO, Cursiefen C, Epstein D, Kruse FE. Corneal higher-order aberrations after Descemet’s membrane endothelial keratoplasty. Ophthalmology. 2012;119(3):528–539. Epub 2011 Dec 22.
van der Meulen IJ, Patel SV, Lapid-Gortzak R, Nieuwendaal CP, McLaren JW, van den Berg TJ. Quality of vision in patients with Fuchs endothelial dystrophy and after Descemet stripping endothelial keratoplasty. Arch Ophthalmol. 2011;129(12):1537–1542.
Progression of cataracts Phakic DSEK induces progression of cataracts, particularly in patients with narrow anterior chambers (<3.0 mm), so combined DSEK and cataract extraction has been recommended in patients older than 50 years or in the presence of mild to moderate cataract. In a large series of patients with Fuchs corneal dystrophy, DSEK combined with cataract extraction did not increase the risk of graft dislocation, endothelial cell loss, or other complications.
Terry MA, Shamie N, Chen ES, et al. Endothelial keratoplasty for Fuchs’ dystrophy with cataract: complications and clinical results with the new triple procedure. Ophthalmology. 2009;116(4):631–639.
Tsui JY, Goins KM, Sutphin JE, Wagoner MD. Phakic Descemet stripping automated endothelial keratoplasty: prevalence and prognostic impact of postoperative cataracts. Cornea. 2011;30(3):291–295.
Primary graft failure The primary graft failure rate seen in published reports varies between 3% and 12%; higher rates are associated with surgeons in the early stages of the learning curve, and lower rates are associated with more experienced surgeons. The lower rates probably reflect better surgical technique, which results in less tissue manipulation and a lower rate of graft dislocations and thus less endothelial trauma.
Corneal graft rejection The incidence of corneal graft rejection in DSEK appears to be lower than that in PK, with an average rejection rate of 1%–10%, depending on the series. The lower incidence may be related to the lack of corneal sutures, which reduces the risk of inflammation due to suture erosion and secondary vascularization. The absence of donor epithelial cells may also play a role. Long-term follow-up is necessary to confirm this observation. The clinical presentation of graft rejection in DSEK also differs from that in PK, as the classic endothelial rejection line is not seen; instead, typically, multiple keratic precipitates scattered across the cornea are observable (Fig 15-24).
