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Keratoconus 2016


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keratoconus diagnosis and management discussed .

Published in: Health & Medicine
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Keratoconus 2016

  3. 3. Normal corneal layers
  4. 4. Noninflammatory Ectatic Disorders •They are keratoconus, , , and . • first three disorders may actually represent variations in phenotypic expression of same pathogenetic mechanism. •Corneal thinning is a hallmark of these ectatic diseases. area of maximal thinning, relative to location of maximal corneal protrusion, is helpful in differentiating these conditions.
  6. 6. Noninflammatory Ectatic Disorders •Distortion of the anterior corneal curvature occurs in keratoconus, pellucid marginal degeneration, and keratoglobus . •The resultant reduction in visual function can vary from mild to severe. •Computer-assisted topographical and pachymetric analyses have dramatically improved the sensitivity of detection of these ectatic disorders, particularly in the case of keratoconus. This has prompted debate on appropriate terminology for the patient .
  7. 7. Noninflammatory Ectatic Disorders • debate on appropriate terminology for Pt with topographical evidence of inferior steepening, eccentric elevation or thinning, but without clinical signs of keratoconus. Keratoconus suspect or subclinical keratoconus are commonly used terms. •Visual correction begins with glasses, followed by contact lens fitting. Failing these modalities, a surgical approach, designed to restore a more normal corneal contour, is planned.
  8. 8. KERATOCONUS Keratoconus is a condition in which cornea assumes a conical shape because of thinning and protrusion. Cellular infiltration and vascularization do not occur. It is usually b/l and, although it involves central two-thirds of cornea, apex of cone is usually centered just below visual axis. This results in mild to marked impairment of visual function.
  9. 9. Prevalence, distribution, & course • 50 to 230 per 100 000 , • occurs bilaterally. u/l cases occur 2–4% • onset of keratoconus occurs at age of puberty. cornea begins to thin and protrude, resulting in irregular astigmatism. Typically, over a period of 10 to 20 years the process continues until progression gradually stops. If a faint, broad iron ring is present, it becomes a thinner, more discrete ring. rate of progression is variable. severity of disorder at time progression stops can range from very mild irregular astigmatism to severe thinning, protrusion, and scarring requiring keratoplasty
  10. 10. •KC occurs with increased frequency with systemic and ocular conditions: 1. Systemic disorders: •Down’s syndrome, Turner syndrome, Ehlers- Dunlos syndrome, Marfan syndrome,atopy, osteogenesis imperfecta, and mitral valve prolapse. 2. Ocular associations: •Vernal disease, retinitis pigmentosa, blue sclera, aniridia, and ectopia lentis
  11. 11. • onset is at puberty and progresses slowly thereafter, it may become stationary . •The hallmark of KC is central or paracentral stromal thinning, apical protrusion,& irregular astigmatism. This results in impairment in both quantity and quality of vision because of the progressive nature of the disease. •In advanced KC with corneal opacities , corneal grafting can be the only surgical alternative. •modern managements have been developed to stop the progression of the disease
  12. 12. Clinical Findings •Munson’s sign : When the patient is asked to look downward toward the floor, a V-shaped profile of the lower lid margin can be seen . Moderate-to severe KC tends to produce Munson’s sign, while mild cases will not produce this sign . •Rizzuti’s sign : This sign is observed by seeing a light on the nasal anterior sclera when the light is directed into the cornea from the temporal direction
  13. 13. Retinoscopy Signs • scissoring effect of the retinal reflex seen with retinoscopy is highly diagnostic of KC (and of all forms of irregular astigmatism). It is best seen when the pupils are dilated. Unlike Munson’s sign, scissoring effect is considered to be sensitive to even mild forms of KC
  14. 14. Slit Lamp Biomicroscopy Signs • Focal thinning : •focal thinning occurs at the cone apex,which is usually located inferior to the center of cornea; in pellucid marginal degeneration (PMD), this focal thinning is located in the lower third of the cornea. • Fleischer’s ring : • It is due to accumulation of ferritin particles in corneal basal epithelial cells. It encircles the base of the cone.
  15. 15. Vogt’s striae, hydrops cornea, and corneal scaring •As cornea continues to thin and bulge out,“stretch marks” may develop in form of thin,bright lines located deep in the stroma adjacent to Descemets’ membrane called Vogt’s striae . Vogt’s striae are a sign of corneal stretching and protrusion. When cornea is depressed, Vogt’s striae often disappear. These striae are sometimes called stress lines.
  16. 16. •Anterior stromal scars may develop due to continuous protrusion of the cornea. These scars may be small or large . • The size and location of the scars determines its impact on visual function. •If stretching becomes excessive, the cornea may eventually tear in the Descemets’ membrane leading to fluid accumulation within the stroma and therefore to hydrops cornea .
  17. 17. Corneal hydrops This intense stromal edema often results in an acutely blurred vision since the tears often occur centrally. •When the endothelium migrates to cover the tear,edema resolves and a posterior scar may form. •Tears can occur in corneal periphery which may have minimal impact on vision
  20. 20. Forme Fruste Keratoconus •Forme Fruste Keratoconus (FFKC) is a subclinical disease and is not a variant of KC. Although clinicians use many other terms such as mild KC, early KC, and subclinical KC, their exact meanings and applications are less certain. These terms are not universally accepted. •The diagnosis of KC is a clinical one that is aided by topography, while the diagnosis of FFKC is topographic.
  21. 21. TWO OPINIONS REGARDING THE DEFINITION • FFKC is a completely normal cornea with neither clinical nor topographical risk factors, but this cornea is able to develop KC when treated by laser. •The fellow eye may be keratoconic or there may be a family history of KC
  22. 22. TWO OPINIONS REGARDING THE DEFINITION • FFKC is an abnormal cornea. Corneal topography or corneal hysteresis or both are abnormal; i.e., there are risk factors but the case is still not a clinically obvious KC.
  23. 23. Pellucid Marginal Degeneration (PMD) & Pellucid-like Keratoconus (PLK) •PMD is a b / l , non-inflammatory, peripheral corneal thinning disorder characterized by a peripheral band of thinning of the inferior cornea. The cornea in and adjacent to the thinned area is ectatic.The etiology of PMD has not been clearly established, but collagen abnormalities, as seen in KC, have been reported. Patients usually are aged 20–40 years at the time of clinical presentation
  24. 24. Keratoglobus •It is a generalized thinning of cornea . thinning is marked at limbus, extending circumferentially for 360°; this makes it different from the globus morphological pattern of the KC.• The whole cornea protrudes, in contrast to the regional thinning seen in KC and the inferior paralimbal thinning in PMD.
  25. 25. Keratoglobus. A generalized bulging and thinning of the cornea
  26. 26. Terrien marginal degeneration •It affects an age group similar to that affected by PMD ,can be bilateral. • Although this condition can be associated with large amounts of astigmatism, it can be differentiated from PMD because the superior cornea is predominantly affected & because the area of thinning is often associated with vascularization and lipid deposition.
  27. 27. Terrien marginal degeneration. Note the lipid deposition
  28. 28. Furrow degeneration: •It has some features of PMD. • An intact epithelium is present, and area of corneal thinning is not vascularized, at least in the acute phase. differentiating feature is that area of thinning is closer to limbus with virtually no intervening zone of normal cornea, unlike findings in PMD.
  29. 29. •Peripheral corneal melting disorders, such as Mooren ulcer, or peripheral melting secondary to rheumatologic disorders are characterized by pain. This pain may be severe in cases of Mooren ulcer. • Associated findings include an epithelial defect over the area of thinning and corneal vascularization adjacent to the area of thinning in the acute phase.
  30. 30. Pathology •Fragmentation of the Bowman's layer seen with scanning electron microscopy has been described as specific to keratoconus and an early change leading to the disease. •A hallmark of keratoconus is the Fleischer ring found at the base of the cone . brown iron ring can be seen histopathologically. Light and electron microscopy reveal that ferritin particles accumulate within and between the epithelial cells, particularly in the basal epithelium
  31. 31. The Fleischer ring in keratoconus Hemosiderin pigment deposited in basal epithelium
  32. 32. Diagnosis • The diagnosis of keratoconus depends first on the suspicion of the condition and then on careful evaluation employing various available diagnostic tools including biomicroscopy, keratometry, keratoscopy, pachymetry, and computer-assisted topography & tomography . • an affected patient in the teens or twenties seeks consultation for symptoms of progressive visual blurring and/or distortion. • Photophobia, glare, monocular diplopia, and ocular irritation are also presenting symptoms. • Early in the course of the disease, visual acuity may be normal even in symptomatic patients.
  33. 33. Diagnosis •Contrast sensitivity measurement may, however, uncover visual dysfunction before Snellen visual acuity loss can be measured. •High, irregular myopic astigmatism with a scissoring reflex on retinoscopy in keratoconus. •In advanced keratoconus corneal protrusion may angulate lower lid on downgaze. (Munson's sign ).
  34. 34. SLIT LAMP EXAMINATION •Slit lamp examination reveals characteristic findings. •An eccentrically located ectatic protrusion of the cornea is noted . •While the apex is usually inferior to an imaginary horizontal line drawn through the pupillary axis, it can be located in the central cornea. corneal topography has revealed that superior flattening is associated with inferior steepening in keratoconus.
  35. 35. SLIT LAMP EXAMINATION •Corneal thinning from one-half to one-fifth of normal thickness is observed at the apex of the protrusion . Two types of cones have been described. •The round or nipple-shaped cone is smaller in diameter . •the larger oval or sagging cone may extend to the limbus and is more prone to contact lens fitting problems.
  36. 36. Thinning at cone apex Apex of cone in inferior paracentral cone
  37. 37. SLIT LAMP EXAMINATION •In advanced cases, deeper opacities can be seen at the apex of the cone resulting from ruptures in Descemet's membrane. • Acute keratoconus or corneal hydrops results from stromal imbibition of aqueous through these defects . The edema may persist for weeks or months, usually diminishing gradually. Eventually, it is replaced by scarring which in some cases may result in flattening of the conical contour.
  38. 38. KERATOMETER • keratometer is an invaluable tool for measuring corneal curvature. Inability to superimpose central keratometric rings suggests irregular corneal astigmatism, a hallmark of keratoconus. There is no keratometric value beyond which diagnosis of keratoconus is definite. There are patients with steep corneas and high astigmatic errors who do not have keratoconus and, conversely, patients with keratoconus who have central corneas of normal steepness.
  39. 39. KERATOMETER . Inferior corneal steepening is also an early sign of keratoconus. By performing central keratometry, followed by keratometry with the patient in upward gaze, steepening in the inferior cornea can be identified . • Keratoscopy or videokeratography, based on Placido disk, can show In early keratoconus, a focal area of increased corneal curvature as an isolated area of smaller ring spacing and distortion. ring spacing decreases overall and becomes increasingly irregular on progression
  40. 40. Keratoscopy &Photokeratoscopy Signs •Keratoscopy uses a pattern of concentric rings (mires) called a Placido disk with nine alternating bright and dark rings. •The rings are reflected off the anterior cornea surface via Purkinje image number one and viewed directly by the clinician. •The Placido disk is nothing more than a simple, inexpensive hand-held device with a central peep-hole for the clinician through which to look
  41. 41. Treatment •The management of keratoconus begins with spectacle correction. Once glasses fail to provide adequate visual function, contact lens fitting is required. Contact lens wear improves visual function by creating a new anterior refractive surface . Contact lenses do not prevent progression of corneal ectasia. While they seem to be associated with the development of keratoconus in some cases, this important mode of therapy should never be withheld for fear of causing progressive disease.
  42. 42. Treatment •Contact lenses must be tailored to individual's visual needs & comfort tolerance. Given ample time & motivation, fitting expertise, & access to all available contact lens modalities, many keratoconus patients can be successfully refitted, achieving good visual function .ens. •Relatively flat-fitting, rigid gas-permeable (RGP), hard contact lenses with light apical corneal touch, so-called technique, remain mainstay of contact lens treatment for keratoconus
  43. 43. Treatment •An apical clearance fitting technique is also commonly used. Other options include soft toric lenses, standard bicurved hard lenses, custom-back toric lenses, piggyback systems, hybrid lenses made of combined hard lens with a soft skirt, scleral lenses. •Hybrid lenses, such as the SoftPerm lens (CIBA Vision Corp., Duluth, GA) and the newer SynergEyes KC lens (SynergEyes, Inc., Carlsbad, CA) may be more comfortable for patients who cannot tolerate an RGP alone.
  44. 44. Corneal Collagen Cross-linking •Cross-linking of collagen refers to the ability of collagen fibrils to form strong chemical bonds with adjacent fibrils. In the cornea, collagen cross-linking occurs naturally with aging due to an oxidative deamination reaction that takes place within the end chains of collagen. Collagen cross-linking in the cornea is also observed in patients with diabetes due to glycation
  45. 45. Corneal Collagen Cross-linking • The original method of therapeutic corneal cross-linking was developed in Germany in 1998.the Dresden protocol, involves the use of UVA light and riboflavin to form bonds between collagen fibrils. Although the exact mechanism is unknown, it is believed that riboflavin causes the release of oxygen radicals that in turn induces an oxidation reaction to create new cross-linking bonds between collagen molecules
  46. 46. Corneal collagen cross linking CXL •CXL is an upcoming and safe treatment for corneal ectatic disorders. It is a technique which uses ultraviolet (UV) light and a photosensitizer to form strong chemical bonds with adjacent collagen fibrils. The goal is to halt progression. Human studies with CXL began in 2003 in Dresden, and early results were promising. The initial pilot study enrolled 16 patients with rapidly progressive keratoconus.
  47. 47. Corneal collagen cross linking CXL •Human studies with CXL began in 2003 in Dresden, and early results were promising. The standard treatment of Dresden protocol uses 0.1% Riboflavin in 20% Dextran drops on a de-epithelised cornea every two minutes for 30 minutes followed by UV A irradiation at 3Mw/cm 2 for 30 minutes at wavelength of 370nm.
  48. 48. Indications • mild to moderate keratoconus, post refractive ectasia, PMD , pseudophakic bullous keratopathy, infective keratitis, The main indication for CXL is progressive keratoconus. It is also used for the treatment of other progressive corneal ectatic disorders, such as post–LASIK ectasia and pellucid marginal degeneration. CXL has also been used for infectious corneal melts because of the collagen-stabilizing effect of CXL and the anti-infective effect of UVA light.
  49. 49. Indications It has been used for the treatment of pseudophakic bullous keratopathy by applying CXL after dehydrating the cornea in an attempt to delay or avoid the need for a penetrating keratoplasty. Traditional age criteria is older than 18 years, but it has been used in pediatric patients with good result
  50. 50. Contraindications • A minimum stromal thickness of 400 μm after epithelial removal is required for safe CXL. • In patients with corneas thinner than this, conventional CXL cannot be performed. For such patients, either contact lens– assisted CXL (CACXL) or hypotonic CXL is performed.
  51. 51. Contraindications • CXL is also not performed in patients with stable, nonprogressive keratoconus. Keratoconus is generally likely to be nonprogressive in patients older than 35 years because of naturally occurring cross- linking occurring with age. • In such patients, it is indicated only if progression is documented
  52. 52. CCC EFFECTS 300 µM DEPTH OF CORNEA Corneal thickness µm
  54. 54. C/I
  57. 57. IMBIBITION
  59. 59. POST CCC STEP 4
  63. 63. CONCLUSION
  64. 64. CROSSLINKING IN THIN CORNEAS •Corneas with a stromal thickness of less than 400 µm are excluded from standard treatment so as to avoid damaging the endothelial cells with the UV radiation. Various methods of CXL have been developed to treat this patient population. Studies have been done in patients with corneal thickness less than 400 µm with the use of hypo-osmolar Riboflavin 0.1% in 20% dextran solution. The method of instillation is similar to standard CXL protocol .
  65. 65. Contact Lens–Assisted Collagen Cross-Linking •It is possible that some corneas do not swell enough to make hypo-osmolar CXL possible. •CACXL has advantage of not being dependent on swelling properties of the cornea . In CACXL, thickness of cornea is artificially increased by increasing amount of riboflavin- containing substance anterior to the stroma, increasing functional corneal thickness. using precorneal riboflavin film, a riboflavin-soaked soft contact lens , and a pre–contact lens riboflavin film
  66. 66. Technique • Preoperatively, lidocaine 2% & pilocarpine 2.0% are instilled twice to aid in epithelial • removal and to promote miosis and reduce UVA exposure to the lens and retina. The central 9 mm of corneal epithelium is abraded. Iso-osmolar riboflavin 0.1% in dextran T500 drops is applied every 3 minutes for 30 minutes. a Sof lens Daily Disposable soft contact lens is immersed in
  67. 67. Technique •At the end of 30 minutes, adequate corneal saturation with riboflavin is confirmed by visualization of a green flare in the anterior chamber using a slit lamp.The riboflavin- soaked contact lens is then applied on the corneal surface & thickness is remeasured. Once confirmed to be more than 400 μm, treatment is continued. central 9 mm of cornea is exposed to UVA light of 370 nm with an irradiance of 3 mW/cm2 for 30 minutes.
  70. 70. Conclusion •In CXL corneas thinner than 400 μm, despite a reduction in irradiance from the corneal surface toward the deeper layers of the corneal stroma, irradiation levels still exceed the endothelial toxic threshold. CACXL adds artificially to corneal thickness using a riboflavin-soaked contact lens and a precorneal riboflavin film of known thickness, thereby increasing safety. It extends the benefit of safely undergoing cross-linking to a larger number of patients with thin corneas .
  71. 71. Accelerated CXL KXL •Accelerated CXL is based on reciprocity law of Bunsen Roscoe & has advantages of decreasing treatment time while increasing intensity, keeping total energy constant . trend is shifting towards aiming at shorter duration of CXL treatment. The accelerated CXL device (KXL™) significantly reduces treatment time from one hour to a few minutes, while maintaining same treatment dose as in conventional CXL.
  72. 72. Accelerated CXL KXL As an alternative to riboflavin formulations containing dextran, the KXL uses riboflavin 0.1% in hydroxypropyl methylcellulose (Vibex Rapid™, Avedro, Inc.). initial procedure is similar to conventional CXL of epithelial debridement. Vibex is then administered topically for 10 minutes. The cornea is then exposed to 365 nm UVA light with the CXL system for three minutes at an irradiance level of 30 mW/cm2 (accelerated CXL).
  73. 73. Accelerated CXL KXL
  74. 74. LASIK Xtra •Kanellopoulos in 2009 introduced concept of simultaneous CXL with conventional LASIK. This has now been termed as LASIK Xtra. The procedure is indicated for individuals who are at higher risk of post LASIK ectasia or regression. The patients included in this high risk group are: High myopes , Borderline corneal pachymetry , Asymmetry topography, Hyperopes , Family history of keratoconus , History of chronic ocular allergy .
  75. 75. Procedure for LASIK Xtra •A variation of Riboflavin formulation is used which comes by the name Vibex Xtra. This is 0.1%Riboflavin diluted in saline instead of Dextran. After lifting the LASIK flap, the flap is folded over itself in order to prevent absorption of Riboflavin by the flap. A single drop of Vibex Xtra is placed over the exposed stromal bed and carefully spread.
  76. 76. Procedure for LASIK Xtra •Soaking of Riboflavin is continued for one minute and then the flap is repositioned. Remaining Riboflavin is thoroughly washed from the stromal bed. Next high fluence cross linking is carried out at irradiation of 30 Mw/cm2 for 80 seconds.
  77. 77. INTRACORNEAL RING SEGMENTS •ICRs are tiny ring segments made of PMMA . They are inserted into cornea to regularize its surface & achieve refractive correction. ICRS is safe & reversible procedure that does not affect central visual axis of cornea. •It is considered as an alternative aiming at •delaying the need for corneal grafting procedures in KC patients. However, long- term stability remains the concern of many studies.
  78. 78. ICRS
  83. 83. MECHANISM
  84. 84. CONDITIONS
  85. 85. CONDITIONS
  87. 87. MYORING
  88. 88. MECHANISM
  91. 91. LKP •In KC, the corneal endothelium is generally intact and healthy, even after many cases of acute hydrops and that most rejection episodes are invariably endothelial in origin. It is for these reasons that there has been a trend •over recent years to perform lamellar Techniques.Such procedures offer replacement of the diseased (stromal) part of the keratoconic cornea.
  92. 92. LKP •LKP has been shown to result in less endothelial cell loss, less IOP problems than PKP , a reduction in rejection episodes, &, in some cases, a reduction of induced astigmatism. •However, while some series have achieved comparable visual outcomes, others have demonstrated that penetrating techniques slightly outperform deep lamellar procedures
  93. 93. LKP • Indications of DALK regarding KC: • Anterior corneal scars • Advanced disease with stress lines and clear cornea • K-max > 65 dpt • Thinnest location < 350 m • Very high refractive error (sphere > −6 and/or cylinder > −6)
  94. 94. PK •Between 10% & 25% of cases of KC progress to point where visual rehabilitation is no longer possible, especially in those who present at a young age (younger than 20) and with keratometry measurements > 60 dpt & corneal thickness < 400 m at the thinnest location. In the past, such patients have had only one option: a full thickness corneal transplant . KC is one of the most common •indications for penetrating keratoplasty accounting for 15–25% of such surgeries.
  95. 95. PKP •As the cornea is avascular, the donor and host do not have to be tissue matched and eye banks – after checking for communicable diseases and tissue quality – can provide suitable tissue within a few days or weeks. Following surgery, visual recovery takes several weeks/ months, with full stabilization often taking up to a year after which time the sutures can be removed.
  96. 96. PKP •Corneal transplantation in KC is considered relatively low risk, in terms of graft rejection and other postoperative complications, as these eyes do not typically exhibit corneal neovascularization. •Despite these facts, there are reported •complications such as allograft rejection, iatrogenic astigmatism, significant endothelial cell loss .
  97. 97. PKP • when the life expectancy is long, side effects caused by long-term use of topical steroids (e.g., secondary glaucoma and cataract), and recurrence of KC on the graft itself. Clear grafts are obtained in 95% of cases but optical outcomes may be unsatisfactory because of the iatrogenic astigmatism and anisometropia. Between 30% and 50% of grafted eyes still require contact lens correction for best acuity or further keratorefractive surgical procedures.
  98. 98. Global Consensus on Keratoconus 2015
  99. 99. •Keratoconus and ectatic corneal diseases have been recognized for more than 150 years. Over the last 2 decades, there has been a revolution in the knowledge related to the diagnosis and management of these conditions. the advent of corneal topography, and more recently corneal tomography, has increased the ability to identify corneal ectasia at a much earlier stage than was previously possible. Previously established prevalence of keratoconus of 1/2000 has been challenged with much higher prevalence rates found in many parts of world.
  100. 100. surgical treatment for keratoconus the use of intrastromal corneal ring segment (ICRS), corneal crosslinking (CXL),therapeutic excimer treatments including Phototherapeutic keratectomy and photorefractive keratectomy (PRK) , and phakic intraocular lenses (IOL) alone or in combination have been proposed to delay or even prevent the need for corneal transplantation. new techniques of Keratoplasty have been developed such as deep anterior lamellar keratoplasty (DALK)& femtosecond laser-assisted corneal transplantation .
  101. 101. mandatory to diagnose keratoconus •Abnormal posterior elevation •Abnormal corneal thickness distribution •Clinical noninflammatory corneal thinning •tomography ( Scheimpflug or OCT ) is currently best and most widely used test to diagnose early keratoconus
  102. 102. •Central pachymetry is the least reliable indicator for diagnosing keratoconus •Keratoconus can be present in a cornea of normal central thickness •Posterior corneal elevation abnormalities must be present to diagnose early or subclinical keratoconus. •True unilateral keratoconus does not exist
  103. 103. Ectasia progression •consistent change in at least 2 of following parameters where magnitude of change is above normal noise of testing system •Progressive steepening of the anterior corneal surface •Progressive steepening of the posterior corneal surface •Progressive thinning.
  104. 104. Surgical Approaches Based on Different Case Scenarios
  105. 105. Young (eg, 15-year-old) patient with stable KCN with satisfactory vision with glasses •Prescribe glasses only or in combination with contact lenses or CXL
  106. 106. Young (eg, 15-year-old) patient with progressive KCN with satisfactory vision with glasses •Perform CXL and prescribe glasses ± contact lenses
  107. 107. Older (eg, 55-year-old) patient with stable KCN with satisfactory vision with glasses •Prescribe glasses only or with contact lenses
  108. 108. Older (eg, 55-year-old) patient with progressive KCN with satisfactory vision with glasses •Perform corneal cross-linking only or with prescription of glasses/ contact lenses
  109. 109. Patient with stable KCN with unsatisfactory vision with glasses but satisfactory vision with rigid contact lenses and tolerates them well This patient has a spherical equivalent of moderate myopia [eg, - 5 diopters (D)] •Prescribe contact lenses (including scleral lenses)
  110. 110. Patient with stable KCN with unsatisfactory vision with glasses but good vision with rigid contact lenses, and tolerates them well This patient has a spherical equivalent of high myopia (eg, -15 D) •Prescribe contact lenses (including scleral lenses
  111. 111. Patient with stable KCN with unsatisfactory vision with glasses and contact and scleral lenses, or who does not tolerate contact or scleral lenses This patient has a spherical equivalent of moderate myopia (eg, -5 D) •Perform dDALK. •Consider ICRS in eyes with adequate corneal thickness and minimal to no scarring
  112. 112. Patient with stable KCN with unsatisfactory vision with glasses and contact and scleral lenses, or who does not tolerate contact or scleral lenses .This patient has a spherical equivalent of high myopia (eg, - 15 D) •Perform dDALK
  113. 113. Patient with stable severe KCN with unsatisfactory vision with glasses and contact and scleral lenses. This patient has moderate anterior corneal scarring but no evidence of previous corneal hydrops •Perform dDALK
  114. 114. Patient with stable severe KCN with unsatisfactory vision with glasses and contact and scleral lenses. This patient has moderate anterior and deep corneal scarring with evidence of previous corneal hydrops •PK alone •or attempt pdDALK
  115. 115. Final summary •anyone with progressive ectasia should undergo CXL no matter what age or level of vision (assuming the eye was an appropriate candidate). •not to proceed with surgery (other than CXL) if patients were satisfied with their vision with glasses or contact lenses. ICRS may be considered. phakic IOLs should be used less often.
  116. 116. Final summary • a strong preference for DALK when a corneal transplant was needed, unless eye had previous compromise of Descemet membrane (most commonly from acute hydrops), at which point the preference is for a PK. • pdDALK may be considered even in the presence of previous hydrops.