Ectasia Risk in Topography: Difference between revisions

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For a better approach and specially in not clear cut cases other index and parameters must be evaluated.
For a better approach and specially in not clear cut cases other index and parameters must be evaluated.
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The article published by Marconi Santiago, propose a metric for calculating the  risk of ectasia in patients where LASIK  is to be performed. The percent of tissue altered (PTA) that describes the interaction between flap thickness (FT), the ablation depth (AD) and the central corneal thickness (CCT) interaction during excimer laser refractive surgery, is described in the following equation: '''PTA = (FT + AD) / CCT '''. This metric formula represents a more accurate way of calculating the risk of corneal ectasia after LASIK than taking into account the individual components that comprise it.<ref name=":8" />
The article published by Marconi Santiago proposes a metric for calculating the  risk of ectasia in patients where LASIK  is to be performed. The percent of tissue altered (PTA) describes the interaction between flap thickness (FT), the ablation depth (AD) and the central corneal thickness (CCT) interaction during excimer laser refractive surgery and is described in the following equation: '''PTA = (FT + AD) / CCT '''. This metric formula represents a more accurate way of calculating the risk of corneal ectasia after LASIK than taking into account the individual components that comprise it.<ref name=":8" />


Using the Orbscan technology Randleman et al. Propose  the following risk factors  for ectasia in  order of importance:   
Using the Orbscan technology Randleman et al. Propose  the following risk factors  for ectasia in  order of importance:   

Revision as of 13:24, July 31, 2020

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Article initiated by:
Adrián Mauricio Aldrete López, MD
All contributors:
Alejandro Rodríguez-García, MD., Adrián Mauricio Aldrete López, MD, Vatinee Y. Bunya, MD, MSCE, Maria A. Woodward, MD, Julio C. Hernandez-Camarena, MD, Vandana Reddy, MD, Alain Saad, MD, Masako Chen, MD, Praneetha Thulasi, MD, Deena Shaath, MD
Assigned editor:
Erica Bernfeld M.D., Vandana Reddy, MD
Review:
Assigned status Update Pending
 by Vandana Reddy, MD on July 31, 2020.


Increased area of corneal power surrounded by concentric areas of decreasing power. Asymmetric inferior-superior power. Skewing of the steepest radial axes above and below the horizontal meridian.

LASIK and PRK induced ectasia is preventable if the preoperative topography and pachymetry indexes for high-risk are identified on time.[1][2][3]

Disease Entity

Refractive surgery induced ectasia is probably the most feared complication of laser in situ keratomileusis (LASIK) and photorefractive keratectomy (PRK). It presents as a progressive eccentric thinning of the corneal stroma with consequent steepening of the posterior surface of the cornea. The disorder is considered irreversible and may reduce significantly uncorrected and spectacle-corrected visual acuity.[3] Although the general prevalence of postoperative ectasia is unknown, there are several reports that show a prevalence rate that vary from 0.02% to 0.6% .[4][5] Risk factors for the development of post-LASIK/PRK ectasia include a personal or family history of keratoconus (KC), abnormal corneal topography (form frusta keratoconus), high myopia, low-residual stroll bed (RSB <300 microns), excessive stroll ablation (>100 microns), high percentage of tissue altered (PTA >0.40); deep primary keratotomy resulting in a thick corneal flap and low preoperative corneal thickness (<500 microns).[3] [6][7][8]

Even when risk factors for ectasia after refractive surgery have been identified, reports of individuals developing ectasia without any of the proposed risk factors have emerged, this specific group of patients have shown a tendency to be younger.[3][9][10][11]

Etiology

Corneal ectasia induced by excimer laser refractive surgery is thought to be the result of the alteration of the corneal surface and anterior stroma in corneas with previous biomechanical abnormalities.[12] Histologic and ultrastructural findings explain the pathophysiology of post-LASIK or post-PRK ectasia by interlamellar and inter fibrillar biomechanics slippage induced by excimer laser disruption (interlamelar and inter fibrillar fracture) and not to primary collagen fibrillar failure.[12] Besides geometric corneal parameters, new techniques permit a better understanding of the corneal bio-mechanics in order to get a better prediction of the corneal response to surgical or therapeutic interventions and to assist in the detection of early KC. [13][14][15]

Risk Factors

There is an integrated relationship between preoperative corneal thickness, ablation depth, and flap thickness in determine the relative amount of bio-mechanical change that has occurred after a LASIK/PRK procedure.[16][17][18][19][20][21] Since there first reported cases of corneal ectasia after LASIK, numerous authors have reported the eye characteristics of these patients making emphasis on preoperative high myopia, RSB thickness lower than 250 microns, low preoperative corneal thickness (<500 microns) and abnormal topography (forme fruste keratoconus).[22][23][24][25] Randleman et al, compared normal uneventful LASIK patients with those developing corneal ectasia after LASIK or PRK and observed that the latter had significant abnormal preoperative corneal topographies, were younger (< 34 years), were more myopic (>8 diopters of mean refractive spherical equivalent), had thinner corneas before surgery (mean, 521 microns) and had less RSB thickness (256 microns).[3] Logistic regression analysis on their data showed abnormal topography as the most significant factor that discriminated cases from controls. [1] [3] 

Santiago et al,  found that the percent of tissue altered (PTA) ≥40% during LASIK (derived from [PTA = (FT + AD)/CCT] where FT is flap thickness, AD is ablation depth and CCT is central corneal thickness) is strongly associated with the development of ectasia in eyes with otherwise normal topography.[16]

Down syndrome, family history of connective tissue disorders, ocular allergy, and mechanical factors such as eye rubbing and floppy eyelid syndrome, have also been identified as risk factors for corneal ectasia. [26]

General Pathology

Pointing out a patient with FFK and early KC is of major importance in the preoperative assessment, as most refractive procedures are contraindicated in patients with an ectasic preoperative condition due to the high-risk of induction and/or progression of the ectasia after the procedure.[27]

Pathophysiology

Electron microscopic studies have proved the Z-shaped pattern interruptions at the level of Bowman´s layer, it is believed are caused by brakes in the epithelial layer with posterior growing of the epithelial layer into Bowman´s layer and collagen growing anteriorly into the epithelial layer.[28]

The fragmentation observed in the Bowman´s layer with the electron microscopy scanner tend to be specific of keratoconus, and it is believed to be the initial change leading for developing ectasia.[29]


Atypical hystopathogical variant has been described, where brakes in Bowman´s layer are not present, although clinically is the same pathology. Among different histopathologic variants the scarring of Bowman´s layer and anterior stroma positively correlate with fragmentation of collagen fibers and fibroblastic activity.[29][30]

It has been suggested that collagen lamellae released from their attachments to Bowman´s layer and become free to slide. This results in thinning without collagenolysis. [31]

The basis of the histologic and ultra-structural findings proposed by Dawson et al.[32], in the pathophysiology of post-LASIK or post-PRK ectasia is explained by interlamellar bio-mechanical slippage followed by subsequent interfibrillar bio-mechanical slippage as opposed to direct primary collagen fibril failure. This chronic bio-mechanical failure process is similar to that of interlamellar and interfibrillar slippage described with keratoconus.[33][34][35]

Diagnosis

PTA formula formula for calculating ectasia risk in Lasik. For a better approach and specially in not clear cut cases other index and parameters must be evaluated.

The article published by Marconi Santiago proposes a metric for calculating the risk of ectasia in patients where LASIK is to be performed. The percent of tissue altered (PTA) describes the interaction between flap thickness (FT), the ablation depth (AD) and the central corneal thickness (CCT) interaction during excimer laser refractive surgery and is described in the following equation: PTA = (FT + AD) / CCT . This metric formula represents a more accurate way of calculating the risk of corneal ectasia after LASIK than taking into account the individual components that comprise it.[16]

Using the Orbscan technology Randleman et al. Propose the following risk factors for ectasia in order of importance:

  1. Abnormal preoperative topography
  2. Low Residual Stromal Bed (RSB) thickness
  3. Young age
  4. Low preoperative corneal thickness
  5. High myopia.


Table The Ectasia Risk Score System designed by Randelman

A screening strategy that weighs all of these factors was proposed: Ectasia Risk Factor Score System. Given a score between 0 to 4 to each one of the factors. [1]

The scoring is a useful but still controversial index for preoperative LASIK candidates.

There are two main videokeratographies software's used to evaluate pre-operative risk of ectasia in the first place the one developed by Rabinowitz[36] and in second place the one developed by Maeda and Klyce at the LSU Eye Center in New Orleans, Louisiana.[37][38]

Using the Keratoconus Prediction Index (KPI) The system developed by Maeda and Klyce was able to differentiate keratoconus from a wide variety of other pathologies with a false positive rate of 98.7% and a false negative rate of 98.4%.[38]

The Rabinowitz software differs from the Maeda-Klyce system in three aspects:

  • Attempts to differentiate keratoconus from healthy corneas, not from other pathologies in a non-contact lens wearing patient.
  • Evaluates both eyes.
  • The indices were developed from videokeratographs of patients with clinical signs of keratoconus.[36]

History

Marc Amsler In 1938, with a photographic placido disk, was the first to describe early corneal topographic changes in keratoconus before clinical or bio-microscopic signs could be noted. His classical studies of keratoconus documented the progression of the disease, from minor corneal surface changes to clinically identifiable keratoconus.

He classified keratoconus into clinical stages and an earlier latent stage identifiable only with the placido disk evaluation of corneal topography. The early stages were subdivided into two categories:

  • Keratoconus fruste. In which there is a 1–4 degree deviation of the horizontal axis of the placido disk.
  • Early or mild keratoconus. Which has a 4–8 degree deviation.


Amsler reexamined 286 eyes 3–8 years after the diagnosis, and only 20%, including 66% of the latent cases, show progression.

Progression was most likely to occur in patients between 10 and 20 years of age and decreased tendency to progression between ages 20 and 30, and low incidence of progression after 30 years old.[39]

Levene suggests that instrument tilt or poor alignment (hand held needed) of the keratoscope may result in incorrect observations of the corneal shape in the horizontal axis. Creating intra-observer and inter-observer discrepancies. [40]

In the 70´s Donaldson published a new technique for keratography: The photokeratoscope produces a topographic record of 55–80% of the total corneal contour, but it provides little information about the central 2-3 mm of the cornea.[41] Rowsey et al. used this instrument to study keratoconus in 827 patients.[42]

The ophthalmometer or keratometer, provides information from 3 points approximately 3 mm apart, calculating anterior corneal curvatures being a simple and useful tool for detecting keratoconus. Typically showing a progressive central or inferior steepening.

Krachmer et al. documented increasing in corneal curvature over time using the keratometer as a sensitive indicator of keratoconus.[43]

In 1984 the classic publication of Klyce et al. set the basis for the later development of computer-assisted videokeratoscopes algorithms. The computed process demonstrate to be a useful quantitative method with which to determine corneal shape, for clinical evaluation particularly in corneal surface irregularities.[44]

Current corneal imaging modalities: Scheimpflug, optical coherence tomography (OCT) offer more information than were previously available with placido based anterior corneal analysis. This new tomographic information allows for earlier identification of disease and has changed our perception of what constitutes keratoconus, improving the specificity to exclude false positive cases.[45]

Optical Coherence Tomography. (OCT) RTVue: Optovue, Inc, Fremont, CA. Is an infrared high definition imaging technique: Offering reliable topographic renders and pachymetric measurements

OCT and Scheimpflug photography allows measurements of both the anterior and posterior cornea, corneal thickness maps, providing greater corneal coverage than possible with videokeratoscopes.[46]

Of these, rotating Scheimpflug photography currently provides the most useful information for diagnosing early ectatic change. It is also a technique that is rapid and easy to perform, which would be a requisite for use as a screening tool.[47][48][45]

Clinical diagnosis

In 2015 international cornea specialist gathered efforts to define key points in the global consensus on keratoconus and ectatic diseases.[26] According to Dr. Rapuano Moderate to severe KC is easy to diagnose clinically “You can see it at the slit lamp; you don’t even need topography.” But to recognizing mild, subclinical disease it is necessary the information of computed systems such as Scheimpflug imaging or OCT, which can detect posterior corneal abnormalities.

The panelist group agreed that the mandatory findings for KC diagnosis include posterior corneal elevation abnormalities, in addition to abnormal distribution of corneal thickness and noninflammatory corneal thinning.[26]

Keratoconus, from greek: (kerato- horn, cornea; and konos cone) is a condition in which the cornea assumes a conical shape due to noninflammatory thinning of the stroma, Producing an irregular astigmatism, myopia, and protrusion, progressively deteriorating vision. Tipically affecting both eyes. [43]

Munson’s sign and Rizzuti’s classical clinical signs are observed in latter stages. Munson’s sign is a V-shaped deformation of the lower lid produced by the corneal conic protrusion in down-gaze. Rizzuti’s sign is a sharply focused beam of light near the nasal limbus.[49]

Fleischer ring are pigmented rings in the peripheral cornea.[50] Resulting from iron deposition in basal epithelial cells, in the form of hemosiderin. They are usually yellowish to dark-brown, and may be complete or broken. Fleischer ring is present in most keratoconus corneas whereas prominent nerves are less frequent and specific for keratoconus.[51][52]

Diagnostic procedures

It has been estimated that up to 6% of patients with some sort of pre-clinically ectatic condition show up in clinical settings for refractive evaluation. [53][54][55]

Classical topography patterns for keratoconus and post-lasik ectasia rely mainly on three characteristics:

  1. Increased area of corneal power surrounded by concentric areas of decreasing power.
  2. Asymmetric inferior-superior power.
  3. Skewing of the steepest radial axes above and below the horizontal meridian.


Keratometry

Central 3 mm curvature zone readings are a very useful tool in pre-operatory evaluation. Manual keratometry is very sensitive indicator of astigmatism. Increased 0.5 diopters or more per year should make the clinician to be conservative and gather more information over time.[56]

Computed Topography.

Up to date the most important element of pre-operative evaluation. The mapping of the corneal surface, renders the calculated corneal dimensions.

There are two principal corneal topographic techniques:

  • Pentacam: Scheimpflug rotatory camera (Oculus Inc, Wetzlar, Germany).
  • Orbscan: Slit lamp scanner monochromatic blue light based (Bausch & Lomb, Technolas, Müngen, Germany).


Optic Coherence Tomography (OCT)

  • RTVue: Infrared based high definition imaging technique (Optovue, Inc, Fremont, CA.)

Differential diagnosis

Meticulous slit lamp examination may distinguish from keratoglobus, pellucid marginal degeneration and Terrien marginal degeneration. But topographic evidence is necessary in early presentations or non typical cases.[57]

Pellucid Marginal Degeneration.

Typically described by a peripheral band of thinning of the inferior cornea, there is an uninvolved area between the thin corneal area and sclero-corneal limbus. Central corneal thickness usually normal.

As well as keratoconus, pellucid marginal degeneration is a progressive condition affecting both eyes. Most of the times the affection tends to be asymmetric.

The topographic pattern of the cornea classically resemble a butterfly, with against the rule astigmatism. [55]

Terrien Marginal degeneration

Terrien marginal degeneration is a slow-progressing, bilateral asymmetric degeneration of the peripheral cornea. Male over 40 years are more commonly affected. Stromal thinning, vascularization, lipid deposition, and against-the-rule astigmatism are classic signs. Though typically noninflammatory, a variant form characterized by prominent inflammation exists. [58]

Keratoglobus

Keratoglobus is a rare bilateral disorder in which the entire cornea is thinned most markedly near the corneal limbus, in contrast to the localized thinning centrally or paracentrally in keratoconus. [43]

Most often keratoglobus is a congenital disease, but it may be secondarily acquired. This corneal pathology tend to produce extreme myopia, irregular astigmatism, and corneal scarring due to hydrops.[59]

Additional Resources[60]

References

  1. ↑ Jump up to: 1.0 1.1 1.2 Randleman JB, Trattler WB, Stulting RD. Validation of the Ectasia Risk Score System for Preoperative Laser in Situ Keratomileusis Screening. American journal of ophthalmology. 2008;145(5):813-818. doi:10.1016/j.ajo.2007.12.033.
  2. ↑ Randleman JB, Russell B, Ward MA, Thompson KP, Stulting RD. Risk factors and prognosis for corneal ectasia after LASIK. Ophthalmology. 2003;110:267–75. [PubMed]
  3. ↑ Jump up to: 3.0 3.1 3.2 3.3 3.4 3.5 Randleman JB, Woodward M, Lynn MJ, Stulting RD. Risk Assessment for Ectasia after Corneal Refractive Surgery. Ophthalmology. 2008;115:37–50. [PubMed]
  4. ↑ Binder PS. Analysis of ectasia after laser in situ keratomileusis: risk factors. J Cataract Refract Surg 2007; 33(9):1530–1538.
  5. ↑ Chen MC, Lee N, Bourla N, Hamilton DR. Corneal biomechanics measurements before and after laser in situ keratomileusis. J Cataract Refract Surg 2008; (34)11:1886–1891.
  6. ↑ Ortiz D, Piñero D, Shabayek MH, Arnalich-Montiel F, Alió JL. Corneal biomechanical properties in normal, post-laser in situ keratomileusis, and keratoconic eyes. Journal of Cataract and Refractive Surgery. 2007;33(8):1371–1375.
  7. ↑ González-Méijome JM, Villa-Collar C, Queirós A, Jorge J, Parafita MA. Pilot study on the influence of corneal biomechanical properties over the short term in response to corneal refractive therapy for myopia. Cornea. 2008;27(4):421–426.
  8. ↑ Kirwan C, O’Keefe M. Corneal hysteresis using the Reichert ocular response analyser: findings pre- and post-LASIK and LASEK. Acta Ophthalmologica. 2008;86(2):215–218.
  9. ↑ Argento C, Cosentino MJ, Tytiun A, et al. Corneal ectasia after laser in situ keratomileusis. J Cataract Refract Surg 2001;27:1440–8.
  10. ↑ Wang JC, Hufnagel TJ, Buxton DF. Bilateral keratectasia after unilateral laser in situ keratomileusis: a retrospective diagnosis of corneal ectasia . J Cataract Refract Surg 2003;29:2015–8
  11. ↑ Piccoli PM, Gomes AA, Piccoli FV. Corneal ectasia detected 32 months after LASIK for correction of myopia and asymmetric astigmatism. J Cataract Refract Surg 2003;29:1222–5.
  12. ↑ Jump up to: 12.0 12.1 Dawson DG1, Randleman JB, Grossniklaus HE, O'Brien TP, Dubovy SR, Schmack I, Stulting RD, Edelhauser HF. Corneal ectasia after excimer laser keratorefractive surgery: histopathology, ultrastructure, and pathophysiology.Ophthalmology 2008;115(12):2181-2191
  13. ↑ Garcia-Porta, N., Fernandes, P., Queiros, A., Salgado-Borges, J., Parbfita-Mato, M., & González-Méijome, J. M. (2014). Corneal Biomechanical Properties in Different Ocular Conditions and New Measurement Techniques. ISRN Ophthalmology, 2014, 724546. http://doi.org/10.1155/2014/724546
  14. ↑ Luce DA. Determining in vivo biomechanical properties of the cornea with an Ocular Response Analyzer. Journal of Cataract and Refractive Surgery. 2005;31(1):156–162.
  15. ↑ Piñero DP, Alcón N. In vivo characterization of corneal biomechanics.J Cataract Refract Surg. 2014 Jun;40(6):870-87.
  16. ↑ Jump up to: 16.0 16.1 16.2 Santhiago MR, Smadja D, Gomes BF, Mello GR, Monteiro ML, Wilson SE, Randleman JB. Association between the percent tissue altered and post-laser in situ keratomileusis ectasia in eyes with normal preoperative topography. Am J Ophthalmol. 2014 Jul;158(1):87-95.e1. doi: 10.1016/j.ajo.2014.04.002. Epub 2014 Apr 13. PubMed PMID: 24727263.
  17. ↑ Santhiago MR, Wilson SE, Hallahan KH, et al. Changes in custom biomechanical variables after femtosecond laser in situ keratomileusis and photorefractive keratectomy for myopia. J Cataract Refract Surg. http://dx.doi.org/10.1016/j.jcrs.2013.11.030.
  18. ↑ Smadja D, Santhiago MR, Mello GR, Roberts CJ, Dupps WJ Jr, Krueger RR. Response of the posterior corneal surface to myopic laser in situ keratomileusis with different ablation depths. J Cataract Refract Surg 2012;38(7): 1222–1231.
  19. ↑ Reinstein DZ, Archer TJ, Randleman JB. Mathematical model to compare the relative tensile strength of the cornea after PRK, LASIK, and small incision lenticule extraction.J Refract Surg 2013;29(7):454–460.
  20. ↑ Randleman JB, Hebson CB, Larson PM. Flap thickness in eyes with ectasia after laser in situ keratomileusis. J Cataract Refract Surg 2012;38(5):752–757.
  21. ↑ Saad A, Gatinel D. Bilateral corneal ectasia after laser in situ keratomileusis in patient with isolated difference in central corneal thickness between eyes. J Cataract Refract Surg 2010;36(6):1033–1035.
  22. ↑ Seiler T, Koufala K, Richter G. Iatrogenic keratectasia after laser in situ keratomileusis. J Refract Surg 1998;14:312–7.
  23. ↑ Seiler T, Quurke AW. Iatrogenic keratectasia after LASIK in a case of forme frusta keratoconus. J Cataract Refract Surg 1998;24:1007–9.
  24. ↑ Buzard KA, Tuengler A, Febbraro JL. Treatment of mild to moderate keratoconus with laser in situ keratomileusis. J Cataract Refract Surg 1999;25:1600 –9.
  25. ↑ Geggel HS, Talley AR. Delayed onset corneal ectasia following laser in situ keratomileusis. J Cataract Refract Surg 1999;25: 582–6.
  26. ↑ Jump up to: 26.0 26.1 26.2 Gomes JA, Tan D, Rapuano CJ, Belin MW, Ambrósio R Jr, Guell JL, Malecaze F, Nishida K, Sangwan VS;Global consensus on keratoconus and ecstatic diseases. Group of Panelists for the Global Delphi Panel of Keratoconus and Ectatic Diseases. Cornea. 2015 Apr;34(4):359-69. doi: 10.1097/ICO.0000000000000408. PMID: 25738235
  27. ↑ Lafond G, Bazin R, Lajoie C. Bilateral severe keratoconus after laser in situ keratomileusis in a patient with forme fruste keratoconus. J Cataract Refract Surg. 2001 Jul;27(7):1115-8. PubMed PMID: 11489585.
  28. ↑ Kanai A, Kaufman HE. Electron microscopic studies of corneal stroma: aging changes of collagen fibers. Ann Ophthalmol. 1973 Mar;5(3):285-7 passim. PubMed PMID: 4694913.
  29. ↑ Jump up to: 29.0 29.1 Sawaguchi S, Fukuchi T, Abe H, Kaiya T, Sugar J, Yue BY. Three-dimensional scanning electron microscopic study of keratoconus corneas. Arch Ophthalmol. 1998 Jan;116(1):62-8. PubMed PMID: 9445209.
  30. ↑ Pouliquen Y, Graf B, Hamada R, Giraud JP, Offret G. [Fibrocytes in keratoconus. Morphological aspect and modification of the extra-cellular space. Study with light and electron microscopy]. Arch Ophtalmol Rev Gen Ophtalmol. 1972 Aug-Sep;32(8):571-86. French. PubMed PMID: 4267199.
  31. ↑ Polack FM. Contributions of electron microscopy to the study of corneal pathology. Surv Ophthalmol. 1976 May-Jun;20(6):375-414. Review. PubMed PMID: 779087.
  32. ↑ Dawson DG, Randleman JB, Grossniklaus HE, O'Brien TP, Dubovy SR, Schmack I, Stulting RD, Edelhauser HF. Corneal ectasia after excimer laser keratorefractive surgery: histopathology, ultrastructure, and pathophysiology. Ophthalmology. 2008 Dec;115(12):2181-2191.e1. doi: 10.1016/j.ophtha.2008.06.008. Epub 2008 Aug 9. PubMed PMID: 18692245.
  33. ↑ Bron AJ. The architecture of the corneal stroma. Br J Ophthalmic 2001;85:379–81.
  34. ↑ Bron AJ. Keratoconus. Cornea 1988;7:163–9.
  35. ↑ Patey A, Salvoldelli M, Pouliquen Y. Keratoconus and normal cornea: a comparative study of the collagenous fibers of the corneal stroma by image analysis. Cornea 1984;3:119–24
  36. ↑ Jump up to: 36.0 36.1 Rabinowitz, YS. Videokeratographic indices to aid in screening for keratoconus. J Refract Surg. 1995;11: 371–379
  37. ↑ Maeda, N, Klyce, SD, Smolek, MK, and Thompson, HW. Automated keratoconus screening with corneal topography analysis. Invest Ophthalmol Vis Sci. 1994;35: 2749–2757
  38. ↑ Jump up to: 38.0 38.1 Maeda, N, Klyce, SD, and Smolek, MK. Comparison of methods for detecting keratoconus using videokeratography. Arch Ophthalmol. 1995; 113: 870–874
  39. ↑ Amsler, M. Le keratocone fruste au javal. Ophthalmologica. 1938; 96: 77–83
  40. ↑ Levene, JR. An evaluation of the handheld keratoscope as a diagnostic instrument for corneal astigmatism. Br J Physiol Opt. 1962; 19: 237–251
  41. ↑ Donaldson, DD. A new instrument for keratography. Arch Ophthalmol. 1972; 88: 425–428
  42. ↑ Rowsey, JJ, Reynolds, AE, and Brown, R. Corneal topography. Corneascope. Arch Ophthalmol. 1981; 99: 1093–1100
  43. ↑ Jump up to: 43.0 43.1 43.2 Krachmer, JH, Feder, RS, and Belin, MW. Keratoconus and related noninflammatory corneal thinning disorders. Surv Ophthalmol. 1984; 28: 293–322
  44. ↑ Klyce, SD. Computer-assisted corneal topography. High resolution graphic presentation and analysis of keratoscopy. Invest Ophthalmol Vis Sci. 1984; 25: 1426–1435
  45. ↑ Jump up to: 45.0 45.1 Belin MW, Ambrósio R. Scheimpflug imaging for keratoconus and ectatic disease. Indian Journal of Ophthalmology. 2013;61(8):401-406. doi:10.4103/0301-4738.116059.
  46. ↑ Kim SW, Sun HJ, Chang JH, Kim EK, Anterior segment measurements using Pentacam and Orbscan II 1 to 5 years after refractive surgery. J Refract Surg. 2009 Dec; 25(12):1091-7.
  47. ↑ Yazici AT, Bozkurt E, Alagoz C, Alagoz N, Pekel G, Kaya V, Yilmaz OF, Central corneal thickness, anterior chamber depth, and pupil diameter measurements using Visante OCT, Orbscan, and Pentacam. J Refract Surg. 2010 Feb; 26(2):127-33.
  48. ↑ Belin MW, Khachikian SS. Corneal diagnosis and evaluation with the OCULUS pentacam. Highlights Ophthalmol. 2007;35:5–7.
  49. ↑ Maguire LJ, Meyer RF: Ectatic corneal degenerations, in Kaufman H (ed): The Cornea. 1988, pp 485–510
  50. ↑ Fleischer, B (1906). «Über Keratokonus und eigenartige Pigmentbildung in der Kornea». Münchener medizinische Wochenschrift, 53, s. 625–626.
  51. ↑ Kriszt A, Losonczy G, Berta A, Takcas L. Presence of Fleischer ring and prominent corneal nerves in keratoconus relatives and normal controls. 2015;8(5):922-927
  52. ↑ Zadnik K, Barr JT, Gordon MO, Edrington TB. Biomicroscopic signs and disease severity in keratoconus. Collaborative Longitudinal Evaluation of Keratoconus (CLEK) Study Group. 1996;15(2):139-146
  53. ↑ Nesburn AB, Bahri S, Salz J, et al: Keratoconus detected by videokeratography in candidates for photorefractive keratectomy. J Refract Surg 11:194–201, 1995
  54. ↑ Wilson SE, Klyce SD: Screening for corneal topographic abnormalities before refractive surgery. Ophthalmology 101:147–152, 1994
  55. ↑ Jump up to: 55.0 55.1 Rabinowitz, Yaron S. Keratoconus. Survey of Ophthalmology, Volume 42, Issue 4, 297 - 319
  56. ↑ Gimbel HV, Iskander NG, Peters NT, Penno EA. Prevention and Management of Microkeratome-related Laser in situ Keratomileusis Complications. J Refract Surg. 2000 Mar 2;16(2 Suppl):S226-9. doi: 10.3928/1081-597X-20000302-05. PubMed PMID: 24364840.
  57. ↑ Rabinowitz YS, Wilson SE, Klyce SD (eds): Corneal Topography: Interpreting Videokeratography. New York, Tokyo, Ig- aku Shoin, 1993
  58. ↑ Chan AT, Ulate R, Goldich Y, Rootman DS, Chan CC. Terrien Marginal Degeneration: Clinical Characteristics and Outcomes. Am J Ophthalmol. 2015 Nov;160(5):867-872.e1. doi: 10.1016/j.ajo.2015.07.031. Epub 2015 Jul 23. PubMed PMID: 26210866.
  59. ↑ Baillif S, Garweg JG, Grange JD, Burillon C, Kodjikian L. [Keratoglobus: review of the literature]. J Fr Ophtalmol. 2005 Dec;28(10):1145-9. Review. French. PubMed PMID: 16395211.
  60. ↑ Asbell, P., & Petratos, T. (2015, August 28). Keratoconus (L. Rose, Ed.). Retrieved December 26, 2015, from http://eyewiki.org/Keratoconus
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