2 Tear Film and Corneal Disorders Abstract This chapter touches upon a select few of the myriad contributors to postoperative refraction inaccuracies including the visual and keratometric impacts of a compromised tear film as well as the visual contributions and consequences of corneal disorders in the cataract surgery setting. Keywords: cataract refractive outcomes, IOL selection, CDED, OSD, osmolarity, keratometry, keratometric errors, IOL calculation errors, wound healing, corneal nerves, growth factors, wavefront, aberrometry, scatter Despite advanced equipment, sophisticated formulae, and significant surgeon effort in choosing the ideal intraocular lens (IOL) power, postcataract surgical refractive outcomes are not as precise as we desire and expect. Crowdsourced online super formulae have improved predictability such that approximately 90% of cases result in refractive outcomes ±0.5 diopters of target refraction. Myriad dynamic and static factors contribute to suboptimal cataract surgery results. Two broad categories of topics will be used to review common and clinically significant factors that contribute to suboptimal post cataract outcomes: tear film disorders and corneal disorders. The most common tear film disorder is chronic dry eye disease (CDED; Standard high-contrast visual acuity testing is inadequate for exploring and understanding the quality of visual performance. Recent technological advances in devices such as wavefront analysis and point spread function analysis capture visual quality and provide insight into the dissatisfied 20/20 postoperative cataract patient. As reviewed by Koh,3 analysis of optical performance can help bridge the gaps in the sign/symptom disconnect in CDED. Light scatter can occur as forward or as backward light scatter. With respect to CDED, both phenomena occur and can be used to help explain suboptimal subjective visual complaints. Koh reported the amount of anterior or forward light scatter is statistically significantly higher for CDED with unstable tear film (rapid tear breakup time, or TBUT) and also for CDED with superficial punctate keratopathy (SPK) compared to normal individuals. Forward light scatter contributes to subjective glare. However, posterior light scatter is associated with subjective blur and is statistically significantly worse only in SPK and not with rapid TBUT. Higher order aberrations in wavefront analysis contribute to blur and fluctuations. Eye fatigue encompasses glare, blur, and fluctuations. Fig. 2.2 Topographic and keratometric maps demonstrating the impact of hyperosmolarity associated with inflammation and chronic dry eye disease. Note the changes in topography, keratometry values as well as axis of astigmatism. Patient was interested in a premium intraocular lens (IOL). If a toric IOL had been calculated based off the first readings, cylinder overcorrection and incorrect axis placement would have resulted as well as a 1.0-diopter postcataract refractive error. (Case and image provided courtesy of Blake Williamson, July 28, 2017.) A healthy ocular surface is under homeostatic control of the lacrimal functional unit. A healthy system is designed to withstand environmental, traumatic, and microbial insults by mounting a stress response and an amplification response while also modulating a damage and repair/remodeling phase before finally returning to homeostatic control.1 With CDED, homeostasis-maintaining mechanisms and signals are compromised, resulting in a chronically activated stress response (nuclear factor-κB, mitogen-activated protein kinase, interleukin-1 [IL-1], tumor necrosis factor [TNF]) and chronically elevated damage phase (IL-17, g-IFN-γ, TNF-α), which leads to damage to the goblet cells, epithelium, and sub-basal corneal nerve plexus. IL-1 and TNF induce nerve growth factor (NGF) from the human limbal basal epithelium. When NGF is chronically upregulated in response to CDED, corneal nerve dysmorphology and epithelial cell apoptosis occur via high-affinity and low-affinity NGF receptors, respectively. Recent confocal microscopy evidence indicates that epithelial cell density, keratocyte activation, and corneal nerve dysmorphology improve after 6 months of treatment with topical cyclosporine A.5 This has implications for an appropriate postoperative wound and nerve healing response. Visual performance is subjective; however, optical analysis can provide objective insight as discussed earlier. Data gathered from the Progression of Ocular Findings (PROOF) study6 (designed to study the natural history of progression of CDED) indicate a significant component of subjective visual fluctuations (57.6%) in level 2 CDED patients compared to controls (10.5%) despite 20/20 vision (PROOF). CDED is increasingly considered a vision disease. The literature also indicates a significant impact of CDED on keratometric repeatability,4 which can induce IOL calculation errors and thereby affect postoperative refractive outcomes (
2.1 Introduction
2.2 Tear Film Disorders
Fig. 2.1). The Tear Film & Ocular Surface (TFOS)/Dry Eye Workshop II (DEWS II) report1 provides a complete scientific literature review and consensus-based organization of the current state of knowledge on dry eye. Trattler et al2 found in a multicenter prospective study that approximately 80% of patients presenting for cataract surgery had evidence of CDED. Additionally, 50% had central corneal staining, which would be associated with backward light scatter as a contributor to subjective blur, discussed later.2,3 CDED impacts preoperative keratometry,4 IOL calculations, and postsurgical visual performance as well as patient satisfaction and quality of life.1
2.2.1 Optical Aberrations: Higher Order Aberrations and Light Scatter as Mechanisms of Visual Disturbance in CDED
2.2.2 Keratometric Aberrations
2.2.3 Visual Performance and Patient Satisfaction
Fig. 2.2). Additionally, patient satisfaction, visual performance, productivity and quality of life are impacted by CDED.1 Arguably, all of these factors are potentially implicated in suboptimal results following cataract surgery.
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