September 30, 2016 Conference
AM session INTRODUCTION TO DMEK – THE THINNER FUTURE
This talk will review the progression of eye bank posterior lamellar corneal graft preparation, beginning with the introduction of eye bank based microkeratome assisted DSAEK graft preparation, through the most recent graft preparation techniques for DMEK. Trends in posterior lamellar corneal transplant tissue utilization will be reviewed, with emphasis toward future demands on eye banks, potential limitations to the allogeneic transplant tissue supply (domestically and internationally), as well as potential measures and developments that may expand the available tissue pool. Emphasis will be given to the importance of rigorous validation of corneal graft preparation techniques, including in depth description of the development, validation and subsequent incorporation of the S-Stamp for DMEK.
DMEK is a partial thickness corneal transplant involving selective removal and replacement of Descemet’s Membrane and endothelium. It is indicated when vision is decreased due to endothelial cell dysfunction. The most common conditions treated with DMEK are Fuchs’ Dystrophy and Pseudophakic Bullous Keratopathy. Successful unrolling and centration of the graft tissue is achieved using pneumatic and/or fluid manipulation under a shallow anterior chamber. The presence of anterior chamber lenses and tube shunts will significantly hinder proper graft positioning. Eyes with a history of vitrectomy, trabeculectomy, iris defects, or aphakia will raise additional obstacles for graft handling and successful outcomes. Patients that are ideally suited to undergo DMEK are those that have good potential postoperative visual acuity, are already pseudophakic, and have minimal other ocular comorbidities. Patient selection for DMEK will depend on the patient’s presenting history and the individual surgeon’s comfort with the procedure.
Anterior segment optical coherence tomography (AS-OCT) is becoming an integral part in post-operative and intra-operative management in patients undergoing corneal transplantations, in particular in patients with endothelial keratoplasties. Endothelial keratoplasties are evolving techniques to selectively replace diseased endothelial layers of the cornea. In recent years the popularity of endothelial keratoplasties, especially Descemet Membrane Endothelial Keratoplasty (DMEK), Descemet Stripping Automated Endothelial Keratoplasty (DSAEK) have increased significantly, as these procedures result in the reduction of intra- and postoperative complications and achieve faster visual recovery. Nevertheless, these surgical procedures are delicate, not standardized and corneal edema may result in poor visualization of the graft in the anterior chamber. Novel AS-OCT imaging devices may substantially aid in the standardization of these procedures intra-operatively and in post-operative management, and may further reduce both intra- and postoperative complications and potentially improve outcomes. This review summarizes use of intra-operative and post-operative AS-OCT imaging for corneal transplantation.
My presentation will review the surgical techniques of my standardized technique of DMEK for good results with a low complication rate. Results of the technique will be reviewed and emphasis will be placed on key steps to prevent and manage intraoperative complications. Surgical video will be shown to illustrate key talking points.
DMEK is a relatively new procedure with a novel postoperative course; management of common complications as well as standard post op management will be reviewed. Emphasis will be placed on patient positioning, posted medications, and dealing with graft detachments. Strategies to achieve an optimal outcome and maintain clinical eppiciency will be emphasized.
Jason S. Rothman
Optimizing the ocular surface prior to cataract surgery can improve the postoperative outcome and patient satisfaction. Diagnosing the dry eye patient can be challenging as signs and symptoms often times do not correlate. Some patients may be asymptomatic or only experience vision fluctuation. Utilizing a questionnaire, such as the Ocular Surface Disease Index (OSDI), along with a careful examination of blink dynamics, the lids, tear film and use of vital dyes are important. Point of care testing may improve diagnostic accuracy and some allow for a metric to determine therapeutic efficacy. Tear film interferometry and meibography are useful for both diagnosis and patient education. Strategic use of tear supplements, lacrimal occlusion, topical and systemic anti-inflammatory therapies, as well as improved treatments for meibomian gland dysfunction can improve both preoperative measurements and postoperative outcome. Awareness of its high prevalence, advances in diagnostics and better classifications of dry eye and blepharitis continue to allow for more effective and directed management of our dry eye patients.
The introduction of presbyopia-correcting and toric IOLs provided a learning curve during which we had the opportunity to gain experience with unexpected visual results and patient disappointment. One way to resolve those problems has been better patient selection and pre-operative analysis, including especially the Angle Alpha. However, there is still a cadre of patients who despite excellent preparation have vision challenges and seek improvement. The cause of many of these problems is refractive in nature begging the question whether we can resolve them with exchanging the multifocal implant, modifying it with a piggyback, or adjusting the vision with laser correction. When a toric IOL is involved the optics are more complicated and considerations must be given to limbal relaxing incisions, laser correction and lens rotation.
PM session Neuro-Ophthalmology
Professional practice gaps: The content and format of this educational activity has been specifically designed to fill the practice gaps in the audientce's current and potential scope of professional activities by:
1. Increasing the competenece of the audience regarding the recognition and diagnosis of key cortical visual syndromes.
2. Improving the performance of the audience in participating in collaborative management of various neurological disorders that affect vision.
3. Improving outcome sin the area of patient care, specifally for complex patients with visual impairment resulting from specific congnitive neurological disorders.
Neural forms of blindness can occur from lesions anywhere along the retino-calcarine visual pathway or even beyond into the visual association cortices. Specific case examples will be discussed to exemplify the clinical features that enable a clinician to distinguish blindness caused by lesions at different sites along the visual pathway. The clinical cases will be supported by neuroimaging of various disorders. With the clinical tools in hand to distinguish different forms of visual loss, the presentation will then include a discussion about the most appropriate management.
Ischemic stroke commonly affects afferent and efferent visual pathways of the cerebral hemispheres and brainstem. Particularly in the setting of acute stroke, if visual symptoms are dominant, ophthalmologists may be the first to evaluate, triage, and manage such patients. The management of ischemic stroke is separated into primary treatment and secondary prevention strategies.
Anton Syndrome Anton Syndrome refers to cortical blindness without awareness of the deficit. Patients have complete visual loss from bilateral occipital lesions, yet they do not directly complain of the deficit. They often confabulate answers when asked about their visual experience. The profound denial is usually transient, and recovery of vision depends upon the underlying etiology. Riddoch Syndrome The Riddoch Syndrome describes preserved ability to detect motion in an otherwise blind visual field.20 There is ‘statokinetic dissociation,’ in which the patient can perceive an object only if it is moving. Form and color cannot be appreciated. The cortical area specialized for processing motion is called V5 and is situated dorsal to the primary visual cortex in the occipital lobe. This area is spared in patients with Riddoch Syndrome, although it remains controversial how visual inputs may arrive there. Alexia Without Agraphia Alexia Without Agraphia refers to the loss of the ability to read, although the ability to write remains spared. Remarkably, patients will not be able to read a sentence that they have written themselves. This defect is limited to the perception of written language; production and comprehension of spoken language is fully preserved. Prosopagnosia Human beings are expert at extracting information from a face in order to accurately and effortlessly identify it. This expertise is the result of a specialized group of neurons in the ventral processing stream, known as the Fusiform Face Area. Prosopagnosia is a specific form of visual agnosia in which face perception is impaired, while other aspects of vision are intact. It results from lesions affecting both (or sometimes just the right) occipital-temporal lobes (specifically the FFA). Patients may be unable to recognize even their own face when looking at a photograph or in the mirror. Typically, patients identify individuals using other clues, such as gait, physical mannerisms, clothing, or voice. Balint Syndrome The Balint Syndrome is a profound disruption of visual attentional mechanisms resulting from bilateral parietal lesions. Although elementary aspects of vision, including acuity and object recognition, remain preserved, patients are profoundly affected by an inability to disengage and shift their attention to various parts of a visual scene. The features of Balint syndrome include optic ataxia (impaired reaching under visual guidance); ocular apraxia (poorly coordinated saccades when shifting gaze between targets); and simultanagnosia (inability to perceive its global elements of a scene, or “missing the forest for the trees.”) Charles Bonnet Syndrome Charles Bonnet Syndrome refers to “release” hallucinations that occur in the context of visual loss. The hallucinations are typically nonthreatening, and patients often describe seeing small people, animals, or flowers. Functional imaging studies have shown spontaneous increases in activity in visual association areas in the ventral extrastriate cortex that temporally correlate with the reported hallucinations.39 These findings lend credence to the idea that in the absence of receiving external sensory information (deafferentation), the visual system can generate internally formed hallucinations instead.
Cortical lesions characteristically result in homonymous visual field loss occurring in both eyes. The anatomy of the central visual pathways and the pattern of visual field loss due to various cortical lesions will be reviewed.
Neoplasms of the central nervous system can compromise the afferent and the efferent function of the visual system. Their management is dependent on the type of tumor and its location in the nervous system. The management is often multimodal and includes surgical resection, chemotherapy, radiation therapy, supportive medical management, and symptom palliation. Adverse effects of chemotherapy such as toxic optic neuropathy, stroke, venous sinus thrombosis with resulting papilledema, and sequelae of radiation such as radiation retinopathy and optic neuropathy, vascular disease, cavernous angiomas, and secondary tumors may also affect the visual system. Attention to their prophylaxis and monitoring is an important part of the ophthalmologist’s role throughout the course of a cerebral tumor management.
Patients with neurodegenerative disorders which affect cortical centers that are involved in processing vision may present with vague visual complaints. Though these patients describe major difficulty with vision, they may have relatively intact visual acuities and a seemingly unremarkable examination. As these patients are often initially seen by eye care professionals, it is important for ophthalmologists to be familiar with different manifestations of these visual integrative disorders.
Cortical visual impairment (CVI) is characterized by dysfunction of visual processing due to an injury of the visual pathways. Common etiologies include perinatal events which result in hypoxic injury to the visual system that result in periventricular leukomalacia to insults of the visual cortex and beyond. Increasingly, CVI is emerging as one of the most common causes of significant visual impairment in children and yet continues to remain undiagnosed as an entity. The goals of this talk will be to present the salient clinical characteristics of CVI, discuss recent endeavors towards understanding the neuroanatomic basis of CVI, and review recent revisions made by the MA Commission for the Blind to recognize CVI in children as a cause of legal blindness.
Visual field defects often result from stroke and brain injury. The resulting visual impairment can be debilitating for patients, impeding daily activities like reading and mobility. Historically, it was believed that there was little opportunity for restoration of function following visual system damage. However, development of various visual rehabilitative strategies suggests that visual field defects are partially repairable and a certain degree of function can be improved. While this provides hope for patients, many of these strategies have been met with skepticism within the clinical and scientific community. Further development of these strategies through carefully designed studies could validate their efficacy and reveal underlying mechanisms.