ESCRS - Dry eye after LASIK (1) ;
ESCRS - Dry eye after LASIK (1) ;

Dry eye after LASIK

Tips for managing common post-op dry eye complaints

Dry eye after LASIK
Leigh Spielberg
Leigh Spielberg
Published: Wednesday, February 1, 2017
[caption id="attachment_7270" align="alignnone" width="180"]Penny Asbell MD Penny Asbell MD[/caption]   The most common complaint after LASIK surgery is dry eye disease, Penny A Asbell MD, FACS, MBA told delegates at the XXXIV Congress of the ESCRS in Copenhagen, Denmark. Almost everyone has symptoms at one week post-op, and between 20% and 40% of patients still have complaints at six months. But a great deal of it is likely missed, pointing to a need for new diagnostic techniques, said Dr Asbell, Director of Cornea and Refractive Services, Department of Ophthalmology, Icahn School of Medicine at Mount Sinai, New York, USA. “We need new tools to evaluate the ocular surface. After all, early post-phaco cystoid macular oedema was only noted after optical coherence tomography (OCT) became available. The situation is likely to be similar regarding detection and differentiation of ocular surface disease, which is often difficult to identify when typical signs are lacking,” she said. “Documenting symptoms can be accomplished by getting a good patient history and including patient-completed Ocular Surface Disease Index (OSDI),” she added. Once a problem has been identified therapy can better be targeted and personalised if a specific cause can be determined. Most of the risk factors for post-LASIK dry eye disease are well known: pre-existing dry eye disease, older age, female sex, lid lag and/or a history of contact lens intolerance. It helps to identify other, less obvious, risk factors such as diabetes and systemic medications. “Dry eye disease is twice as common in diabetic patients, and among diabetics, it is more common among females,” she said. Understanding the pathogenesis of post-LASIK ocular surface disease helps you and your patient understand potential treatments and the prognosis: surgical disruption of afferent nerve fibres leads to hypoesthesia and subsequent disruption of the lacrimal functional unit. This disruption causes both decreased basal and reflex tear secretion and decreased blink reflex, resulting in changes in tear film composition and quality as well as goblet cell damage. The end result is hyperosmolarity and inflammation, which is the ultimate cause of ocular surface damage. She referred to research showing that corneal sensation, necessary for proper lubrication of the epithelial surface, can take months for recovery and in some people nerve abnormalities persist long-term. NEUROPATHIC PAIN But what if ocular surface disease is not even the actual cause of the complaints? “Post-LASIK pain is most often due to ocular surface disease. But once ocular disease has been ruled out, we have to consider neuropathic pain,” she said. Neuropathic pain is due to a lesion of the corneal neurons themselves. Dr Asbell contrasted this to nociceptive pain, which is pain caused by damage to non-neural tissue, such as a scratched cornea. Symptoms of neuropathic pain are often chronic, continuing from two to five years after LASIK. They are out of proportion to the signs on ocular exam. The pathogenesis is initiated by environmental stress, leading to inflammation and an immune cell influx. This causes altered gene expression and the release of nerve growth factor. The result is sensitisation of first peripheral and then central nerves. Risk factors for neuropathic corneal pain, especially chronic pain, include female sex, younger age, genetic factors and anxiety or depression. Diagnosis can be suggested by altered neuronal density and morphology on confocal microscopy, which shows corneal nerve dysplasia. But before advanced examinations are performed, more basic tests can be carried out, such as the proparacaine challenge test. The failure of topical anaesthetic to decrease symptoms is very suggestive for neuropathic pain, she explained. Management is difficult. Treatment of the concomitant ocular surface and lid disease is of course essential. Anti-inflammatory agents might help break the cycle, and scleral lenses can decrease stimuli. Furthermore, Dr Asbell recommends peripheral nerve regenerative therapy, which may consist of autologous serum eye drops, nerve growth factor, and platelet-rich plasma. If this all proves insufficient, systemic pharmacotherapy for pain might be necessary. Penny A Asbell: penny.asbell@mssm.edu
Tags: cornea, dry eye
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