Corneal Protection during General Anesthesia for Nonocular Surgery

Grixti, Andre; Sadri, Maziar; Watts, Mark

doi:10.1016/j.jtos.2012.10.003

Cited by 51 publications

(45 citation statements)

References 44 publications

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“…Research into the underlying pathophysiology of more common causes of POVL, such as CA, has led to more effective prevention strategies and fewer malpractice claims (1, 21, 22) (Table 1). …”

Section: Resultsmentioning

confidence: 99%

“…Longer procedures, as well as prone or lateral positioning during surgery, are shown to increase the risk of CA (21). Many institutions have developed prevention strategies for CA (18).…”

Section: Resultsmentioning

confidence: 99%

“…No intervention is completely effective in protection of CA during surgery, but eyelid taping is the single best used protective method. Proper placement of eyelid protection has been shown to decrease the risk of CA (21). CA claims from 1990 or later received a median compensation of $12,000.…”

Section: Resultsmentioning

confidence: 99%

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Revisiting Postoperative Vision Loss following Non-Ocular Surgery: A Short Review of Etiology and Legal Considerations

et al. 2017

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Postoperative vision loss (POVL) following non-ocular surgery is a serious complication where the causes are not fully understood. Studies have identified several causes of POVL as well as risk factors and prevention strategies. POVL research is made difficult by the fact that cases are often subject to malpractice claims, resulting in a lack of public access to case reports. This literature review was conducted in order to identify legal issues as a major barrier to studying POVL and address how this affects current knowledge. Informed consent provides an opportunity to overcome legal challenges by reducing malpractice litigation through educating the patient on this outcome. Providing pertinent information regarding POVL during the informed consent process has potential to reduce malpractice claims and increase available clinical information.

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Section: Resultsmentioning

confidence: 99%

“…Longer procedures, as well as prone or lateral positioning during surgery, are shown to increase the risk of CA (21). Many institutions have developed prevention strategies for CA (18).…”

Section: Resultsmentioning

confidence: 99%

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Revisiting Postoperative Vision Loss following Non-Ocular Surgery: A Short Review of Etiology and Legal Considerations

et al. 2017

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“…Loss of innervation causes a loss of sensation [47] and the development of spontaneous corneal abrasions [55]. Damage to corneal nerves can be caused by diabetes [29], pharmacotherapeutics such as paclitaxel [14], vision correction surgery [37], or accidental injury [20] that causes damage to the ocular surface. Studies examining injury-induced changes in corneal nerves find conflicting and paradoxical results when trying to correlate altered nerve structure to ocular pain.…”

Section: Introductionmentioning

confidence: 99%

Acute Hyperalgesia and Delayed Dry Eye After Corneal Abrasion Injury

Hegarty

Hermes

Morgan

et al. 2018

Preprint

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Corneal nerves mediate pain from the ocular surface, lacrimation, and blinking, all of which protect corneal surface homeostasis and help preserve vision. Corneal nerve density correlates with neuropathic pain states and is used as an assessment of small fiber neuropathies. Because pain, lacrimation and blinking are rarely assessed at the same time, it is not known if their regulatory mechanisms have similar temporal dynamics after acute corneal injury. We examined changes in corneal nerve density, evoked and spontaneous pain, and ocular homeostasis in Sprague-Dawley male rats after a superficial epithelial injury with heptanol that acutely abolished nerve endings within the central cornea. Despite a profound loss of epithelial nerve endings, pain was transiently enhanced after abrasion injury, while basal tear production was normal. We found no relationship between epithelial nerve density and pain or homeostatic responses. Axotomy following corneal abrasion increased expression of both ATF3 (a nerve injury marker) and CGRP (a nociceptive peptide) in trigeminal ganglia 24 hours after injury. These molecular changes were absent on the contralateral side, despite reductions in corneal epithelial nerve density in the uninjured eye. ATF3 and CGRP levels in trigeminal ganglion were normal at one week post-injury when pain responses were normal. In contrast, CGRP was upregulated in peripheral corneal endings one week after injury, when dry eye symptoms emerged. Our results demonstrate dynamic trafficking of CGRP within trigeminal sensory nerves, with elevations in the ganglion correlated with pain behaviors and elevations in peripheral endings correlated with dry eye symptoms. peer-reviewed)

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“…Ocular pain can result from corneal exposure to environmental irritants, corneal injuries stemming from accidents, vision correction surgery such as LASIK or general surgery (Altinors, Bozbeyoglu, Karabay, & Akova, 2007;Ang, Dartt, & Tsubota, 2001;Grixti, Sadri, & Watts, 2013). Ocular pain is also seen in chronic conditions such as dry eye disease and normal aging (Chao et al, 2016;Lemp, 2008).…”

mentioning

confidence: 99%

Select noxious stimuli induce changes on corneal nerve morphology

Hegarty

Hermes

Yang

et al. 2017

J of Comparative Neurology

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The surface of the cornea contains the highest density of nociceptive nerves of any tissue in the body. These nerves are responsive to a variety of modalities of noxious stimuli and can signal pain even when activated by low threshold stimulation. Injury of corneal nerves can lead to altered nerve morphology, including neuropathic changes which can be associated with chronic pain. Emerging technologies that allow imaging of corneal nerves in vivo are spawning questions regarding the relationship between corneal nerve density, morphology, and function. We tested whether noxious stimulation of the corneal surface can alter nerve morphology and neurochemistry. We used concentrations of menthol, capsaicin, and hypertonic saline that evoked comparable levels of nocifensive eye wipe behaviors when applied to the ocular surface of an awake rat. Animals were sacrificed and corneal nerves were examined using immunocytochemistry and three-dimensional volumetric analyses. We found that menthol and capsaicin both caused a significant reduction in corneal nerve density as detected with β-tubulin immunoreactivity 2 hr after stimulation. Hypertonic saline did not reduce nerve density, but did cause qualitative changes in nerves including enlarged varicosities that were also seen following capsaicin and menthol stimulation. All three types of noxious stimuli caused a depletion of CGRP from corneal nerves, indicating that all modalities of noxious stimuli evoked peptide release. Our findings suggest that studies aimed at understanding the relationship between corneal nerve morphology and chronic disease may also need to consider the effects of acute stimulation on corneal nerve morphology.

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Corneal Protection during General Anesthesia for Nonocular Surgery

Cited by 51 publications

References 44 publications

Revisiting Postoperative Vision Loss following Non-Ocular Surgery: A Short Review of Etiology and Legal Considerations

Revisiting Postoperative Vision Loss following Non-Ocular Surgery: A Short Review of Etiology and Legal Considerations

Acute Hyperalgesia and Delayed Dry Eye After Corneal Abrasion Injury

Select noxious stimuli induce changes on corneal nerve morphology

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