Anterior Ischemic Optic Neuropathy After Dental Extraction: Comment

I enjoyed reading the recent case report of by Kravitz and Foroozan, entitled 'Anterior ischemic optic neuropathy after dental extraction' (1). The report documented a case of a 19-year-old woman who developed a nonarteritic anterior ischemic optic neuropathy (NAION) after an otherwise uneventful dental extraction using local anesthetic and intravenous sedation (5-mg midazolam, 25-mg ketamine, and 60-mg propofol). Although the authors concluded that they could not be certain as to the etiology of the NAION; they hypothesized that the effects of lidocaine used as a local anesthetic and the possibility of local dental debris impaired blood flow to the optic nerve. The authors discount the possibility of local anesthetic agents acting on the cardiovascular system because of an absence of change in preprocedure and postprocedure blood pressure. The authors did not comment on the potential effect of intravenous anesthetics.

Letters to the Editor Anterior Ischemic Optic Neuropathy After Dental Extraction: Comment I enjoyed reading the recent case report of by Kravitz and Foroozan, entitled "Anterior ischemic optic neuropathy after dental extraction" (1). The report documented a case of a 19-year-old woman who developed a nonarteritic anterior ischemic optic neuropathy (NAION) after an otherwise uneventful dental extraction using local anesthetic and intravenous sedation (5-mg midazolam, 25-mg ketamine, and 60-mg propofol). Although the authors concluded that they could not be certain as to the etiology of the NAION; they hypothesized that the effects of lidocaine used as a local anesthetic and the possibility of local dental debris impaired blood flow to the optic nerve. The authors discount the possibility of local anesthetic agents acting on the cardiovascular system because of an absence of change in preprocedure and postprocedure blood pressure. The authors did not comment on the potential effect of intravenous anesthetics. NAION subsequent to the use of intravenous anesthetics is well documented (2). In many cases, as well as the case from Parc et al, cited by the authors, there was no documented use of local anesthetic in that case, suggesting this is unlikely to play a causative role in NAION. These cases have, however, all occurred in the setting of intravenous anesthetic agents. The role of anesthetic agents on the cardiovascular system is complex. Propofol has been shown to reduce cardiac output through a decrease in cardiac contractility (3). Benzodiazepines, such as midazolam, seem to have a similar but smaller effect on cardiovascular function (3). Systemic cardiovascular effects were discounted by the authors because there was no change in blood pressure between the start and end of the procedure. Nevertheless, given vascular autoregulation, if there were any intraoperative fluctuations in blood pressure, how could anesthetic agents have induced NAION? I suggest that NAION is likely to have developed because of autoregulation and not despite it. Autoregulation is the ability to maintain blood flow across a wide range of blood pressures (4). In the setting of reduced cardiac contractility, the Hagen-Poiseuille equation demonstrates that blood flow can be maintained by an increase in the crosssectional area of blood vessels, namely vasodilation, which is the primary mechanism by which the central nervous sys- 288 tem autoregulates blood supply (4). It is this vasodilation that could potentiate NAION through an arteriolar compartment syndrome or venous occlusion-both of these mechanisms have been implicated in the disease process (5,6). This is particularly relevant given the appearance of a small, crowded optic disc in the contralateral eye of this patient in Figure 2 (1). This hypothesis is supported by the fact that a number of other physiological states that involve vasodilation have been associated with NAION, including prolonged hypotension, nocturnal hypotension, and use of phosphodiesterase-5 inhibitors (6). That the role of intravenous anesthetic agents should be considered in the pathophysiology of this case of NAION is important. The authors minimize the possibility of cardiovascular changes because of the absence of any documented change in blood pressure. However, in the setting of multiple intravenous anesthetic agents, a stable blood pressure may not reflect a physiological cardiovascular state but, rather, the maintenance of homeostasis through central and peripheral autoregulation. Consideration of both local and intravenous anesthetic routes has important implications in how we counsel our patients about the potential risks of different types of anesthesia; such considerations may also help us greatly in the quest to understand the complex pathophysiology of NAION. Joshua P. Harvey, MA(Oxon), BM, BCh Ophthalmology Department, King's College Hospital, London, United Kingdom The author reports no conflicts of interest. REFERENCES 1. Kravitz E, Foroozan R. Anterior ischemic optic neuropathy after dental extraction. J Neuroophthalmol. 2019;39:14-17. 2. Berg KT, Harrison AR, Lee MS. Perioperative visual loss in ocular and nonocular surgery. Clin Ophthalmol. 2010;4:531- 546. 3. Haney M. Cardiovascular Aspects of Anaesthetic Agents. 2012. European Society of Anaesthesiology. Avaliable at: http:// www.esahq.org. Accessed February 26, 2019. 4. Vavilala MS, Lee LA, Lam AM. Cerebral blood flow and vascular physiology. Anesthesiol Clin North Am. 2002;20:247-264. 5. Berry S, Lin WV, Sadaka A, Lee AG. Nonarteritic anterior ischemic optic neuropathy: cause, effect, and management. Eye Brain. 2017;9:23-28. 6. Levin LA, Danesh-Meyer HV. Hypothesis. Arch Ophthalmol. 2008;126:1582. Letters to the Editor: J Neuro-Ophthalmol 2019; 39: 288-289 Copyright © North American Neuro-Ophthalmology Society. Unauthorized reproduction of this article is prohibited.