| OCR Text |
Show Original Contribution Anterior Ischemic Optic Neuropathy After Dental Extraction Elizabeth Kravitz, BSA, Rod Foroozan, MD Background: While often idiopathic, anterior ischemic optic neuropathy occasionally may occur from an identifiable cause. Methods: Observational case report. Results: A 19-year-old woman with unremarkable medical and ophthalmic histories developed visual loss from nonarteritic anterior ischemic optic neuropathy in her right eye after otherwise uneventful dental extraction of the inferior third molars. Conclusions: Anterior ischemic optic neuropathy may rarely occur after dental extraction. Potential pathophysiologic mechanisms of this rare occurrence are discussed. Journal of Neuro-Ophthalmology 2019;39:14-17 doi: 10.1097/WNO.0000000000000711 © 2018 by North American Neuro-Ophthalmology Society A lthough the clinical profile of nonarteritic anterior ischemic optic neuropathy (NAION) is well known, the precise pathophysiology of this optic nerve disorder remains uncertain. It is believed to be multifactorial leading to infarction of the anterior portion of the optic nerve and is not related to vasculitis. We describe a 19-year-old woman with visual loss of her right eye after the dental extraction of her inferior third molars. The clinical findings suggested that the cause of visual loss was NAION. CASE REPORT A 19-year-old woman noted painless visual loss of her right eye immediately after extraction of the inferior third molars (Teeth 17 and 32). The dental extraction was performed with sedation but without general anesthesia. Drugs administered during the extraction included 5 mg midazolam, 8 mg dexamethasone, 25 mg ketamine, and 60 mg From the Baylor College of Medicine (EK, RF), Houston, Texas. The authors report no conflicts of interest. Address correspondence to Rod Foroozan, MD, Baylor College of Medicine, 1977 Butler Boulevard, Houston, TX 77030; E-mail: foroozan@bcm.edu 14 propofol. In total, 3 carpules (1.8 ml/carpule) of lidocaine 2% with epinephrine and 2 carpules of septocaine 2% with epinephrine were injected as inferior alveolar nerve blocks. Her blood pressure was 131/72 mm Hg before the procedure and 134/71 mm Hg at the completion of the procedure. At no time, did she experience symptoms suggestive of systemic hypotension. She had no history of previous medical or ophthalmic problems. The patient was seen 2 days after the procedure by an ophthalmologist who noted optic disc edema in the right eye. She underwent an MRI of the brain and orbits, which was unremarkable. Her blood pressure was 138/79 Hg at this time. Optic neuritis was diagnosed, and she was hospitalized and treated with intravenous methylprednisolone (1 gm/day) for 3 days and then oral prednisone 60 mg per day. She noted no changes in her vision. A lumbar puncture showed an opening pressure of 19 cm of H2O, and cerebrospinal fluid analysis including venereal disease research laboratory, myelin basic protein, and immunoglobulin G (IgG) was normal. The patient had neuro-ophthalmic evaluation 8 days after the dental extractions. At that time, she was taking prednisone 60 mg per day and also had completed a course of clindamycin and doxycycline. Visual acuity was 20/20 in each eye, with a right relative afferent pupillary defect (RAPD) and intact color vision bilaterally. Automated perimetry showed decreased sensitivity throughout the field in the right eye and a few points of reduced sensitivity in the left eye (Fig. 1). There was no evidence of intraocular inflammation, and funduscopy showed diffuse optic disc edema in the right eye and a crowded disc in the left eye (Fig. 2). There was no evidence of maculopathy on optical coherence tomography, and the retinal nerve fiber layer measures were increased in the right eye (206 mm) and normal in the left eye (103 mm). Intravenous fluorescein angiography of the right eye showed normal choroidal filling but delayed filling of the right optic disc with mild leakage in late images (Fig. 3). Prednisone was discontinued, and she was prescribed aspirin 325 mg/day. Kravitz and Foroozan: J Neuro-Ophthalmol 2019; 39: 14-17 Copyright © North American Neuro-Ophthalmology Society. Unauthorized reproduction of this article is prohibited. Original Contribution FIG. 1. Automated perimetry shows superior and inferior arcuate defects in the right eye, while the left visual field is intact. The patient was referred to a rheumatologist and hematologist, neither of whom found evidence of a systemic disease. Her antinuclear antibody was 1:160 (normal ,1:40). The following hematological studies were normal or negative: erythrocyte sedimentation rate, angiotensin-converting enzyme, lupus anticoagulant, protein S, antithrombin 3, factor V Leiden, lupus anticoagulant, anticardiolipin antibodies, homocysteine, rapid plasma regain, fluorescent treponemal antibody absorption (FTA-Abs), fibrinogen, prothrombin G20210A mutation (Factor II mutation), SCL-70 antibodies (Anti-topoisomerase), anti-Ro/SSA antibodies, anti-La/SSB antibodies, antineutrophil cytoplasmic antibody, and serum IgG level. Right optic disc pallor developed over the next 2 months, and during the ensuing 6 months, her visual function remained unchanged. Aspirin was discontinued. DISCUSSION Our patient's clinical course was consistent with NAION. There are few reports of patients developing optic neuropathy following dental procedures. Parc et al (1) described a 16-year-old boy with reduced visual acuity in his right eye with visual field deficits after extractions FIG. 2. The right optic disc is swollen with peripapillary and retinal hemorrhage. There is some engorgement of the retinal venous system. The left fundus is normal. Kravitz and Foroozan: J Neuro-Ophthalmol 2019; 39: 14-17 15 Copyright © North American Neuro-Ophthalmology Society. Unauthorized reproduction of this article is prohibited. Original Contribution FIG. 3. Fluorescein angiography of the right eye demonstrates prompt choroidal filling (A), delayed filling of the optic disc vasculature (B), and leakage of dye from the disc in late images (C). of all 4 third molars. There was sectoral optic disc pallor in the right eye 2 months after the procedure. The authors speculated that the visual deficit was from an optic neuropathy, although retinopathy could not be excluded because the patient was not examined acutely. The extractions were performed under general anesthesia (perfentanyl, propofol, midazolam, and rapacuronium), with no local injection. It was hypothesized that microembolism of dental material traveled through the alveolar arterial network toward the short posterior ciliary circulation during the extraction. Horowitz et al (2) reported 2 additional cases. The first was a 26-year-old woman with a root canal of tooth 27 (left upper jaw) who experienced reduced visual acuity of the left eye to 20/200, with a left RAPD and impaired color vision. After treatment with intravenous and oral steroids, her vision in the left eye returned to 20/20 over 10 days. The authors hypothesized that this was the result of the lidocaine nerve block of the superior alveolar nerve, although the details of the composition of the local anesthesia were not reported. The second case involved a 45-year-old healthy man with left optic neuropathy that did not resolve following a root canal of tooth 25 (left upper jaw). Six hours after the procedure, acuity was 20/100 in the left eye, with a left RAPD, reduced color vision, inferior altitudinal field defect, and a swollen optic disc. One year later, the patient developed NAION in the other eye with final visual acuity of 20/80, right eye, and 20/100, left eye. It was hypothesized that the vasospastic effect of epinephrine (concentrations of lidocaine-epinephrine injection were not specified) may have triggered the optic neuropathy; however, this would not explain the same condition occurring in the other eye. We also found a report of a 51-year-old woman who developed a branch retinal artery occlusion shortly after FIG. 4. Illustration of local anesthesia for a right inferior alveolar nerve block. 16 Kravitz and Foroozan: J Neuro-Ophthalmol 2019; 39: 14-17 Copyright © North American Neuro-Ophthalmology Society. Unauthorized reproduction of this article is prohibited. Original Contribution extraction of her third molar teeth (specific site not specified). Emboli were noted within the involved artery. During the extraction, lidocaine with epinephrine was used (specific concentrations not specified). The authors discussed several potential mechanisms for ocular ischemia related to dental procedures including: the vasospastic effects of intravascular dental anesthesia, embolic occlusion from intravascular dental anesthesia, and emboli from the carotid system caused by cervical hyperextension or a Valsalva maneuver (3). Our patient's dental extractions were different in that they involved the inferior third molars, with anesthesia of the inferior alveolar nerve and without injections involving the other alveolar nerves (Fig. 4). Although the precise cause of the ischemic optic neuropathy was not clear, we believe that the anesthetic could cause ischemia to the optic nerve either by simple diffusion through the pterygomaxillary fossa to the orbit or from inadvertent vascular injection with subsequent involvement of vessels to the eye. The use of a vasoconstrictor, such as epinephrine, in addition to lidocaine is typical in dental extractions to decrease the peak plasma concentration of the local anesthetic, reduce the minimum amount of nerve block necessary, and decrease blood lost during the procedure. Studies have found that local injection of lidocaine 2% with epinephrine (1:100,000) leads to a rapid rise in plasma epinephrine levels, and subsequent cardiovascular changes such as increases in heart rate and mean arterial blood pressure (4). However, these effects are unlikely in our patient given the absence of any documented marked change in blood pressure. In addition, lidocaine has independent vasoactive effects, with evidence suggesting vasodilator properties at clinically relevant concentrations and vasoconstrictor properties at lower concentrations (5). Therefore, we cannot exclude the possibility of vasoactivity from the lidocaine itself, apart from the added epinephrine. Kravitz and Foroozan: J Neuro-Ophthalmol 2019; 39: 14-17 We cannot definitively conclude that the oral nerve block alone was the causative agent. In the case of the 16 year old with ischemic optic neuropathy, reported by Parc et al (1), there was no local injection, indicating that the extractions themselves may have played a contributing role. We were unable to find any reports of patients undergoing less extensive dental procedures, such as a dental filling, that included only an oral nerve block and resulted in an ischemic ocular complication. Therefore, a final possibility is that in extensive dental procedures, such as extractions, dental debris enters the alveolar arterial network and travels to the short posterior ciliary circulation impairing blood flow to the optic nerve. STATEMENT OF AUTHORSHIP Category 1: a. Conception and design: R. Foroozan and E. Kravitz; b. Acquisition of data: E. Kravitz and R. Foroozan; c. Analysis and interpretation of data: E. Kravitz and R. Foroozan. Category 2: a. Drafting the manuscript: E. Kravitz and R. Foroozan; b. Revising it for intellectual content: E. Kravitz and R. Foroozan. Category 3: a. Final approval of the completed manuscript: E. Kravitz and R. Foroozan. REFERENCES 1. Parc C, Allali J, Patel S, Su V, Brèzin AP. Ischèmie du nerf optique compliquant une extraction dentaire. J Fr Ophthalmol. 2004;27:921-923. 2. Horowitz J, Almog Y, Wolf A, Buckman G, Geyer O. Ophthalmic complications of dental anesthesia: three new cases. J Neuroophthalmol. 2005;25:95-100. } urel T, Onaran Z, O gurel R, Ornek }yu }ktortop Gǒkcinar N, 3. Og N, Bu } Ornek K. Branch retinal artery occlusion following dental extraction. Case Rep Ophthalmol Med. 2014;2014:202834. 4. Sisk AL. Vasoconstrictors in local anesthesia for dentistry. Anesth Prog. 1992;6:187-193. 5. Newton DJ, Amyes AK, Khan F, McLeod GA, Bannister J, Belch JJF. Vasoactive properties of lignocaine administered by iontophoresis in human skin. Clin Sci. 2003;105:87-92. 17 Copyright © North American Neuro-Ophthalmology Society. Unauthorized reproduction of this article is prohibited. |
