Journal of Neuro-Ophthalmology, June 1990, Volume 10, Issue 2

Visual loss following intranasal anesthetic injection.

Four patients had visual loss after nasal surgery. There was one instance each of branch retinal artery occlusion, central retinal artery occlusion, anterior ischemic optic neuropathy, and posterior ischemic optic neuropathy. The postulated mechanism is vasospasm. The submucosal injection, under pressure, of an anesthetic with epinephrine is deemed to be causative.

Journal of Clinical Neuro- ophthalmology 10( 2): 140- 144, 1990. Visual Loss Following Intranasal Anesthetic Injection Peter J. Savino, M. D., Ronald M. Burde, M. D., and Richard P. Mills, M. D. @ 1990 Raven Press, Ltd., New York Four patients had visual loss after nasal surgery. There was one instance each of branch retinal artery occlusion, central retinal artery occlusion, anterior ischemic optic neuropathy, and posterior ischemic optic neuropathy. The postulated mechanism is vasospasm. The submu­cosal injection, under pressure, of an anesthetic with epinephrine is deemed to be causative. Key Words: Cranial nerve palsy- Ischemic optic neu­ropathy- Nasal surgery- Retinal artery occlusion- Sub­mucosal injections. From the Neuro- Ophthalmology Service, Wills Eye Hospital, Thomas Jefferson University, Philadelphia, Pennsylvania ( P. J. S.); the Department of Ophthalmology, Albert Einstein Medical Center, Bronx, New York ( R. M. B.); and the Depart­ment of Ophthalmology, University of Washington, Seattle, Washington ( R. P. M.), U. S. A. Address correspondence and reprint requests to Dr. Peter J. Savino, Neuro- Ophthalmology Service, Wills Eye Hospital, Ninth and W;, J"'. ut C; trd · t'. Philadelphia, PA 19107, U. S. A. 140 Visual loss following uncomplicated otolaryn­gologic surgical procedures is an uncommon oc­currence. Most of the visual defects reported oc­curred following the injection of corticosteroids or other solutions containing particulate matter in the nasal cavity. We describe four patients with retinal artery occlusion and optic nerve ischemia follow­ing nasal surgery. None of these patients had in­jections of particulate- containing solutions, and all appear to have suffered permanent visual defects secondary to vasospasm. CASE REPORTS Case 1 A 37- year- old woman awoke from general anes­thesia following rhinoplasy with decreased vision in her left eye. The operative note described infil­tration of the nasal septum pyramidal complex with " Marcaine and adrenalin [ Adrenalin] injec­tion" ( no percentages given). Cocaine pledgets were placed in both nostrils prior to injection. No corticosteroids were injected at any time during the procedure. Neuro- ophthalmologic evaluation 8 days follow­ing surgery showed vision of 20/ 20 in the right eye and 20/ 20 - 1 in the left. External examination, slit­lamp examination, applanation tonometry, and oc­ular motility were normal. The patient missed one Ishihara color plate on the left but none on the right. She had a left relative afferent pupillary de­fect and a left superior altitudinal visual field de­fect ( Fig. 1). Fundus examination showed the area of retinal whitening ( Fig. 2). Follow- up examination 1 year after surgery re­vealed vision of 20/ 20 in both eyes, persistence of the left relative afferent pupillary defect and visual field defect, and thinning of the retinal nerve fiber layer in the area of the previous edema. VISUAL LOSS FOLLOWING INTRANASAL ANESTHETIC INJECTION FIG. 1. Case 1. Superior nasal defect in left eye. LE 20/ 20 .(\, Ilt1' _ 141 Case 2 A 26- year- old man underwent bilateral naso­polypectomy, ethmoidectomy, and bilateral antral irrigations under general anesthesia. On awaken­ing, he noted poor vision in his right eye. The operative note described " some injection of 1% Xy­locaine with epinephrine ... into the inferior tur­binates and the anterior septal membranes." No steroids were injected. Evaluation 6 hours postoperatively showed vi­sion was " hand motions" in the right eye and 201 20 in the left. There were no orbital signs, and ocular motility was normal. There was a right rel­ative afferent pupillary defect. The right retina was described as edematous with a " cherry red" spot at the macula. The superior temporal artery was described as having a " changed reflex suggestive of fluid emboli." Orbital tomography showed no bony fractures. Case 3 In October 1980, a 28- year- old man underwent repair of a deviated septum and removal of the roots of the upper teeth in his maxilla following a motorcycle accident 6 months previously. On awakening from surgery, he complained of de­creased visual acuity in his right eye and double vision. During the surgery under general anesthesia, he received multiple injections of Lidocaine with epi­nephrine into his palate and nasal mucosa. No cor­ticosteroids were injected. Neuro- ophthalmologic evaluation 8 days later revealed " finger counting" vision at 1 m in the right eye and 20/ 20 in the left, with a right relative afferent pupillary defect. There was limitation of ocular movement in the fields of the right medial, inferior, and superior rectus muscles. There was lesser dysfunction of the right superior oblique muscle. Corneal sensation was decreased on the right. A superior altitudinal defect was charted in the right eye and a nasal defect noted in the left, but patient reliability and fixation were poor ( Fig. 3). Subsequent visual fields were consistently nor­mal on the left. The right optic nerve was pale and elevated. FIG. 2. Case 1. Inferior temporal retinal ar­tery occlusion with edema of the retina. 1Clin Neuro- ophthalmol, Vol. 10, No. 2, 1990 142 FIG. 3. Case 3. Superior altitudinal defect that involves fixation on the right. The left nasal defect is an artifact. P. ]. SAVINO ET AL. Mo.. 20/ 2( 1 Examination 2 years later showed vision of 20/ 20 in the right eye and 20/ 15 in the left, a right relative afferent pupillary defect, persistent altitudinal vi­sual field loss on the right, and optic atrophy on the right with a decreased nerve fiber bundle layer inferiorly. His ocular motility was normal. Case 4 A 44- year- old woman with a history of chronic sinusitis underwent bilateral nasal antral windows and a right myringotomy on March 30, 1983. Im­mediately postoperatively, the patient noted de­creased vision in the right eye. Surgery was per­formed under general endotracheal anesthesia. The nose was packed with cocaine pledgets, and a local block of 1.5% Lidocaine with 1: 200,000 epi­nephrine was injected into the inferior meatus in the floor of the nose for further vascular constric­tion. Corticosteroids were not injected during the procedure. Neuro- ophthalmologic consultation revealed vi­sion of " finger counting" at 1 m in the right eye and 20/ 20 in the left. She had right upper lid ptosis and was unable to elevate the right eye. The pa­tient could not identify any of the Ishihara pseu-doisochromatic color plates with the right eye, and there was a right relative afferent pupillary defect. Goldmann kinetic perimetry showed an inferior is­land of vision remaining in the right eye and a full visual field in the left ( Fig. 4). Dilated fundus ex­amination was normal bilaterally. Fluorescein angiography was normal. A high­resolution computed tomography ( CT) scan and polytomography failed to reveal any orbital path­ologic findings or fractures. The patient was treated with high- dose oral corticosteroids, but de­spite this, vision did not return. The ocular motil­ity disturbances and the ptosis completely re­solved. One year following the episode the vision remained unchanged, and optic atrophy had de­veloped on the right. DISCUSSION Visual loss occurring during nasal surgery is an uncommon event. Several mechanisms are impli­cated as the cause of visual loss ( Table 1). Griffin and associates ( 1) described two patients with visual loss attributable to fractures in the optic canal. Their first patient had a left vidian nerve section and postoperatively experienced a partial FIG. 4. Case 4. Superior altitudinal defect that involves fixation on the right. . ' I' VISUAL LOSS FOLLOWING INTRANASAL ANESTHETIC INJECTION 143 TABLE 1. Clinical summary Patient! Vision Computed age, yrl Other tomography sex Surgery Injection Initial Final manifestation Diagnosis scan 1/ 37/ F Rhinoplasty Marcainel 20/ 20 - 1 20/ 15 None Branch retinal epinephrine artery occlusion 21261M Nasopolypectomyl 1% Xylocainel Hand motions light None Central retinal Polytomography intranasal epinephrine perception artery occl usion results within ethmoidectomy normal limits 31281M Rhinoplasty Lidocainel Finger 20/ 20 IUrd and IVth Anterior ischemic Orbit negative epinephrine counting nerve paresis optic neuropathy 41441F Bilateral lidocainel Finger Finger Superior Posterior ischemic Orbit negative nasal antral epinephrine counting counting division of optic neuropathy windows IUrd nerve left third and sixth nerve palsy as well as an optic neuropathy. Polytomography revealed a fracture of the left optic canal close to the anterior clinoid process. Despite immediate decompression through a frontal craniotomy, the patient re­mained blind in that eye. Their second patient ex­perienced unilateral visual loss following surgery for correction of a congenital left- side choanal atresia. An optic canal fracture was demonstrated on polytomography anterior to the clinoid process. A fracture was also noted through the vidian bone extending toward the superior orbital fissure. Sur­gery was not advised since the authors believed the bony fragments were not mobile and the visual loss was, by the time they examined the patient, 2 weeks old. The patient was given high- dose oral prednisone and recovered from 20/ 200 to 20/ 30 vi­sion. A second and more frequent cause of visual loss following otolaryngologic procedures is embolism to the retinal and choroidal circulation. Several re­ports have appeared and attribute the loss of vi­sion to microembolization of corticosteroids or other particulate matter to the retina and choroid resulting in ischemia in the territory of the central retinal artery ( 2- 4). Mabry ( 5) estimates that this complication occurs with a frequency of 0.006% following otherwise uncomplicated otolaryn­gologic injections. The third and fourth possible mechanisms for visual loss following submucosal injections are re­lated to the properties of the sympathomimetic amines, in this case epinephrine, as well as to the regional blood supply. The vascular connections between the nasal cavity and the optic nerve and retina are via the anterior and posterior ethmoidal arteries. These arteries anastomose with the oph­thalmic artery and the posterior ciliary arteries. Therefore, injection performed under pressure in the area of the inferior turbinates can reflux through the ethmoidal circulation to the ophthal­mic arteries. Antegrade flow can then occur to the retina and optic nerve via the central retinal artery and posterior ciliary circulation and to the ocular motor nerves and extraocular muscles via the vasa nervorum and orbital branches ( 6). Can the injection of a solution containing epinephrine cause sufficient vascular spasm to produce permanent neurologic deficits from either retinal or optic nerve infarction? McGrew and co­workers ( 7), utilizing a canine model, have dem­onstrated that the intracarotid injection of Xy­locaine alone produces no visible change in the fundus, but the injection of 1: 100,000 epinephrine alone or in combination with Xylocaine produces transient vasospasm without a permanent deficit. Although from their experimental work they con­clude that to produce a permanent neurologic def­icit it is necessary to have particulate matter in the injection, the recent article by Magargal and asso­ciates ( 8) belies this conclusion. In addition, the canine blood supply is very different from that of the primate, with a large percentage of the orbital circulation deriving from the external carotid ar­tery. Magargal and associates describe a man in whom a branch retinal artery occlusion secondary to the chronic abuse of 0.5% oxymetazoline hydro­chloride long- acting nasal spray developed. The fourth possible mechanism is epinephrine­induced aggregation with retrograde embolization under pressure. In the patient described by Magar­gal and associates, platelet emboli were reported in the retinal vessels, and they demonstrated en­hanced platelet aggregation of their patient's plate­lets when exposed to epinephrine in vitro. Such a supersensitivity of coagulation may playa role in some instances of complications associated with submucosal injections. Although none of our pa­tients demonstrated evidence of emboli, it is well known since the first reports of C. M. Fisher ( 9) that platelet emboli are, for the most part, evanes­cent and may disappear before observation. The patients described in cases 1 and 2 are un­usual in that they experienced retinal artery occlu- 1Clin Neuro- ophthalmol, Vol. 10, No. 2, 1990 144 P. J. SAVINO ET AL. sions from injection with nonparticulate material with no evidence of embolization. The only other report in the literature of a central retinal artery occlusion following a submucosal injection of an­esthetic epinephrine compound is by Kambic and co- workers ( 10). It is interesting that it was be­lieved that one of the arteries of the patient de­scribed in case 2 was filled with a fluid embolism ( absence of blood column without vascular col­lapse). This patient otherwise had a classic oph­thalmoscopic appearance with cloudy retina and a " cherry red" spot. Our third patient suffered sudden visual loss as­sociated with a pallid swollen optic disc ophthal­moscopically compatible with an anterior ischemic optic neuropathy. The fourth patient experienced visual loss with no ophthalmoscopically visible le­sions. The third and fourth patients also experi­enced ophthalmoparesis, case 3 a third and fourth nerve palsy and case 4 a superior division third nerve palsy. We postulate that the ophthalmopare­sis was on a neurogenic basis rather than on the basis of muscular damage, as not only do the ex­traocular muscles have a luxuriant blood supply, but one of these patients had involvement of the first division of the fifth cranial nerve as well. Both patients were left with significant afferent visual system residua, but the induced ophthalmoparesis and sensory deficit recovered completely. Our fourth patient represents a case of primary optic neuropathy following the intranasal, submu­cosal injection of an epinephrine- containing solu­tion. The only previous report of such an occur­rence is by Evans and co- workers ( 11). The retina was examined on the day of surgery when the pa­tient sustained visual loss, and no evidence of acute retinal infarction was seen; the optic nerve appeared normal, although as expected, later be­came atrophic. Appropriate radiologic studies, in­cluding high- resolution CT scan with bone win­dows, failed to demonstrate evidence of a fracture. It therefore seems likely that retinal and optic nerve ischemia with permanent visual deficits may occur following intranasal injection of anesthetic with epinephrine without corticosteroids, and transient ophthalmoparesis may accompany these occurrences. REFERENCES 1. Griffin JF, Momose J, Wray SH. Optic canal fractures after rhinologic surgery. Am J OphthalmoI1979; 87: 526. 2. Whiteman DW, Rosen DA, Pinkerton RMH. Retinal and choroidal microvascular embolism after intranasal cortico­steroid injection. Am I Ophthalmol 1980; 89: 8510. 3. Byers B. Blindness secondary to steroid injections into the nasal turbinates. 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