- Email: [email protected]
Visual Loss as a Result of Primary Optic Nerve Neuropathy After Intranasal Corticosteroid Injection
VISUAL LOSS AS A RESULT OF PRIMARY OPTIC NERVE NEUROPATHY AFTER INTRANASAL CORTICOSTEROID INJECTION DONALD
E. EVANS, M.D., JOSEPH A. ZAHORCHAK, M.D., AND JOHN S. KENNERDELL, M.D. Pittsburgh, Pennsylvania
Transient or permanent visual loss after injections to the head and neck has seldom been reported. In virtually all cases, ophthalmoscopic examination implicated inadvertent intravascular injection with subsequent retinal embolism. We describe a patient with marked visual loss seen immediately after corticosteroid injection to the concha nasalis inferioris. At no time did the ophthalmoscopic examination suggest retinal embolic disease. To our knowledge, this is the first case report of visual loss secondary to an optic nerve insult after injection to the head or neck. CASE REPORT A 25-year old woman came here for an emergency consultation after acute loss of visual acuity in the right eye. The patient had a long history of sinus disease and was being treated for intermittent nasal obstruction secondary to multiple allergies. As part of her therapy, she periodically received corticosteroid injections to the conchae nasalis inferioris to decrease congestion of the nasal mucosa. Her physician inserted cotton pledgets containing 1% phenylephrine HCI to minimize bleeding and 2% tetracaine to anesthetize the mucosa. Then, using direct visualization, he injected 0.5 ml of a solution containing 20 mg of methylprednisolone acetate into each concha nasalis inferioris at two or three different sites with a 25-gauge sharp needle. He then reinserted the cotton pledgets until hemostasis was adequate. She received such injections on Jan. 25 and Feb. 4, 1980. There were no complications and her symptoms were relieved. On Feb. 19, 1980, she received a third set of injections. She noted a "cloud" over her right eye
From the Departments of Ophthalmology (Drs. Evans and Kennerdell), Neurology (Dr. Kennerdell), and Otolaryngology (Dr. Zahorchak), University of Pittsburgh School of Medicine and Eye and Ear Hospital, Pittsburgh, Pennsylvania. Reprint requests to John S. Kennerdell, M.D., Eye and Ear Hospital, 230 Lothrop St., Pittsburgh, PA 15213.
immediately after the injection and experienced severe visual loss within a few minutes. She was hospitalized and underwent a neuroophthalmologic examination within one hour of the injection. At the time of the initial examination, her visual acuity was R. E.: hand motion, temporally, and L. E.: 6/6 (20/20). There was a 3+ right afferent pupillary defect. There was no blanching or erythema of the ipsilateral face, no blepharoptosis, and no extraocular motor disturbance. The anterior segments were normal. Applanation tonometry showed an intraocular pressure of 16 mm Hg in each eye. The results of an ophthalmoscopic examination were normal; vascular pattern and vessel caliber were normal, without evidence of intravascular emboli, intraretinal hemorrhages, edema, exudates, or nerve fiber layer infarction (Fig. 1). The optic disks were normal. Visual fields disclosed an extensive loss nasally in the right eye, with less constriction temporally, and loss of central fixation (Fig. 2). The left visual field was normal. Orbital B-scan and computed axial tomography displayed a grossly normal optic nerve (Fig. 3). Treatment, already begun by her otolaryngologist A. Z.), consisted of 20 mg of prednisone, orally four times a day; 12 mg of nylidrin HC!, orally twice a day; 2.75 mg of histamine, intravenously; and intermittent 5% carbon dioxide inhalation. The visual acuity in her right eye improved over a
a.
Fig. 1 (Evans, Zahorchak, and Kennerdell). Right eye within two hours of acute visual loss.
AMERICAN JOURNAL OF OPHTHALMOLOGY 90:641--644, 1980
641
642
AMERICAN JOURNAL OF OPHTHALMOLOGY
NOVEMBER, 1980
Fig. 2 (Evans, Zahorchak, and Kennerdell). Visual field within two hours of acute visual loss.
period of several days, stabilizing at 6/15- (20/50-) with a small myopic overcorrection. The afferent pupillary defect became much less prominent but persisted. Her nasal peripheral visual field did not expand but she did regain central fixation (Fig. 4). DISCUSSION
Transient or permanent visual loss after injections to the head and neck is an unusual phenomenon that has been reported with increasing frequency in the past several years. A recent review implicated paraffin, alcohol, local anesthetics, angiographic contrast dye, pro-
Fig. 4 (Evans, Zahorchak, and Kennerdell). Visual field one month after acute visual loss.
Fig. 3 (Evans, Zahorchak, and Kennerdell). Computed axial tomographic scan showing right optic nerve (American Science and Engineering 510 matrix).
caine penicillin, corticosteroid suspensions, and multiple drug combinations. 1 Injections of corticosteroid suspensions have been used in the peritonsillar fossae to decrease postoperative pain,2,3 in the conchae nasalis to treat allergic rhinitis;' and in the scalp to treat alopecia areata, psoriatic plaques, discoid lupus erythematosus, and lichen planopiliaris. Subtenon and, less commonly, retrobulbar injections of corticosteroids have been used for a variety of ophthalmic conditions. Intranasal.P" peritonsillar," scalp.P'" and retrobulbar'! injections have all been implicated as occasional causes of visual loss. The incidence of visual loss following injection into the concha nasalis inferioris has been estimated at 0.006%.13 Several authors'<" have reviewed this phenomenon. They believe that visual loss occurs as the result of high-pressure injection of material with embolic potential into highly vascular tissue. Retrograde arterial flow allows emboli to lodge in vascular beds far distant from the site of injection. Therefore, injections to such
VOL. 90, NO. 5
VISUAL LOSS AFTER INTRANASAL INJECTION
diverse areas as the scalp, peritonsillar fossa, and conchae nasalis can cause visual loss from retinal embolic disease. Results of ophthalmoscopic examinations, which are almost always consistent with embolic disease, support this theory. Retinal vasospasm in the absence of emboli" and optic nerve damage may also playa role. Optic nerve damage may be caused by emboli in the optic nerve vasculature, by optic nerve vasospasm, or by direct neurotoxic effects. Occasional reports of afferent pupillary defects suggest optic nerve involvement in addition to retinal disease, although this could be anticipated with florid retinal embolic disease alone. This clinical pattern can be reproduced in animals by injecting a corticosteroid suspension and epinephrine together. Injection of either agent alone will not reproduce the retinal changes. 15 This suggests that the corticosteroid suspension, with its poor aqueous solubility and, therefore, embolic potential in an aqueous medium, coupled with the vasoconstricting properties of epinephrine greatly enhances the risk of embolic occlusive disease. Many previously described patients have had symptoms suggesting embolic disease, including transient central nervous system defects (altered state of consciousness, focal neurologic defects), and blanching or erythema of the ipsilateral face. The most frequently reported sites of facial injection are all highly vascular and therefore present a small but definite risk of inadvertent intra-arterial injection, regardless of technique. Injecting a significant volume of material into a small space requires sufficient force to propel retrograde intra-arterial emboli to distant vascular beds. Pretreating the nasal mucosa with vasoconstrictors (1% phenylephrine, 5% cocaine) theoretically lowers the risk of intravascular injection.
643
Subclinical emboli may be more common than recognized, for this diagnosis is usually considered only when the function of vital structures is affected, that is, the retina or central nervous system, and it is confirmed by direct visualization only in the retina. The patient described here is, to the best of our knowledge, unique in that her retina and optic disk were normal throughout the entire course of observation. The afferent pupillary defect, less prominent as visual acuity improved, strongly suggested that the optic nerve was the site of damage. We believe this is the first case report of visual loss after facial injection caused by optic nerve injury. Whether the insult causes emboli in the optic nerve vasculature or whether they are secondary to vasospasm is speculative, although the former seems more likely. Why the optic nerve circulation is so profoundly affected without any effect on the retinal circulation is also unclear. SUMMARY
A 25-year-old woman experienced acute visual loss after injection of methylprednisolone suspension into the concha nasalis inferioris. Results of ophthalmoscopic examinations were normal throughout the observation period, a finding not reported previously in cases of visual loss after head or neck injections. An afferent pupillary defect, which diminished as visual acuity improved, implicated optic nerve damage, as did the visual field defect which also improved slightly. This is, to our knowledge, the first case report ofacute visual loss caused by optic nerve neuropathy after injection to the head or neck. REFERENCES 1. McGrew, R. N., Wilson, R. S., and Havener, W. H.: Sudden blindness secondary to injections of common drugs in the head and neck. Clinical experiences. Trans. Am. Acad. Ophthalmol. Otolaryngol. 86:147, 1978.
644
AMERICAN JOURNAL OF OPHTHALMOLOGY
2. Smith, J. P.: Alleviation of post tonsillectomy pain and infection. A preliminary report. Laryngoscope 73:461, 1963. 3. Smith, J. P., King, J. T., Gershon, N. I., and Fisher, W. R.: Alleviation of pain and prevention of infection after tonsillectomy. A controlled clinical study of a novel injectable combination. Trans. Am. Acad. Ophthalmol. Otolaryngol. 68:65, 1964. 4. Wall, J. W., and Shure, N.: Intranasal cortisone. Preliminary study. Arch. Otolaryngol. 56:172, 1952. 5. Osentreich, N., Sturm, H. M., Weidman, A. L., and Pelzig, A.: Local injection of steroids and hair regrowth in alopecias. Arch. Dermatol. 82:894, 1960. 6. Hager, G., and Heise, G.: A severe complication with permanent practical blindness of one eye following an intranasal injection. H.N.O. 10:325, 1962. 7. Rowe, R J., Duster, J. W., and KinkeIla, A. M.: Visual changes and triamcinolone. J.A.M.A. 201:333, 1967. 8. McCleve, D. E., Goldstein, J. C., and Silver, S.: Corticosteroid injections of the nasal turbinates. Past experience and precautions. Trans. Am. Acad. Ophthalmol. Otolaryngol. 86:851, 1978. 9. Ellis, P. P.: Visual loss following tonsillectomy.
NOVEMBER, 1980
Possible association with injections in tonsillar fossae. Arch. Otolaryngol. 87:436, 1968. 10. vonBahr, G.: Multiple embolisms in the fundus of an eye after an injection in the scalp. Acta Ophthalmol. 41:85, 1963. 11. Baran, M. L. R: Le risque d'amaurose au cours du traitement local des alopecies par corticotherapie injectable. Bull. Soc. Fr. Dermatol. Syph. 71:25, 1964. 12. Francois, J., and Van Longenhave, E.: Embolism of the central retinal artery of the retina following a retrobulbar injection of methylprednisolone acetate. Bull. Soc. Beige Ophtalmol. 155:517, 1970. 13. Mabry, R L.: Intranasal corticosteroid injection. Indications, technique, and complications. Otolaryngol. Head Neck Surg. 87:207, 1979. 14. Selmanowitz, V. J., and Osentreich, N.: Cutaneous corticosteroid injection and amaurosis. Analysis for cause and prevention. Arch. Dermatol. 110:729, 1974. 15. McGrew, R N., Wilson, R S., and Havener, W. H.: Sudden blindness secondary to injections of common drugs in the head and neck. 11 animal studies. Trans. Am. Acad. Ophthalmol. Otolaryngol. 86:152, 1978.
E. EVANS, M.D., JOSEPH A. ZAHORCHAK, M.D., AND JOHN S. KENNERDELL, M.D. Pittsburgh, Pennsylvania
Transient or permanent visual loss after injections to the head and neck has seldom been reported. In virtually all cases, ophthalmoscopic examination implicated inadvertent intravascular injection with subsequent retinal embolism. We describe a patient with marked visual loss seen immediately after corticosteroid injection to the concha nasalis inferioris. At no time did the ophthalmoscopic examination suggest retinal embolic disease. To our knowledge, this is the first case report of visual loss secondary to an optic nerve insult after injection to the head or neck. CASE REPORT A 25-year old woman came here for an emergency consultation after acute loss of visual acuity in the right eye. The patient had a long history of sinus disease and was being treated for intermittent nasal obstruction secondary to multiple allergies. As part of her therapy, she periodically received corticosteroid injections to the conchae nasalis inferioris to decrease congestion of the nasal mucosa. Her physician inserted cotton pledgets containing 1% phenylephrine HCI to minimize bleeding and 2% tetracaine to anesthetize the mucosa. Then, using direct visualization, he injected 0.5 ml of a solution containing 20 mg of methylprednisolone acetate into each concha nasalis inferioris at two or three different sites with a 25-gauge sharp needle. He then reinserted the cotton pledgets until hemostasis was adequate. She received such injections on Jan. 25 and Feb. 4, 1980. There were no complications and her symptoms were relieved. On Feb. 19, 1980, she received a third set of injections. She noted a "cloud" over her right eye
From the Departments of Ophthalmology (Drs. Evans and Kennerdell), Neurology (Dr. Kennerdell), and Otolaryngology (Dr. Zahorchak), University of Pittsburgh School of Medicine and Eye and Ear Hospital, Pittsburgh, Pennsylvania. Reprint requests to John S. Kennerdell, M.D., Eye and Ear Hospital, 230 Lothrop St., Pittsburgh, PA 15213.
immediately after the injection and experienced severe visual loss within a few minutes. She was hospitalized and underwent a neuroophthalmologic examination within one hour of the injection. At the time of the initial examination, her visual acuity was R. E.: hand motion, temporally, and L. E.: 6/6 (20/20). There was a 3+ right afferent pupillary defect. There was no blanching or erythema of the ipsilateral face, no blepharoptosis, and no extraocular motor disturbance. The anterior segments were normal. Applanation tonometry showed an intraocular pressure of 16 mm Hg in each eye. The results of an ophthalmoscopic examination were normal; vascular pattern and vessel caliber were normal, without evidence of intravascular emboli, intraretinal hemorrhages, edema, exudates, or nerve fiber layer infarction (Fig. 1). The optic disks were normal. Visual fields disclosed an extensive loss nasally in the right eye, with less constriction temporally, and loss of central fixation (Fig. 2). The left visual field was normal. Orbital B-scan and computed axial tomography displayed a grossly normal optic nerve (Fig. 3). Treatment, already begun by her otolaryngologist A. Z.), consisted of 20 mg of prednisone, orally four times a day; 12 mg of nylidrin HC!, orally twice a day; 2.75 mg of histamine, intravenously; and intermittent 5% carbon dioxide inhalation. The visual acuity in her right eye improved over a
a.
Fig. 1 (Evans, Zahorchak, and Kennerdell). Right eye within two hours of acute visual loss.
AMERICAN JOURNAL OF OPHTHALMOLOGY 90:641--644, 1980
641
642
AMERICAN JOURNAL OF OPHTHALMOLOGY
NOVEMBER, 1980
Fig. 2 (Evans, Zahorchak, and Kennerdell). Visual field within two hours of acute visual loss.
period of several days, stabilizing at 6/15- (20/50-) with a small myopic overcorrection. The afferent pupillary defect became much less prominent but persisted. Her nasal peripheral visual field did not expand but she did regain central fixation (Fig. 4). DISCUSSION
Transient or permanent visual loss after injections to the head and neck is an unusual phenomenon that has been reported with increasing frequency in the past several years. A recent review implicated paraffin, alcohol, local anesthetics, angiographic contrast dye, pro-
Fig. 4 (Evans, Zahorchak, and Kennerdell). Visual field one month after acute visual loss.
Fig. 3 (Evans, Zahorchak, and Kennerdell). Computed axial tomographic scan showing right optic nerve (American Science and Engineering 510 matrix).
caine penicillin, corticosteroid suspensions, and multiple drug combinations. 1 Injections of corticosteroid suspensions have been used in the peritonsillar fossae to decrease postoperative pain,2,3 in the conchae nasalis to treat allergic rhinitis;' and in the scalp to treat alopecia areata, psoriatic plaques, discoid lupus erythematosus, and lichen planopiliaris. Subtenon and, less commonly, retrobulbar injections of corticosteroids have been used for a variety of ophthalmic conditions. Intranasal.P" peritonsillar," scalp.P'" and retrobulbar'! injections have all been implicated as occasional causes of visual loss. The incidence of visual loss following injection into the concha nasalis inferioris has been estimated at 0.006%.13 Several authors'<" have reviewed this phenomenon. They believe that visual loss occurs as the result of high-pressure injection of material with embolic potential into highly vascular tissue. Retrograde arterial flow allows emboli to lodge in vascular beds far distant from the site of injection. Therefore, injections to such
VOL. 90, NO. 5
VISUAL LOSS AFTER INTRANASAL INJECTION
diverse areas as the scalp, peritonsillar fossa, and conchae nasalis can cause visual loss from retinal embolic disease. Results of ophthalmoscopic examinations, which are almost always consistent with embolic disease, support this theory. Retinal vasospasm in the absence of emboli" and optic nerve damage may also playa role. Optic nerve damage may be caused by emboli in the optic nerve vasculature, by optic nerve vasospasm, or by direct neurotoxic effects. Occasional reports of afferent pupillary defects suggest optic nerve involvement in addition to retinal disease, although this could be anticipated with florid retinal embolic disease alone. This clinical pattern can be reproduced in animals by injecting a corticosteroid suspension and epinephrine together. Injection of either agent alone will not reproduce the retinal changes. 15 This suggests that the corticosteroid suspension, with its poor aqueous solubility and, therefore, embolic potential in an aqueous medium, coupled with the vasoconstricting properties of epinephrine greatly enhances the risk of embolic occlusive disease. Many previously described patients have had symptoms suggesting embolic disease, including transient central nervous system defects (altered state of consciousness, focal neurologic defects), and blanching or erythema of the ipsilateral face. The most frequently reported sites of facial injection are all highly vascular and therefore present a small but definite risk of inadvertent intra-arterial injection, regardless of technique. Injecting a significant volume of material into a small space requires sufficient force to propel retrograde intra-arterial emboli to distant vascular beds. Pretreating the nasal mucosa with vasoconstrictors (1% phenylephrine, 5% cocaine) theoretically lowers the risk of intravascular injection.
643
Subclinical emboli may be more common than recognized, for this diagnosis is usually considered only when the function of vital structures is affected, that is, the retina or central nervous system, and it is confirmed by direct visualization only in the retina. The patient described here is, to the best of our knowledge, unique in that her retina and optic disk were normal throughout the entire course of observation. The afferent pupillary defect, less prominent as visual acuity improved, strongly suggested that the optic nerve was the site of damage. We believe this is the first case report of visual loss after facial injection caused by optic nerve injury. Whether the insult causes emboli in the optic nerve vasculature or whether they are secondary to vasospasm is speculative, although the former seems more likely. Why the optic nerve circulation is so profoundly affected without any effect on the retinal circulation is also unclear. SUMMARY
A 25-year-old woman experienced acute visual loss after injection of methylprednisolone suspension into the concha nasalis inferioris. Results of ophthalmoscopic examinations were normal throughout the observation period, a finding not reported previously in cases of visual loss after head or neck injections. An afferent pupillary defect, which diminished as visual acuity improved, implicated optic nerve damage, as did the visual field defect which also improved slightly. This is, to our knowledge, the first case report ofacute visual loss caused by optic nerve neuropathy after injection to the head or neck. REFERENCES 1. McGrew, R. N., Wilson, R. S., and Havener, W. H.: Sudden blindness secondary to injections of common drugs in the head and neck. Clinical experiences. Trans. Am. Acad. Ophthalmol. Otolaryngol. 86:147, 1978.
644
AMERICAN JOURNAL OF OPHTHALMOLOGY
2. Smith, J. P.: Alleviation of post tonsillectomy pain and infection. A preliminary report. Laryngoscope 73:461, 1963. 3. Smith, J. P., King, J. T., Gershon, N. I., and Fisher, W. R.: Alleviation of pain and prevention of infection after tonsillectomy. A controlled clinical study of a novel injectable combination. Trans. Am. Acad. Ophthalmol. Otolaryngol. 68:65, 1964. 4. Wall, J. W., and Shure, N.: Intranasal cortisone. Preliminary study. Arch. Otolaryngol. 56:172, 1952. 5. Osentreich, N., Sturm, H. M., Weidman, A. L., and Pelzig, A.: Local injection of steroids and hair regrowth in alopecias. Arch. Dermatol. 82:894, 1960. 6. Hager, G., and Heise, G.: A severe complication with permanent practical blindness of one eye following an intranasal injection. H.N.O. 10:325, 1962. 7. Rowe, R J., Duster, J. W., and KinkeIla, A. M.: Visual changes and triamcinolone. J.A.M.A. 201:333, 1967. 8. McCleve, D. E., Goldstein, J. C., and Silver, S.: Corticosteroid injections of the nasal turbinates. Past experience and precautions. Trans. Am. Acad. Ophthalmol. Otolaryngol. 86:851, 1978. 9. Ellis, P. P.: Visual loss following tonsillectomy.
NOVEMBER, 1980
Possible association with injections in tonsillar fossae. Arch. Otolaryngol. 87:436, 1968. 10. vonBahr, G.: Multiple embolisms in the fundus of an eye after an injection in the scalp. Acta Ophthalmol. 41:85, 1963. 11. Baran, M. L. R: Le risque d'amaurose au cours du traitement local des alopecies par corticotherapie injectable. Bull. Soc. Fr. Dermatol. Syph. 71:25, 1964. 12. Francois, J., and Van Longenhave, E.: Embolism of the central retinal artery of the retina following a retrobulbar injection of methylprednisolone acetate. Bull. Soc. Beige Ophtalmol. 155:517, 1970. 13. Mabry, R L.: Intranasal corticosteroid injection. Indications, technique, and complications. Otolaryngol. Head Neck Surg. 87:207, 1979. 14. Selmanowitz, V. J., and Osentreich, N.: Cutaneous corticosteroid injection and amaurosis. Analysis for cause and prevention. Arch. Dermatol. 110:729, 1974. 15. McGrew, R N., Wilson, R S., and Havener, W. H.: Sudden blindness secondary to injections of common drugs in the head and neck. 11 animal studies. Trans. Am. Acad. Ophthalmol. Otolaryngol. 86:152, 1978.