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Show © 1993 Raven Press, Ltd., New York Visual Recovery from Radiation-Induced Optic Neuropathy The Role of Hyperbaric Oxygen Therapy F.-X. Borruat, M.D., N. J. Schatz, M.D., J. S. Glaser, M.D., L. G. Feun, M.D., and L. Matos, M.D. Optic neuropathy resulting in permanent visual loss is an infrequent delayed complication of radiation therapy. Hyperbaric oxygen therapy (HBO) has been used to treat such a complication, but its efficacy is controversial. We report a patient who presented with radiationinduced optic neuropathy 17 months after irradiation for a left maxillary antrum melanoma. HBO fully reversed visual loss in the more recently involved eye, and slightly improved vision in the earlier affected eye. Key Words: Hyperbaric oxygen-Radiation necrosisOptic neuropathy. From the Bascom Palmer Eye Institute, NeuroOphthalmology Unit (F.-X. B., N.j.S., jSG.), Department of Medicine (L.G.F.), Department of Surgery, Division of Hyperbaric Medicine (L.M.), University of Miami, Miami, Florida, U.s.A.; University Eye Clinic (F.-X. B), H6pital Ophtalmique jules Gonin, 1004 Lausanne, Switzerland. Dr. F.-X. Borruat was supported by Swiss funds from H6pital Ophtalmique jules Gonin, Fondation Florian Veney, Societe Academique Vaudoise, Fondation SICPA and, Fondation du 450eme anniversaire de I'Universite de Lausanne. Address correspondence and reprint requests to Dr. joel S. Glaser, 900 NW 17th Street, Miami, FL, 33136, USA. 98 Delayed necrosis of the intracranial optic nerves or chiasm is a recognized complication of ionizing radiation, characterized by abrupt and permanent visual loss affecting one or both eyes (1-3). Intervals from irradiation to symptom onset vary from less than 6 months to 3 years. Treatment of radiation optic neuropathy (RON) with hyperbaric oxygen (HBO) has been shown to stop or reverse the visual loss (4), but its efficacy has been challenged (5,6). We here report the benefits of HBO in a patient who presented with visual loss, occurring 17 months after radiotherapy. CASE REPORT A 45-year-old woman presented in May 1990, with recent onset of left nasal obstruction and bleeding. A melanoma of the left maxillary sinus invading the nasal cavity was found and extensive sinus surgery was performed. Despite postoperative 8-mm inferior displacement of the left orbital contents, visual acuity remained at 20/20 and visual fields were full in both eyes. Between July 5 and August 7 of 1990,5,000 rads were delivered to the left maxillary sinus (20 sessions of 250 rads over 33 days), and 4,250 rads to the left neck (17 sessions of 250 rads over 27 days), without overlap of radiation fields. On October 15, 1990, chemotherapy was commenced with intravenous dacarbazine and oral piritrexim, an experimental folate antagonist (7). Dacarbazine had to be discontinued on August 1991, due to intolerable fatiguability following infusion and the patient remained on only oral piritrexim for the next 7 months. She remained in partial remission and visual function was unchanged in both eyes. Early February 1992, 21 months after surgery and 17 months after completion of irradiation, the HYPERBARIC OXYGEN THERAPY 99 patient noted left visual loss. On February 10, 1992, visual acuity was 20/20 00 and 20/70 OS with a left pupillary afferent defect. Goldmann visual field revealed an arcuate nasal inferior defect in the left eye (Fig. 1, top). The right optic disk was normal and the left showed temporal pallor. No retinal lesions were seen. Magnetic resonance imaging (MRI) was recommended but not carried out. At 15 days later, the patient returned with further visual loss: left vision now "no light percep-tion" (NLP), right acuity still 20/20, but with temporal hemianopia on Humphrey visual field (Fig. 1, middle). MR! performed the same day revealed an enlarged left intracranial optic nerve and left hemichiasm, which enhanced after gadolinium injection (Fig. 2). No recurrence of the tumor was detected either clinically or by MR!. The patient underwent HBO (three periods of 30 minutes of 100% oxygen at 2.4 atm, separated by 2 periods of 10 minutes of normal air breathing twice a day for 2 days, then 5 to 6 times/week, 35 sessions in to- '-. .~ 3/23/92 FIG. 1. Visual fields. Top: Goldmann perimetry: normal visual field in the right eye; the left eye shows an arcuate nasal inferior loss. Middle: Left vision is no light perception. Automated static threshold perimetry (Humphrey, 30-2) reveals a dense temporal hemianopia of the right eye. Bottom: Left vision is light perception. Automated static threshold perimetry (Humphrey, 30-2) shows a remarkable recovery of the temporal hemianopia. I Clill Nrllro-ophthalmol. Vol. 13. No.2. 1993 100 F.-X. BORRUAT ET AL. FIG. 2. Magnetic resonance imaging (Vista 1.5 tesla). T1-weighted images (TR 700. TE 20) after gadolinium injection. A marked enhancement of the swollen left intracranial optic nerve (top) and left half of the chiasm (bottom) is seen on these coronal cuts. tal). The patient also received intravenous methylprednisolone 500 mg q6h for 5 days, followed by oral prednisone, 60 mg daily, tapering over 8 weeks. At 13 days after therapy was initiated, marked resolution of the right temporal hemianopia was noted, further improving 2 weeks later (Fig. 1, bottom). Three weeks after completion of HBO therapy, vision was 20/20 aD and light perception as; the right visual field (Humphrey, 30-2) was normal. MRI was repeated and showed decreased swelling of the left intracranial optic nerve and chiasm with only slight enhancement after gadolinium injection. DISCUSSION Delayed necrosis of the optic nerves and chiasm is a well-recognized complication of radiotherapy. I Clin Ne""",'phihaimoi. Vol. 13. No.2. 1993 Irradiation causes tissue ischemia secondary to a progressive obliterative endarteritis of the microvasculature. Pathology studies demonstrate myointimal and endothelial proliferation of small arteries and narrowing of the vessel lumen with fibrinoid necrosis (8). Skin biopsies from irradiated areas showed the presence of hypocellular and hypovascular tissue that is unable to regenerate supportive vessels and transcutaneous oxygen measurement in irradiated areas revealed tissue oxygen tension at 30% of nonirradiated areas (9). Despite the presence of an endarteritis, the role of high-dose steroids is uncertain as no cases of RON has been reported to improve with steroids only. RON has been reported to occur as early as 2 months and as late as 7 years after completion of radiotherapy (Fig. 3). However, 90% of RON cases occur within 3 years of irradiation with a mean onset at 12 months (2,3,5,10). In the present case, HYPERBARIC OXYGEN THERAPY 101 12 10 -UI 8 C .C-D - 6 CO a. ~ 4 2 0 6 12 18 24 36 48 60 Latency (months) visual loss began suddenly 17 months after completion of irradiation. A left retrobulbar optic neuropathy evolved rapidly, progressing to no light perception. Two weeks later, evidence of chiasmal involvement occurred with a dense temporal hemianopia, but preserved visual acuity in the right eye. MRI revealed enlarged left intracranial optic nerve and swollen left chiasm, both enhanced with gadolinium (Fig. 2). These MRI characteristics have been previously demonstrated in RON (10). No other cerebral involvement was detected on MRI and no local recurrence of the sinus melanoma was evident. HBO therapy produces a steep oxygen gradient between irradiated and non-irradiated tissues. Such an oxygen gradient directly enhances fibroblastic activity, collagen synthesis, and neovascularization in the irradiated tissues (9). HBO is presently the only available treatment capable of creating an environment that allows the reversal of radiation-induced tissue damage. From 20 to 30 sessions of 100% oxygen breathing at 2.4 atm for 90 min each day has been successfully used for problem wounds in oral and maxillofacial surgery following irradiation (9). Since angiogenesis is a progressive event with an initial lag phase, we suggest the use of twice-daily treatments during the first week if vision is deteriorating. Guy and Schatz (4) first reported visual improvement in RON when treated early with HBO after onset of visual loss, within 2 days if possible. The effectiveness of HBO in RON was challenged by Roden and coworkers (5), but in that report all patients were treated 2 to 12 weeks following visua1loss and breathing oxygen at only 2.0 atm. Our patient was treated 15 days after the onset FIG. 3. Latency for the development of radiation-induced optic neuropathy: the cumulative data for 50 patients with radionecrosis of optic nerve and/ or chiasm are plotted on this histogram (2, 3, 5, 10, and present case). Median latency is 12 months; 90% of cases presented within 3 years of radiation. 72 84 of left visual loss and 2 days after the loss of the right temporal visual field. There was full recovery of the right hemifield and the left vision slightly improved to light perception. The role of early therapy of RON is emphasized; the key element is the commencement of HBO therapy as soon as vision starts to deteriorate. The dramatic visual recovery in our case emphasized both the benefits of hyperbaric oxygen therapy and the need for starting therapy soon after visual loss, within 2 days, if possible. REFERENCES 1. Schatz Nj, Lichtenstein S, Corbett JJ. Delayed radiation necrosis of the optic nerves and chiasm. Neuro-Ophthalmology 1975;8:131-9. 2. Kline LB, Kim JY, Ceballos R. Radiation optic neuropathy. Ophthalmology 1985;92: 111&--26. 3. Warman R, Glaser JS, Quencer RM. Radionecrosis of optieo- hypothalamic glioma. Neuro-Ophthalmology 1989;9:21926. 4. Guy j, Schatz NJ Hyperbaric oxygen in the treatment of radiation-induced neuropathy. Ophthalmology 1986;93: 1083-8. 5. Roden D, Bosley TM, Fowble B, et al. Delayed radiation injury to the retrobulbar optic nerves and chiasm: clinical syndrome and treatment with hyperbaric oxygen and eorticosteroids. Ophthalmology 1990;97:346-51. 6. Guy j, Schatz NJ. Effectiveness of hyperbaric oxygen in treating radiation injury to the optic nerves and chiasm. [Letter]. Ophthalmology 1990;10:1246-7. 7. Feun LG, Gonzalez R, Savaraj N, et al. Phase II trial of piritrexim in metastatic melanoma using intermittent lowdose administration. I Clin OncoI1991;9:464-7. 8. De Reuck j, Van der Eecken H. The anatomy of the late radiation encephalopathy. Eur Neurol 1975;13:481-94. 9. Marx RE, Johnson RP. Problem wounds in oral and maxillofacial surgery: the role of hyperbaric oxygen. In: Davis Je. Hunt TK, eds. Problem wounds: the role of oxygen. New York: Elsevier Science; 1988:6~123. 10. Zimmerman CF, Schatz Nj, Glaser JS. Magnetic resonance imaging of radiation optic neuropathy. Am I Ophthalntol 1990;110:389-94. , eli" NellY(HJI'htJzalmol, Vol. 13. No.2, 1993 |
