NEWS & EVENTS
Retinal Review, Issue 40
CASE NUMBER 40
A 42 year old man was referred for sudden vision loss in his right eye. He underwent a vasectomy three weeks before presentation. He was hospitalized one week after the procedure for an infection and was treated with intravenous antibiotics. He was discharged on a one week course of oral antibiotics and noted the vision loss shortly after discharge. Past ocular history is unremarkable. Past medical history is normal as well. On examination VA was OD: 20/100 and OS: 20/20. IOP’s were normal OU. The slit lamp examination was normal OU. A 2+ right relative afferent papillary defect was noted on pen light examination. Visual fields with a 24-2 program showed a dense inferior altitudinal defect OD and had mild inferior depression OS.
Dilated examination was significant for a clear lens and vitreous OU. The right optic nerve was diffusely swollen with a few overlying cotton wool spots. The vessels were not engorged. The left optic nerve had a small cup with mild hyperemia and possible edema.
The patient was diagnosed with optic neuropathy OD and possibly OS. This was a confusing case in that the altitudinal visual field loss suggested an ischemic process (AION), yet the nerve was diffusely rather than segmentally swollen, and the other nerve was also possibly involved. Furthermore, was the infection following the vasectomy playing a role or was it just a “red herring” and unrelated to the optic neuropathy? AION is untreatable. There have been numerous studies looking at medical, surgical, and topical interventions for AION. Unfortunately no treatment is beneficial. So rather than diagnosing the patient with an untreatable problem we went a different route. Given the fact that both nerves were involved and that the patient recently had a systemic infection, we diagnosed the patient with a post infectious optic neuropathy. Patients can develop either inflammation of the optic nerve or demyelination of the optic nerve after a severe infection. Vision can be reduced mildly or dramatically. Inflammation or demyelination can both respond to systemic steroids. There was also a possibility that there was an infectious process in the spinal fluid resulting in optic neuropathy, but the patient did not exhibit any meningeal signs. We started the patient on 80mg of oral prednisone with a rapid taper over two weeks. Within several days the nerves began to defervesce and vision returned to normal. Visual fields were repeated a week later and the altitudinal defect disappeared.
Our patient had an unusual post infectious optic neuropathy which luckily responded to oral steroids. Optic nerve edema as well as acuity reduction and the altitudinal visual field defect fully resolved. This case underscores the need to fully evaluate treatment options for acute optic nerve disease. Although treatment should not be instituted for untreatable conditions such as AION, the unusual aspects of this case made us consider other treatable causes of optic neuropathy. His vision has remained normal after the steroid taper.