A possible relationship has been observed between ischemic optic neuropathy and the use of nitric oxide inhibitors, such as sildenafil, for erectile dysfunction. The visual loss has occurred within 24 h of taking the drug and is usually unilateral. According to Pomeranz and colleagues, all affected patients have had risk factors for vascular disease such as hypertension, diabetes, or hyperlipidemia, but there have been exceptions, and these risk factors are likely to be present in older men who are also likely to use the drug.
Massive blood loss or intraoperative hypotension, particularly in association with the use of cardiac surgery with a bypass pump, may also produce visual loss, and ischemic infarction of the retina and optic nerve. Prolonged laminectomy operations, performed with the patient in the prone position, are another situation that can be complicated by severe unilateral or bilateral ischemic optic neuropathy. Obese individuals and those with small optic cups are seemingly at risk for this complication. The reported cases have been summarized from a registry by Lee and coworkers.
Temporal, or giant cell, arteritis is another important cause of ischemic optic neuropathy (see also Chap. 9 on the related headache and Chap. 33 for a discussion of cerebrovascular disease in association with giant cell arteritis). Fleeting premonitory symptoms of visual loss (amaurosis fugax) may precede infarction of the nerve. Infarction caused by cranial arteritis may affect both optic nerves or retina in close succession and also, less often, impair ocular motor function.
A number of disease processes adjacent to the orbit and optic nerve can cause blindness, usually with signs of compression or infarction of the optic and oculomotor nerves. They are seen far less frequently than are ischemic optic neuropathy and optic neuritis. Septic cavernous sinus thrombosis (see “Cavernous Sinus Thrombosis” in Chap. 33), for example, may be accompanied by loss of vision in one or both eyes. Visual loss may present days after the development of chemosis and oculomotor palsies from the venous sinus occlusion. The mechanism of visual loss, which can occur without swelling of the optic nerve head, is unclear but most likely relates to retrobulbar ischemia of the nerve.
Similarly, optic and oculomotor disorders may rarely complicate ethmoid or sphenoid sinus infections. Severe diabetes with mucormycosis or other invasive fungal or bacterial infection is the usual setting for these complications. Extensive sinus disease may occasionally produce optic neuropathy; for example, Slavin and Glaser described a case of loss of vision from a sphenoethmoidal sinusitis with cellulitis at the orbital apex. Visual symptoms in these exceptional circumstances can occur prior to overt signs of local inflammation. An otherwise benign sphenoidal mucocele may cause a compressive optic neuropathy, usually with accompanying ophthalmoparesis and slight proptosis.