Toxic/Nutritional Optic Neuropathy Treatment & Management

Based on the literature, one standard treatment for patients who have nutritional optic neuropathy is not apparent, as various authors have had success with a variety of regimens.

Improved nutrition clearly is the key, as dietary deficiency is the common denominator in these patients. A well-balanced diet, which is high in protein, also should be supplemented with B-complex vitamins. Others believe that thiamine may contribute to recovery, even in patients who continue to abuse alcohol or tobacco.

Injections of hydroxycobalamin have been successful in treating patients with tobacco amblyopia, even when smoking continues.

It cannot be overemphasized to patients that stopping, or at least reducing, their smoking or consumption of alcohol is critical to their recovery. The latter, combined with an improved diet (green leafy vegetables and fruit daily) and vitamin supplementation, are the mainstay of therapy in nutritional optic neuropathy. Therefore, specific therapy includes thiamine 100 mg PO bid, folate 1 mg PO qd, a multivitamin tablet daily, and the elimination of any causative agent (eg, tobacco, alcohol).

Vitamin B-12 injections are reserved for patients with pernicious anemia. If pronounced nerve fiber layer dropout is present, treatment is futile.

Toxic optic neuropathies

For cases of toxic optic neuropathies, the treatment is more definitive; the goal is to identify and remove the offending substance.

Other than stopping the causative drug or substance, no specific treatment is available for the optic neuropathy caused by ethambutol. Once this is accomplished, most patients will recover, and this may take weeks to months. However, there are reports that vision may still decline or fail to recover even when the drug is stopped ^[13] if damage is severe enough.

For isoniazid, vision also improves when administration of the drug is ceased. In some patients, the administration of pyridoxine has been used to help reverse the toxicity of isoniazid, but this improvement may be simply related to stopping it and not the pyridoxine. Because these drugs may be given concurrently in the treatment of tuberculosis, and both may produce a toxic optic neuropathy, physicians should remember that if stopping one does not result in the improvement of a patient's vision, then the other drug also should be stopped.

If an optic neuropathy is diagnosed in a patient taking both isoniazid and ethambutol, the latter drug should be discontinued first. If visual symptoms persist, then the isoniazid must also be discontinued. ^[2]

Prompt discontinuation of amiodarone (in consultation with the patient's cardiologist) is essential if compelling evidence exists of toxic optic neuropathy from the drug. The visual symptoms, along with the disk swelling, can improve ^[5] gradually over the next several months, rather than immediately. Conversely, visual loss or associated field defects reportedly can be permanent despite discontinuation of the drug, ^{[14, 6]} with the disc swelling progressing to optic nerve pallor. Of note, some patients have developed disc edema and subsequent optic neuropathy even after cessation of the drug. ^{[5, 6]}

When considering a nutritional optic neuropathy in a patient, especially elderly patients, one must always consider that folate or vitamin B-12 deficiencies may be responsible. In such cases, a hematologic consultation is warranted before treatment is undertaken, especially in the presence of a normal hematocrit.

A neurologist may be consulted to look for neurologic manifestations of nutritional deficiencies, neurological consequences of pernicious anemia, or toxicities from systemic medications and to determine whether further tests, such as cerebrospinal fluid studies, are indicated.

With respect to patients on amiodarone, it is strongly recommended to consult with the patient's cardiologist before discontinuing the drug. The ophthalmologist, in conjunction with the cardiologist, should determine whether the less established visual complications of the drug outweigh its highly proven cardiac clinical benefits.

See Medical Care.

No complications are associated with the aforementioned therapy. The only complication of not seeking or complying with therapy is profound bilateral visual loss but never total blindness.

Patients in whom ethambutol or isoniazid is indicated for tuberculosis need to have a baseline ophthalmologic examination before treatment is instituted and should be monitored by their ophthalmologist periodically as long as they are on the drug to detect any optic nerve toxicity as soon as possible. Patients should also be made aware of the potential ocular adverse effects of these drugs and should be encouraged to seek medical attention as soon as visual symptoms become apparent.

Any patient for whom amiodarone is being considered for treatment requires a baseline ophthalmic examination before the drug is initiated. Furthermore, once on the drug, patients should be evaluated at least every 6 months. Even if a patient presents with corneal changes associated with the drug, their decreased vision should never be attributed to this until any pathology of the optic nerve has been excluded.

Patients should seek assistance from their primary physician on methods to stop or reduce their smoking and/or alcohol intake.

Patients with toxic/nutritional optic neuropathy should be observed initially every 4-6 weeks and then, depending on their recovery, every 6-12 months. At each visit, the patient's visual acuity, color vision, visual fields, pupils, and optic nerves should be assessed. Optical coherence tomography may be used to quantify nerve fiber layer or ganglion cell structure.