eMedicine Specialties > Ophthalmology > Optic Nerve

Toxic/Nutritional Optic Neuropathy: Treatment & Medication

Author: Aftab Zafar, MD, Consulting Staff, Department of Ophthalmology, St Mary's General Hospital
Contributor Information and Disclosures

Updated: Aug 27, 2008

Treatment

Medical Care

  • 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 hydroxocobalamin 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 at this institution 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.
  • 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 drug, 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 stopped9 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 improve5 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,10,6 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

Consultations

  • 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 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.

Diet

See Medical Care.

Medication

The goals of pharmacotherapy are to reduce morbidity and to prevent complications.

Vitamin supplements

Given to those patients who are deficient in a particular vitamin or those who are suspected of having a particular vitamin deficiency.


Folic acid (Folvite)

Important cofactor for enzymes used in production of red blood cells.

Adult

1 mg PO qd

Pediatric

0.1-0.4 mg PO qd

Increase in seizure frequency and subtherapeutic levels of phenytoin reported when used concurrently

Documented hypersensitivity; patients with pernicious anemia

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Benzyl alcohol may be contained in some products as a preservative (associated with a fatal gasping syndrome in premature infants); resistance to treatment may occur in patients with alcoholism and deficiencies of other vitamins


Thiamine (Thiamilate)

Essential coenzyme that combines with ATP to form thiamine pyrophosphate.

Adult

100 mg PO qd

Pediatric

10-50 mg PO qd for 2 wk; then, 5-10 mg PO qd for 1 mo

Pregnancy

A - Fetal risk not revealed in controlled studies in humans

Precautions

Sensitivity reactions can occur (intradermal test dose recommended in suspected sensitivity); deaths have resulted from IV use; sudden onset or worsening of Wernicke encephalopathy, following glucose, may occur in patients with thiamine deficiency; administer before or together with dextrose-containing fluids in suspected thiamine deficiency

More on Toxic/Nutritional Optic Neuropathy

Overview: Toxic/Nutritional Optic Neuropathy
Differential Diagnoses & Workup: Toxic/Nutritional Optic Neuropathy
Treatment & Medication: Toxic/Nutritional Optic Neuropathy
Follow-up: Toxic/Nutritional Optic Neuropathy
References
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References

  1. Lim SA. Ethambutol-associated optic neuropathy. Ann Acad Med Singapore. Apr 2006;35(4):274-8. [Medline].

  2. Orssaud C, Roche O, Dufier JL. Nutritional optic neuropathies. J Neurol Sci. Nov 15 2007;262(1-2):158-64. [Medline].

  3. Murphy MA, Murphy JF. Amiodarone and optic neuropathy: the heart of the matter. J Neuroophthalmol. Sep 2005;25(3):232-6. [Medline].

  4. Macaluso DC, Shults WT, Fraunfelder FT. Features of amiodarone-induced optic neuropathy. Am J Ophthalmol. May 1999;127(5):610-2. [Medline].

  5. Nagra PK, Foroozan R, Savino PJ, et al. Amiodarone induced optic neuropathy. Br J Ophthalmol. Apr 2003;87(4):420-2. [Medline].

  6. Nazarian SM, Jay WM. Bilateral optic neuropathy associated with amiodarone therapy. J Clin Neuroophthalmol. Mar 1988;8(1):25-8. [Medline].

  7. Santaella RM, Fraunfelder FW. Ocular adverse effects associated with systemic medications : recognition and management. Drugs. 2007;67(1):75-93. [Medline].

  8. Zoumalan CI, Agarwal M, Sadun AA. Optical coherence tomography can measure axonal loss in patients with ethambutol-induced optic neuropathy. Graefes Arch Clin Exp Ophthalmol. May 2005;243(5):410-6. [Medline].

  9. Chai SJ, Foroozan R. Decreased retinal nerve fibre layer thickness detected by optical coherence tomography in patients with ethambutol-induced optic neuropathy. Br J Ophthalmol. Jul 2007;91(7):895-7. [Medline].

  10. Johnson LN, Krohel GB, Thomas ER. The clinical spectrum of amiodarone-associated optic neuropathy. J Natl Med Assoc. Nov 2004;96(11):1477-91. [Medline].

  11. Danesh-Meyer H, Kubis KC, Wolf MA. Chiasmopathy?. Surv Ophthalmol. Jan-Feb 2000;44(4):329-35. [Medline].

  12. Glaser JS. Nutritional and toxic optic neuropathies. In: Glaser JS, ed. Neuro-ophthalmology. 3rd ed. Philadelphia: Lippincott; 1999.

  13. Grant WM, Schuman JS. Toxicology of the Eye. 4th ed. Springfield, Ill: Charles C Thomas Publisher; 1993.

  14. Kerrison JB. Optic neuropathies caused by toxins and adverse drug reactions. Ophthalmol Clin North Am. Sep 2004;17(3):481-8; viii. [Medline].

  15. Lessell S. Nutritional deficiency and toxic optic neuropathies. In: Albert DM, Jakobiec FA, eds. Principles and Practice of Ophthalmology. 2nd ed. Philadelphia: WB Saunders Co; 2000.

  16. Mantyjarvi M, Tuppurainen K, Ikaheimo K. Ocular side effects of amiodarone. Surv Ophthalmol. Jan-Feb 1998;42(4):360-6. [Medline].

  17. Melamud A, Kosmorsky GS, Lee MS. Ocular ethambutol toxicity. Mayo Clin Proc. Nov 2003;78(11):1409-11. [Medline].

  18. Miller NR. Anterior toxic optic neuropathies. In: Walsh and Hoyt's Clinical Neuro-Ophthalmology. 4th ed. Baltimore: Lippincott Williams & Wilkins; 1982:254-260.

  19. Miller NR. Retrobulbar toxic and deficiency optic neuropathies. In: Walsh and Hoyt's Clinical Neuro-ophthalmology. 4th ed. Baltimore: Lippincott Williams & Wilkins; 1982:289-307.

  20. Phillips PH. Toxic and deficiency optic neuropathies. In: Miller NR, Newman NJ, eds. Walsh and Hoyt's Clinical Neuro-ophthalmology. 6th ed. Baltimore: Lippincott Williams & Wilkins; 2005:447-463.

  21. Rizzo JF 3rd, Lessell S. Tobacco amblyopia. Am J Ophthalmol. Jul 15 1993;116(1):84-7. [Medline].

  22. Sadun AA. Metabolic optic neuropathies. Semin Ophthalmol. Mar 2002;17(1):29-32. [Medline].

  23. Woon C, Tang RA, Pardo G. Nutrition and optic nerve disease. Semin Ophthalmol. Sep 1995;10(3):195-202. [Medline].

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Further Reading

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Keywords

toxic/nutritional optic neuropathy, toxic-nutritional optic neuropathy, toxic and nutritional optic neuropathy, toxic optic neuropathy, nutritional optic neuropathy, optic neuropathy, optic neuropathies, metabolic optic neuropathy, nutritional deficits, undernutrition, nutritional amblyopia

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Contributor Information and Disclosures

Author

Aftab Zafar, MD, Consulting Staff, Department of Ophthalmology, St Mary's General Hospital
Aftab Zafar, MD is a member of the following medical societies: Canadian Medical Association, Canadian Ophthalmological Society, College of Physicians and Surgeons of Ontario, Ontario Medical Association, and Royal College of Physicians and Surgeons of Canada
Disclosure: Nothing to disclose.

Medical Editor

Andrew W Lawton, MD, Medical Director of Neuro-Ophthalmology Service, Section of Ophthalmology, Baptist Eye Center, Baptist Health Medical Center
Andrew W Lawton, MD is a member of the following medical societies: American Academy of Ophthalmology, Arkansas Medical Society, and Southern Medical Association
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: Nothing to disclose.

Managing Editor

Brian R Younge, MD, Professor of Ophthalmology, Mayo Clinic School of Medicine
Brian R Younge, MD is a member of the following medical societies: American Medical Association, American Ophthalmological Society, and North American Neuro-Ophthalmology Society
Disclosure: Nothing to disclose.

CME Editor

Ralph Garzia, OD, Assistant Dean for Clinical Programs, Associate Professor, School of Optometry, University of Missouri at St Louis
Ralph Garzia, OD is a member of the following medical societies: American Academy of Optometry and American Optometric Association
Disclosure: Nothing to disclose.

Chief Editor

Hampton Roy Sr, MD, Associate Clinical Professor, Department of Ophthalmology, University of Arkansas for Medical Sciences
Hampton Roy Sr, MD is a member of the following medical societies: American Academy of Ophthalmology, American College of Surgeons, and Pan-American Association of Ophthalmology
Disclosure: Nothing to disclose.

 
 
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