Toxic and Metabolic Optic Neuropathies

Chapter 25

TOXIC AND METABOLIC OPTIC NEUROPATHIES


Valerie Ann Purvin


Toxic-metabolic optic neuropathy is a broad category that includes visual loss due to environmental exposure (Table 25–1), a variety of medications (Tables 25–2 and 25–3), and nutritional deficiencies (Tables 25–4 and 25–5).1 These different entities are usually grouped together because their clinical manifestations are so similar and also because they often coexist, making the relative contribution of each difficult to define.24 Recognition is important because visual loss in these disorders is potentially reversible, particularly with early intervention. In addition, optic neuropathy may be the first manifestation of toxicity or nutritional deficiency, and its prompt recognition and treatment may prevent the development of other neurologic or systemic sequelae.


URGENCY OF EVALUATION


Because the onset is usually insidious, most patients will have already been symptomatic for weeks or months prior to seeking medical attention. Evaluation within 2 weeks of presentation is advisable. The exception is acute methanol toxicity, which should be treated as an emergency if seen acutely, and referred for management of metabolic status.


DIAGNOSIS


DEMOGRAPHICS


Optic neuropathy secondary to nutritional deficiency is more prevalent in lower socioeconomic groups and in individuals on unusually restricted diets (e.g., vegans). Tobacco-alcohol optic neuropathy occurs most commonly in middle-aged men. Vitamin B12 deficiency due to pernicious anemia more often affects middle-aged women, particularly those of Scandinavian descent.


SYMPTOMS


Visual Loss

Usually presents with subacute, painless, bilateral central visual loss. Desaturation of colors is common.






TABLE 25–1 TOXINS ASSOCIATED WITH OPTIC NEUROPATHY

Arsenicals


Carbon disulfide


Carbon tetrachloride


Ethyl alcohol


Ethylene glycol


Lead


Methanol


Thallium


Tobacco


Trichloroethylene






TABLE 25–2 MEDICATIONS ASSOCIATED WITH OPTIC NEUROPATHY

Chlorambucil


Chloramphenicol


Cisplatin


Disulfiram


Ethambutol


Halogenated hydroxyquinolones


Isoniazid


Penicillamine


Streptomycin


Sulfonamides


Vincristine






TABLE 25–3 TOXIC OPTIC NEUROPATHIES THAT CAUSE DISC EDEMA

α-Interferon11


Amiodarone12


Cyclosporin13


Ornithine-ketoacid transaminase (OKT) 314


Tacrolimus (FK 506)15


 


Neurologic Deficits

Some patients have coexisting peripheral neuropathy, manifest as “glove-and-stocking” numbness and paresthesias. Patients with vitamin B12 deficiency may also experience cognitive decline.


Systemic

Gastrointestinal symptoms are common in pernicious anemia, including abdominal pain, diarrhea, and glossitis.


SIGNS


Visual Acuity

The papillomacular bundle is preferentially affected, causing loss of acuity.5 Visual loss is bilateral and symmetric; the severity varies.


Color Vision

Prominently affected.


Visual Field (Fig. 25–1)

Bilateral central or cecocentral scotomas. Rarely bitemporal scotomas are seen, e.g., ethambutol.6






TABLE 25–4 CAUSES OF VITAMIN B12 DEFICIENCY

1. Nutritional deficiency


Mostly vegan diet


Takes > 10 years to develop


2. Gastric disorders


Absence of intrinsic factor


Congenital


Pernicious anemia


Gastroplasty


3. Small bowel disease


Diphyllobothrium latum infection


Ileal resection (e.g., for Crohn’s disease)


 


Pupils

A relative afferent pupillary defect is rarely found because of the symmetry of the visual loss, but the pupillary light reactions may be bilaterally sluggish if there is significant disease.


Fundi

Acutely the optic discs may look normal or may have a hyperemic appearance similar to that seen in Leber’s hereditary optic neuropathy (Fig. 25–2). Over time, if untreated and permanent visual loss ensues, temporal pallor develops (Fig. 25–3). Diffuse pallor is unusual.


Red Flags

image Bitemporal deficits, which may resemble cecocentral scotomas, suggest a compressive chiasmal syndrome (Fig. 25–4).


image Unilateral or markedly asymmetric visual loss suggests an alternative diagnosis such as Leber’s hereditary optic neuropathy, compressive optic neuropathy, or optic neuritis.

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Jun 4, 2016 | Posted by in OPHTHALMOLOGY | Comments Off on Toxic and Metabolic Optic Neuropathies

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