Chapter 25 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.2–4 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. 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. 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. Usually presents with subacute, painless, bilateral central visual loss. Desaturation of colors is common.
TOXIC AND METABOLIC OPTIC NEUROPATHIES
URGENCY OF EVALUATION
DIAGNOSIS
DEMOGRAPHICS
SYMPTOMS
Visual Loss
Arsenicals Carbon disulfide Carbon tetrachloride Ethyl alcohol Ethylene glycol Lead Methanol Thallium Tobacco Trichloroethylene |
Chlorambucil Chloramphenicol Cisplatin Disulfiram Ethambutol Halogenated hydroxyquinolones Isoniazid Penicillamine Streptomycin Sulfonamides Vincristine |
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
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
Bitemporal deficits, which may resemble cecocentral scotomas, suggest a compressive chiasmal syndrome (Fig. 25–4).
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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