Acquired dyschromatopsia
Specialty: Ophthalmology.
Why it occurs
- Macular drug toxicity (especially induced by ethambutol, hydroxychloroquine or digitalis)
- Demyelinating or ischemic optic neuritis in acute or resolving phase
- Toxic-nutritional optic neuropathy (associated with chronic alcohol and tobacco abuse with folate deficiency)
- Progressive wet or dry senile maculopathy
- Advanced open angle glaucoma with loss of retinal fibers
- Pathology of the cortical visual pathway (e.g., infarction of the fusiform gyrus)
Initial workup
Ishihara pseudoisochromatic slide test (useful for rapid screening of the red-green axis); Farnsworth-Munsell ordering test of 100 hue (or its simplified version of 15 or 28 hue for a precise quantitative analysis of dyschromatopsia in the protan, deutan and tritan axes of confusion); Optical Coherence Tomography (OCT) of the optic nerve and macula; Visual Evoked Potentials to measure abnormalities in axonal transmission speed.
red flags
Sudden or subacute loss of red and green color discrimination in a patient under active treatment for tuberculosis with ethambutol, requiring immediate suspension of the medication to prevent irreversible optic atrophy.
Standard management
- There is no drug that restores color perception altered by structural damage. The treatment consists of immediately removing the toxic agent
- Folic acid (5 mg orally per day) associated with Vitamin B12 (hydroxycobalamin 1000 mcg intramuscularly weekly in the attack phase, followed by monthly administration, indicated in nutritional optic neuropathy to provide metabolic support to the myelin sheath of the optic nerve).
Educational guidance for study. It is NOT a prescription recommendation. The actual choice depends on the cause, the patient, and current guidelines.
- Area
- Ophthalmology
- Listed causes
- 6
- Treatment options
- 2