An old friend revisited: chloramphenicol optic neuropathy
A 66-year-old woman presented on October 2011 with a 10-day history of painless bilateral visual loss of subacute onset (over 48 h). She also described paraesthesiae of the limbs for a similar duration.\nShe has rheumatoid arthritis, treated with methotrexate (since 2002) and etanercept (2003–2009), and she required bilateral knee replacements in 2009. Her right knee replacement was revised and underwent six washouts for persistent infection. Previous antibiotics used for her knee infection included ceftriaxone, fusidic acid, amoxicillin, vancomycin and daptomycin. Chloramphenicol 4 g daily was started 14 weeks before the occurrence of visual loss.\nChloramphenicol had been discontinued five days before presentation. Her other medications included methotrexate, folic acid, tramadol, paracetamol, aspirin and omeprazole. She smokes 10 cigarettes daily and does not drink alcohol. She has a varied balanced diet. There is no relevant family history.\nOn examination at 10 days after onset of visual loss, she had a best corrected visual acuity of 3/24 (Snellen) bilaterally and centrocaecal scotomas on examination by confrontation with a red hat pin. None of the Ishihara colour plates could be read, not even the control plate. Both her optic discs were hyperaemic (see Figure ). The rest of her cranial nerves and neurological examination of limbs were normal, except for bilateral L5 dermatomal loss to pinprick and abnormal proprioception at the great toe. Both temporal arteries were normal to palpation.\nInvestigations showed normochromic normocytic anaemia (haemoglobin 10.9 g/dL, mean corpuscular volume 94 fL). C-reactive protein was elevated at 54.7 mg/L (normal <5). The rest of blood tests were unremarkable including vitamin B12, folate, methylmalonic acid, homocysteine, autoantibodies (antinuclear antibody, extractable nuclear antigen and antineutrophil cytoplasmic antibody) and a genetic screen for Leber Hereditary Optic Neuropathy mutations.\nMagnetic resonance imaging (MRI) of brain and orbits was normal and MRI spine showed mild degenerative changes at cervical spine only. Cerebrospinal fluid examination was normal. A visual evoked potential was performed after recovery and this was normal, as were nerve conduction studies.\nA diagnosis of toxic optic neuropathy secondary to chloramphenicol was suspected. As stated above, the chloramphenicol had been stopped five days before presentation to us, i.e. on day 6 of visual symptoms. Four weeks after stopping chloramphenicol, vision improved to acuities of 6/5 (right), 6/6 (left) and normal visual fields, but reading of the Ishihara colour plates remained impaired at 8/13 bilaterally.\nThe patient elected to have an above knee amputation of her right leg, and is now mobilizing with a prosthetic limb and rehabilitation. At the onset of visual symptoms she developed paraesthesiae of limbs. Although the paraesthesiae improved, she is still symptomatic with this and the sensory loss in the left foot is impairing her prosthesis use.