Cocaine Orbitopathy Complicated by Orbital Wall Defects, Bilateral Naso-Orbital Fistulas, Phthisis, and Bilateral Vision Loss.

Abstract

A 64-year-old male with a 40-year history of daily intranasal cocaine use presented with painless, gradually worsening binocular diplopia. External examination showed a severe saddle-nose deformity. Ophthalmologic exam was notable for visual acuity of 20/40 in OU, with restrictive strabismus, esotropia, and hypotropia in the OD. Neuroimaging revealed extensive nasal septal destruction with erosion of bilateral medial and orbital floors. The patient was lost to follow-up and presented 3 years later with progression of vision loss, now light perception vision OD and count fingers vision OS. There was now complete absence of the nasal bridge and medial orbital walls with large naso-orbital fistulas bilaterally, and phthisis of the right globe with complete corneal neovascularization. Laboratory work-up, including perinuclear anti-neutrophil cytoplasmic antibodies, cytoplasmic anti-neutrophil cytoplasmic antibody, erythrocyte sedementation rate, c-reactive protein, and chest X-ray, were unremarkable. The patient continually refused drug testing. Repeat neuroimaging revealed progression of the nasal midline destruction and further loss of the medial and orbital floors (panels A and B). These findings were consistent with anatomic destruction of the orbital bony walls and subsequent ocular necrosis, perforation, and ischemia related to long-term cocaine use (panel C). Cocaine use can result in tissue damage through its alpha agonist and inflammatory properties leading to a prothrombotic state, vasoconstriction, and subsequent ischemia. The authors present a severe case of presumed cocaine orbitopathy resulting in extensive midline structural loss, destruction of the medial and inferior orbital walls, naso-orbital fistulas, and subsequent phthisis bulbi resulting in vision loss.