Acute macular neuroretinopathy following intranasal use of cocaine.

Abstract

Originally described by Bos & Deutman (1975), acute macular neuroretinopathy (AMN) is a rare condition characterized by paracentral scotomas corresponding to flat, reddish, wedge-shaped intraretinal lesions usually pointing towards the fovea. These lesions are best seen using infrared (IR) reflectance imaging and show typical optical coherence tomography (OCT) findings (Fawzi et al. 2012). We have observed two cases of bilateral AMN following intranasal cocaine insufflations in two young otherwise healthy women. A 24-year-old woman (Case 1) presented 3 days after sudden onset of paracentral scotomata in both eyes at her awakening. Her past medical history was unremarkable and she did not take any medication, including oral contraceptives. The patient admitted to intranasal cocaine use the evening before the onset of symptoms. She was an occasional user and she denied any history of alcohol abuse or other drugs use. Best-corrected visual acuity (BCVA) was 20/20 in both eyes. On clinical examination, IR and OCT signs of AMN (Fawzi et al. 2012) were detected in both eyes (Fig. 1, A1-A4). After 1 month, the scotomata were subjectively unchanged, BCVA remained stable, and OCT showed slight interruption of the outer retinal layers (Fig. 1C). A 25-year-old woman (Case 2) was referred to our Department for persistent paracentral scotomata from 9 days. She did not take any medication, including oral contraceptives, and she had no history of ocular or systemic diseases. The ocular symptoms occurred during a 7 days trip abroad. On inquiring about drug use, the patient admitted to intranasal cocaine use few hours before the onset of symptoms. She stated it was her first time. Her BCVA was 20/20 in both eyes. On clinical examination, IR and OCT signs of AMN (Fawzi et al. 2012) were detected in both eyes (Fig. 1, B1–B4). After 40 days, the scotomata were subjectively unchanged, BCVA remained stable, and OCT showed partial recovery of the outer retinal layers (Fig. 1C). Pathogenesis of AMN is unclear. A recent study (Fawzi et al. 2012) demonstrated superficial involvement at the level of the outer plexiform layer and the Henle fibre layer. The authors proposed ischaemia of the deep capillary plexus (DCP), located in the outermost portion of the inner nuclear layer, as the cause of early outer plexiform layer lesions (Fawzi et al. 2012). As far as we know, this is the first report on AMN following intranasal use of cocaine. The increasing abuse of cocaine in Western countries has led to an increase of reported medical (including ocular) complications. In our cases, the close temporal association between cocaine use and onset of AMN suggests a causal relationship. Cocaine may induce arterial spasm (Isner & Chokshi 1989) that may result in decreased ocular perfusion at the level of the DCP. Moreover, intranasal use of cocaine has been reported to be associated with central retinal artery occlusion in a young woman with a history of systemic arterial hypertension (Wallace et al. 1992). Recently, our team (Querques et al. 2014) showed evidence of retinal artery transient occlusion on fluorescein angiography in a variant of AMN (paracentral acute middle maculopathy); the occlusion was transient because it resolved 3 days after presentation, despite persistence of the typical OCT findings. The cases here reported presented to our attention 3 and 9 days, respectively, after symptoms onset. Even though we could not see a transient artery occlusion, we may speculate that a decreased ocular perfusion at the level of the DCP following use of cocaine might play a key role in the pathogenesis of AMN. Adrenomimetic response associated with the intranasal use of cocaine (Wallace et al. 1992) may have also contributed to the pathogenesis of AMN, as intranasal injection of epinephrine during rhinosurgery has been reported to be associated in a case of AMN (Wessel et al. 2013). Given that the macula is supplied by a dual circulation, a choroidal contribution to the pathogenesis of AMN could be speculated. However, indocyanine green angiography did not show any abnormalities in our two cases (Fig. 1). In conclusion, we reported two cases of AMN following intranasal use of cocaine in two otherwise healthy women. Cocaine use should be considered as a possible risk factor of AMN.