Acute macular neuroretinopathy (AMN) related to energy drink consumption

Abstract

This case identifies a newly found association between energy drinks and acute macular neuroretinopathy (AMN). Our patient, a 34-year-old woman with no significant ocular or previous medical history, presented with a 3-day history of decreased vision after consumption of multiple energy drinks. After near infrared and optical coherence tomography imaging, we were able to diagnose her with AMN. Our patient’s vision improved over a 2-month course with no intervention. Our case aims to emphasise the effect of caffeine on the retina, as well as encourage clinicians to consider energy drinks as a causative agent of AMN.

Background

Acute macular neuroretinopathy (AMN) is a retinal disorder characterised by sudden onset paracentral scotomas and reddish-brown, petalloid macular lesions.¹ It most commonly occurs in young, healthy women and is most easily identified by wedge-shaped parafoveal lesions on near-infared imaging. Patients may present with changes in visual acuity or scotoma that spontaneously resolve within a few months.² Associations include preceding flu-like illness, oral contraceptives, antecedent trauma, caffeine, injection of epinephrine or epinephrine, pseudoephedrine, hypovolemia and pregnancy-induced hypertension.^{1 3} We describe a case of AMN that developed after our patient consumed caffeine-based energy drinks.

Case presentation

A 34-year-old woman with no relevant previous medical or ocular history presented with a 3-day history of a scotoma in the left eye. She reported that she had been anxious about upcoming examinations and had recently consumed multiple energy drinks. In addition, the patient denied any current or previous use of oral contraceptives or other medications. On examination, her best-corrected visual acuity was 20/30 in the right eye and 20/40 in the left eye. There was no afferent pupillary defect. Slit-lamp biomicroscopy was unremarkable, intraocular pressure was 22 in both eyes and funduscopic examination was unremarkable in both eyes.

Optical coherence tomography showed a parafoveal hyperreflective band in the outer retinal layers of the left eye without retinal thickening (figure 1). Near-infrared photography showed a wedge-shaped parafoveal lesion pointing to the fovea.

Figure 1.

(A) Near-infrared imaging of the left eye with white arrows identifying the wedge-shaped parafoveal lesion. (B) Optical coherence tomography corresponding to the level of the wedge-shaped lesion in panel (A), with white arrows identifying the lesion.

Outcome and follow-up

The patient was monitored clinically. She was monitored and by 2 months after presentation, symptoms had improved and lesions had resolved (figure 2).

Figure 2.

(A) Near-infrared imaging of the left eye with white arrows identifying the resolving lesion after 2 months of observation alone. (B) Optical coherence tomography corresponding to the level of the resolving lesion in panel (A).

Discussion

AMN is a rare retinal pathology more commonly affecting women of reproductive age. Patients usually present with decreased vision, paracentral scotoma and flu-like symptoms. A variety of causative agents have been reported, most commonly including oral contraceptives.⁴ Our case report aims to bring attention to the effect of caffeine on the retinal architecture, specifically identifying caffeine in energy drinks as a possible causative agent of AMN.

AMN has been previously shown to be associated with caffeine usage. In their review, Bhavsar et al reported two cases of AMN associated with caffeine usage—10 cups per day in one case and 2−3 cups per day in another.¹ Our patient drank multiple caffeine-based energy drinks a few days prior to the beginning of her symptoms.

Recent reports using optical coherence tomography angiography have shown that AMN may be associated with choroidal or deep retinal ischaemia. Lee et al showed 11 eyes with AMN that had inner choroidal flow voids on optical coherence tomography angiography that corresponded to hyporeflectance on en-face near-infared imaging.⁵ Casalino et al also used optical coherence tomography angiography in seven patients and confirmed inner choroidal vascular flow void as well as focal impairment in the deep capillary plexus within the AMN lesions.⁶ The deep capillary plexus flow voids seen in patients with AMN have been shown to resolve on follow-up.⁷ Retinal vasoconstriction after caffeine ingestion has been shown through the blue field stimulation technique.⁸ More recently, oral caffeine intake has also been shown to be associated with significant reduction in macular flow area in the superficial vascular plexus, deep vascular plexus and choriocapillaris on OCT angiography.⁹ It is likely that the reduction in blood flow associated with caffeine intake causes macular ischaemia that is the likely pathophysiological cause of AMN.

In conclusion, this case reinforces the importance of asking patients with suspected AMN whether they have been exposed to caffeine or caffeine-based substances. It also identifies the need to include energy drink consumption when inquiring about caffeine consumption. Caffeine usage contributing to development of AMN supports the adrenergic hypothesis involved in the pathogenesis of AMN.

Learning points.

• Energy drinks may be a possible causative agent for acute macular neuropathy.

• Caffeine consumption, including energy drinks, should be considered in patients presenting with acute macular neuropathy.

• Though mostly known for their cardiovascular effects, highly caffeinated energy drinks can also affect vision.