Sir,

I read with interest the excellent series by Davies et al,1 describing maculopathy in patients using ‘poppers.’ Together with two recent series from France,2, 3 their report provides important evidence for an association between abuse of alkyl nitrite compounds and specific, sub-foveal changes. Whether this association is causal remains to be determined, and Davies et al suggest causality is likely.

What I find most striking about the cases attributed to ‘poppers maculopathy’ in the Davies series (and which is consistent with the two series from France) is the SD-OCT imaging—which has an uncanny resemblance to photic maculopathy (Figure 1). In both ‘poppers maculopathy’ and photic maculopathy, there is focal disruption of the IS-OS junction centred at the fovea.1, 2, 3, 4 Moreover, the size, shape, echogenicity, and temporal evolution of the SD-OCT lesions appear indistinguishable in the two conditions. Patients also present with the same symptoms (scotoma, reduced vision, and phosphenes) and have the same slit-lamp findings (a pale yellow foveal lesion).1, 2, 3, 4 Indeed, it appears that in people using poppers, the two conditions can only be reliably distinguished by eliciting a history of excess light exposure and not by clinical features.

Figure 1
figure 1

A comparison of SD-OCT images in (a) ‘poppers maculopathy’ as presented in Case 2 of Davies et al1 with (b) photic retinopathy in a 30-year-old male who presented to my clinic 2 weeks after sun-gazing. Notice the similarity in location, size, shape, and echogenecity of the respective lesions in the IS-OS junction.

Unfortunately, Davies et al1 did not report to what extent excessive light exposure was specifically queried in their patients. In the two French series,2, 3 all patients ‘denied staring at bright lights’—yet how reliable is their history? Poppers are frequently combined with psychotropic drugs and alcohol, which can alter consciousness and memory, potentially making history unreliable.5 Poppers themselves can cause transient visual hallucinations and heighten sensory perception5—effects that are known to increase light-gazing behaviour in other recreational drugs such as LSD.6 Poppers are frequently used in raves, where bright strobe lights and lasers are common.

Given the points discussed, it should be crucial when considering the diagnosis of ‘poppers maculopathy’ to document a thorough history of the patient’s drug behaviour and light exposure. Do they take multiple drugs? Do they hallucinate or experience altered consciousness? Are they ever entranced by bright lights, candles, or the sun?

The endemic use of poppers4 and the mere handful of reports of maculopathy suggests that compounding factors or susceptibilities may be involved. It is not inconceivable that ‘poppers maculopathy’ represents a sub-group of patients who have unrecognised photic injury. If poppers maculopathy is indeed a distinct entity, then the remarkable ultrastructural similarity with photic injury suggests that the two conditions share a common pathophysiological pathway. Perhaps poppers lower the threshold for retinal phototoxicity or otherwise trigger a biochemical cascade identical to that induced by photic damage.