Sir,

Systemic disease is usually responsible for retinal ischaemic events in patients under 30 years of age. We report the case of a young man with retinal artery occlusion (RAO) secondary to patent foramen ovale (PFO).

Case report

A healthy 17-year-old African-American male presented with sudden, painless loss of vision in his right eye while playing basketball. He denied associated symptoms of headache, pain, or visual disturbance, as well as a history of sickle cell disease or trait, or recreational drug abuse. An examination revealed a visual acuity of hand motions in the affected eye. The fundus had macular pallor and a cherry-red spot in the fovea (Figure 1). Fluorescein angiography was consistent with a RAO (Figures 2 and 3). An optical coherence tomography showed macular edema of 503 μm. The haemotological/infectious work-up, including transthoracic echocardiogram (TTE), was negative. However, a trans-oesophageal echocardiogram (TEE) showed a PFO. The patient underwent a successful percutaneous femoral catheterization to close the defect.

Figure 1
figure 1

Right eye with inner retinal ischaemic whitening in the area supplied by the temporal retinal artery.

Figure 2
figure 2

Corresponding fluorescein angiogram with (a) early and (b) late images, showing non-filling of the temporal artery and a corresponding hypofluorescence from non-perfusion of the area supplied by the artery.

Figure 3
figure 3

Intra-operative trans-oesophageal echography showing percutaneous femoral catheter (thin arrow) in the right atrium and the closure of the defect (curved arrow). The thick arrow indicates flow towards the defect.

Comment

A PFO has been a reported finding in young patients presenting with RAO without risk factors for such an event.1 Autopsy studies report the incidence of PFO to be 17–35% in the general population.2 The association between PFO and embolism has been reported in young adults.3 The source for the emboli is often not found, but is usually attributed to occult thrombosis. Nakagawa et al4 reported a case of RAO in a patient with PFO and deep venous thrombosis. Our patient's history is significant for engagement in the basketball game at the onset of symptoms. This exertion, coupled with a sub-clinical thrombosis, may have resulted in the paradoxical RAO.

Chen et al2 reported a fourfold increased incidence of PFO in patients with ischaemic events compared with that in controls, and a greatly increased sensitivity for detecting PFO with TEE when compared with TTE. Kramer et al5 found TEE to have a higher yield than TTE in the evaluation of patients with RAO. As PFOs are usually asymptomatic, for younger patients presenting with a RAO and in whom the TTE and the corresponding work-up have been negative, a TEE is a more sensitive means of diagnosis.