Sir,

Prepapillary loops (PPLs) are rare. They are usually unilateral, congenital, and uncommonly associated with complications.1 We describe a patient with carotid artery stenosis and a congenital PPL, who developed a branch retinal artery obstruction (BRAO).

A 57-year-old male smoker presented with a 1-week history of a left inferior scotoma associated with photopsia. There was no relevant past ocular or medical history.

On examination, visual acuities were 6/6 OD, 6/4 OS, and a left afferent pupillary defect was present. On fundus examination, a PPL and findings compatible with a BRAO were detected (Figures 1 and 2). An inferior visual field defect was evident on confrontational testing. No emboli were visible. His blood pressure was 160/92 mmHg and a left carotid bruit was audible. Carotid doppler ultrasound scanning subsequently revealed a 50% stenosis of the right common carotid artery, and a greater than 75% obstruction of the left internal carotid artery. Treatment was initiated with aspirin 75 mg daily and the patient underwent left carotid endarterectomy 3 months later. At 5 months following the initial presentation, the visual acuity was unchanged and no major changes in the retina were apparent.

Figure 1
figure 1

Demarcation line between ischaemic oedematous retina (BRAO) and healthy retina (black arrows). Prepapillary loop out of focus (white arrow).

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Figure 2
figure 2

Prepapillary loop extending from left optic nerve (black arrow).

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Comment

PPLs are rare, occurring in 0.01% of the general population. The majority are thought to be congenital in origin;1 however, acquired prepapillary arterial loops have been described following central retinal artery occlusion,2 and in a patient in whom the initial findings were multiple cotton wool spots of unknown origin.3

Although generally asymptomatic, PPLs have been associated with BRAO, central retinal artery occlusion, vitreous haemorrhage, hyphaema, and amaurosis fugax.1, 2, 3, 4, 5

To the best of our knowledge, the coexistence of carotid artery stenosis and prepapillary loops has not been described previously. It is interesting to note that the side with the greater degree of carotid stenosis was the same as that with the PPL and BRAO. We hypothesise that the coil-like structure of the PPL is associated with an increased turbulence of vascular flow through it, predisposing to intraloop thrombosis. The development of carotid artery stenosis would be expected to reduce the perfusion pressure across the loop, further increasing the risk of loop thrombosis.

This case highlights the need for a thorough cardiovascular workup and appropriate intervention in patients with PPLs and retinal vascular occlusions.