According to a recent systemic review of PUR, the most frequent etiologies are trauma and acute pancreatitis. A previous report presented a patient developing PUR after a myocardial infarction with a concomitant transient ischemic attack. Although the exact mechanism of PUR remains unknown, currently the most accepted theory for its pathogenesis attributes to an embolic phenomenon resulting in occlusion of the precapillary arterioles. Air, fat, platelets, fibrin, leukocyte aggregates as well as exogenous particles are all potential embolus. In this case, the present of lacunar infarction brought up a hint that the retinal disorders share the same etiology as the vasculature of retina has similar embryologic origins to the cerebral vasculature.
The diagnosis of PUR is mostly clinical depending on specific medical histories including sudden vision loss after trauma or other special systemic disease and typical funduscopic signs like retinal hemorrhage, cotton wool spots and Purtscher fleckens. Multimode-image inspections including OCT, OCT-A and FA may provide more information for diagnosis and follow-up. Previous researches reported common signs of FA findings in PURs including areas of non-perfusion, retinal ischemia and slower filling of vessels . OCT-A may reveal extensive nonperfusion in the macular area in both inner and deep capillary plexus [5, 6]. This patient also presented a hypoperfusion condition in retina layer. But we found its presentation in choriocapillaris is even characteristic with a notable sign of honeycomb-like hypointense signal pattern indicating the ischemic involvement of the choroid.
Many patients of PUR could regain their visual acuity to normal level spontaneously after the etiology is resolved, while some patients remain poor prognosis despite of various treatments. There is still no exact prognostic factor for PUR. To this case, some special circumstances should be taken into consideration to predict the visual outcomes. Owing to his delayed consultation for 2 weeks, the exact process of the disease was unknowable and the best opportunity for intervention might have lost. And the present of PAMM lesions surrounding the fovea indicated a poor prognosis as this sign represented the ischemia of both inner and deep capillary plexus at the fovea . Furthermore, OCT-A presented a honeycomb-like hypointense signal pattern in choriocapillaris just corresponds with anatomic structures of choroidal lobules. This provided a sign of choroidal lobular infarction as well and explained the restricted recoverability of this patient. At present, there is still no consensus on the treatment of PUR. Most viewpoints consider observation and treatment of the underlying etiology may be the most reasonable therapeutic option without risk of adverse drug effects.
In conclusion, PURs were reported mostly related to trauma or other special systemic conditions. It’s an embolic occlusion disease substantially. This case provides us another perspective to detect for potential embolic etiologies, which makes sense especially for patients in 60s if no trauma or other specific systemic diseases reported. FA and OCT-A provide more information for diagnosis and follow-up visit. The present of PAMM lesion in OCT scan and a honeycomb-like pattern of hypointense signal pattern in OCT-A at the layer of choriocapillaris may indicate a poor visual prognosis because of the ischemia involvement of macula fovea and choroid.