According to a recent systemic review of PUR, the most frequent aetiologies are trauma and acute pancreatitis . A previous report presented a patient who developed PUR after a myocardial infarction with a concomitant transient ischaemic attack . Although the exact mechanism of PUR remains unknown, currently, the most accepted theory for its pathogenesis is an embolic phenomenon resulting in occlusion of the precapillary arterioles . Air, fat, platelets, fibrin, leukocyte aggregates and exogenous particles are all potential emboli. In this case, the presence of lacunar infarction hinted that fundus disorders share the same aetiology as the retinal vasculature has embryologic origins similar to those of the cerebral vasculature. Hypertensive retinopathy is an important differential diagnosis. However, his blood pressure was well controlled at that time and was unilaterally involved without apparent papilloedema; thus, this diagnosis seems less likely.
The diagnosis of PUR is mostly clinical depending on specific medical histories, including sudden vision loss after trauma or other special systemic diseases and typical signs, including retinal haemorrhage, cotton-wool spots and Purtscher flecken. Multimodal-image inspections, including OCT, OCT-A and FA, may provide more information for diagnosis and follow-up. Previous researchers have reported common signs of FA findings in PURs, including areas of non-perfusion, retinal ischaemia and slower filling of vessels . OCT-A may reveal extensive non-perfusion in the macular area in both the inner and deep capillary plexuses [5, 6]. OCT mostly indicates retinal oedema at the macula. Recent studies have reported cystoid macular oedema or even subretinal fluid in patients with PUR . PAMM lesions, a special OCT feature of PUR discovered in recent years, present as hyperreflective bands at the INL in OCT, indicating an ischaemic condition at the outer retinal capillary plexus .
This patient also presented low perfusion in the retina layer. However, the presentation of low perfusion in the choriocapillaris was characteristic with a notable sign of a honeycomb-like hypointense signal pattern in OCT-A, indicating the ischaemic involvement of the choroid. The anatomical features of the lobular blood supply in the choroid from the short posterior ciliary artery may partly explain this phenomenon since the areas of low perfusion are localized and well defined. The reduction in flow in the choriocapillaris is easily considered a projection artefact of cotton-wool spots and flecken of the superficial layer. However, the low perfusion area is more extensive and shows clearer boundaries in D4 than in D2. The projection artefact would not have such sharp edges for low perfusion areas.
Many patients with PUR can regain their visual acuity to normal levels spontaneously after the aetiology is resolved, while some patients have a poor prognosis despite various treatments. There is still no exact prognostic factor for PUR. In this case, some special circumstances should be taken into consideration to predict visual outcomes. Because the patient delayed consultation for 2 weeks, the exact process of the disease was unknowable, and the best opportunity for intervention might have been lost. Additionally, the presence of PAMM lesions surrounding the fovea indicated a poor prognosis as this sign represented the ischaemia of both the inner and deep retinal capillary plexuses at the fovea . Furthermore, OCT-A showed a honeycomb-like hypointense signal pattern in choriocapillaris that corresponds to anatomic structures of choroidal lobules. This finding provided a sign of choroidal lobular infarction 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 aetiology to be the most reasonable therapeutic option without the risk of adverse drug effects. In this case, we prescribed Alprostadil injections, which have been proven to attenuate immunohistochemical and histological repercussions in renal tissue . In addition, we referred him to the internal medicine department for further examination for cerebral infarction and hypertension, which may be the underlying aetiology of PUR.
In conclusion, PURs are reportedly mostly related to trauma or other special systemic conditions. PUR is largely an embolic occlusion disease. This case provides another perspective to detect potential embolic aetiologies, which is especially reasonable for patients in their 60s if no trauma or other specific systemic diseases are reported. FA and OCT-A provide more information for diagnosis and follow-up visits. The presence of PAMM lesions on OCT scans and a honeycomb-like hypointense signal pattern in OCT-A at the choriocapillaris layer may indicate a poor visual prognosis because of the ischaemia in the macular fovea and choroid.