The current view regarding the retinal findings in Purtscher or Purtscher-like retinopathy is centered on the microembolization of the precapillary arterioles, which affects the retinal microvasculature [
3,
10]. The occurrence of embolic occlusion can be attributed to various factors, such as the presence of fat emboli resulting from long bone fractures, the dissemination of pancreatic proteases in the systemic circulation observed in cases of acute pancreatitis, and the activation of C5 and complement factors associated with renal failure and other autoimmune diseases, which ultimately leads to leucocyte aggregation [
11‐
13]. In cases where the emboli are of significant size, they have the potential to obstruct the proximal segment of retinal arterioles, leading to the extensive whitening of the retina observed in individuals diagnosed with branch retinal artery occlusion. Conversely, when the emboli are smaller in size, they have the ability to obstruct the distal segment of retinal arterioles, resulting in the characteristic appearance of cotton-wool spots on fundoscopic examination. In the present instance, substantial contiguous regions of retinal whitening were observed in both eyes, indicating the presence of large emboli. Furthermore, we observed notable opacification of the inner retina, thickening of the inner retina, and disruption of the stratification of the inner retina layer, along with separation of the ILM and the presence of hyperreflective dots in the posterior vitreous in both eyes, as observed using OCT. These findings corresponded to the regions of retinal whitening observed during clinical examination. In instances of central retinal artery occlusion, comparable OCT observations have been documented, suggesting a higher degree of vascular occlusion [
14]. Therefore, it can be inferred that the occlusion severity observed in our case of Purtscher-like retinopathy was substantial. The occurrence of ILM separation or detachment, as well as the presence of posterior vitreous hyperreflective dots, has been previously recorded in cases of more severe central retinal artery occlusion [
8]. The authors put forth a pathogenesis model that suggests that inflammation caused by reperfusion injury is responsible for cellular damage in the inner retina. This damage then could lead to the separation of the ILM and the formation of hyperreflective dots in the posterior vitreous. The identical pathogenesis can be extrapolated to the present instance of Purtscher-like retinopathy. In cases of Purtscher retinopathy, high-dose corticosteroids, administered orally or intravenously, are commonly prescribed and have demonstrated favourable results [
15]. Steroids possess the capacity to stabilize the neuronal membrane and microvascular channels that have been compromised, thereby facilitating a partial restoration of neuronal fibres that have not undergone irreversible damage. Steroids additionally impede the process of granulocyte aggregation and complement activation, both of which are pivotal in the development of this particular disease [
16]. After administering oral systemic steroids, we observed the reattachment of the ILM separation and disappearance of posterior vitreous hyperreflective dots. This supports a possible hypothesis that inflammation resulting from microvascular occlusion could have been the likely underlying cause for the novel OCT findings of ILM separation and posterior vitreous hyperreflective dots in this particular case. The observed discrepancy in visual acuity improvement between the two eyes in our study may be primarily attributed to the varying levels of occlusion severity in each eye and the preservation of papillomacular bundle perfusion in the right eye. Additionally, this difference could potentially be influenced by the varying extent of damage to the outer retinal layer in both eyes. However, additional retinal imaging with fluorescein angiography or optical coherence tomography angiography could have helped to determine the extent of retinal ischemia and a possible explanation for the disparities in visual acuity changes in both eyes.
In summary, this case offers an additional perspective on the underlying mechanisms responsible for the retinal manifestations observed in Purtscher or Purtscher-like retinopathy. The involvement of inflammation in the retinal manifestations of this disease is of significant importance, and the administration of steroids may offer potential benefits in terms of early restoration of retinal structure and improvement in visual acuity.