Obstructed Axoplasmic Transport in Purtscher’s Traumatic Retinopathy

Abstract

2 cases of unilateral traumatic Purtscher’s retinopathy are reported. The pos-traumatic increase of the cephalic venous pressure may cause subconjunctival hemorrhages and retinal venous stasis followed by hemorrhages and ischaemic changes, like capillary non-perfusion and cotton-wool spots. Correlation of the fundus picture with fluorescein angio-grams suggests that the cotton-wool spots found in association with capillary non-perfusion result from the obstruction of both the orthograde and the retrograde axonal flow in the retinal ganglion cell axons. After recovery, funduscopic and perimetric evidence of nerve fibre bundle defect was found.

Interferon‐associated retinopathy in a uniform regimen of natural interferon‐α therapy for chronic hepatitis C

“…IFN‐associated retinopathy is one of these adverse reactions, and retinopathy is probably due to disturbances in retinal microcirculation (15). It is generally accepted that cotton‐wool spots are caused by obstruction of axoplasmic flow secondary to ischemia of the retinal vasculature (17, 18). In the present study, fortunately, only cotton‐wool spots and minor retinal hemorrhage were experienced, but occasionally, retinal capillary nonperfusion, retinal edema, vascular occlusions, microvascular abnormalities, and vascular leakage have been reported (7).…”

Why cotton wool spots should not be regarded as retinal nerve fibre layer infarcts

“…For example, a plethora of CWSs in an annulate distribution some 2-4 mm in radius around the disc sometimes evolves in the immediate aftermath of hyperacute elevation of central (intrathoracic) venous pressure such as might derive from severe chest compression (fig 11). [65][66][67][68][69] The CWSs in Purtscher's traumatic retinal angiopathy have generally been attributed to multifocal retinal arteriolar occlusion, 68 69 but the long held suspicion-that reflux of venous blood through the valveless jugular veins and cavernous sinus somehow underpins these changes 65-69may well be correct. Transient supraphysiological hypertension within, and passive hyperdistension of, the thin walled retinal veins in the peripapillary RNFL might cause compression damage to the axon bundles if their innate protective deformability was to be overwhelmed.…”

Central retinal artery occlusion resembling Purtscher-like retinopathy

“…The pathological mechanism for Purtscher retinopathy remains unknown, but several mechanisms have been hypothesized based on the pathogenesis of more general diseases, eg, occlusion and infarction of the microvascular bed due to small emboli,10,11 disseminated intravascular coagulopathy,12 and leukocyte aggregation due to complement C5a activation 13,14. Raised intrathoracic pressure and venous dilatation have also been suggested to be the cause of Purtscher-like retinopathy 15,16. Previously, Gass proposed that Purtscher-like retinopathy is a subtype of CRAO cause by an endogenous emboli 17.…”