Fibrinoid necrosis

[4][5][6][7] The earliest documented identification of fibrinoid changes dates back to 1880, when it was questioned whether these histological changes resulted from the deposition of a fibrinous exudate, or the degeneration and breakdown of collagen fibers.

Because these stains possess the ability to highlight and identify fibrin, this led to the term fibrinoid, which means "fibrin-like", being used to describe the affected vessels.

[8] The term fibrinoid necrosis is, in fact, considered a misnomer,[1][10] as the intense eosinophilic staining of the accumulated plasma proteins masks the true nature of the underlying changes in the blood vessel, and makes it virtually impossible to definitively determine whether the cells of the vessel wall are actually undergoing necrosis.

[4][14] Fibrinoid infiltration in affected vessels may be confined to the subintimal region, as the ground substance of the intima and the inner elastic lamina often act as a barrier, limiting further penetration of fibrin into the arterial wall.

[2][3][28] This endothelial damage may arise due to a variety of underlying factors; for instance: Endothelial cell damage results in the loss of the normal barrier function, and allows plasma components, including coagulation factors, to escape from the bloodstream and leak out into the blood vessel walls and the surrounding spaces.

Ischemia disrupts RPE function, compromises the blood-retinal barrier and causes fluid leakage into the subretinal space, and the development of exudative retinal detachment.

[40] However, it is to be noted that these histological features tend to progress gradually over time, and a biopsy taken too early or too late might miss the "textbook" full-blown changes of LCV.