Ischaemic ocular necrosis from carotid-cavernous fistula. Pathology of stagnant anoxic "inflammation" in orbital and ocular tissues.

Acute carotid-cavernous fistulae reduce arterial pressure in the ophthalmic artery and cause marked elevation of pressure in the orbital veins (Sanders and Hoyt, I969). Together the effects ofvascular dilatation, oedema, and slowing of orbital circulation impair clearance of cellular metabolites and lead to a stagnant type of anoxia that differs clinically and pathologically from the ischaemic effects caused by arterial insufficiency alone. These stagnant anoxic changes may be aggravated rather than cured by neurosurgical procedures designed to "trap" the fistula by arterial ligations and embolization (Walker and Allegre, I956; Stern, Brown, and Alksne, I967).