postoperative visual loss (POVL)

POVL is vanishingly rare but when it happens its a nightmare on (insert your hospital's street) street.
It occurs typically during prone surgery even when pins are applied and there is clearly no eyeball pressure.
Opth exam shows ischemia of either the retina or the nerve.  predisposing factors include long case, hypotension, bleeding.  notably with longer cases intraocular pressure has been noted to rise.   I have always hunched that it was somehow related to high venous pressure too.  One clue for this was a patient of a colleagues from a few yrs back during thoracic vertebral surgery from an anterior approach they got into bleeding and had to occlude the svc to stop the bleeding. after all the face swelling finally subsided the patient was quite blind with not even light perception.  similarly cavernous carotid fistuas also produce blindness.
So based on the above physiologic considerations for prone cases my approach is to give just enough anesthesthetic to ensure unconsciousness and if that makes the MAP go less than 80 mmHg i run dilute neosynephrine to make it so.  Use bis and keep it at 55.  transfuse to Hb 10.

Comments

[mkeamy]

Your colleague, Warner, I think, gives a very good talk on this topic. Clearly, the phenomenon is ischemic, and hypotension probably plays a significant role. Warner claims that art of the pathophyisology involves pharmacologic paralysis; that paralyzing the extra-ocular muscles causes the globes to hang from the optic nerve, constricting the central retinal artery. I do a lot of complex spine, and I do not use induced hypotension, nor do I paralyze for any longer than necessary to establish exposure; the BIS helps with this. Incidentally, I favor vasopressin over neo- can't tell ya why, just like it.

[mkeamy]

why Bis of 55? why not 45 or 50? why Hgb of 10? If you are worried aout IOP, how about acetazolamide?

[andrew kofke]

lower bis=lower bp
hb of 10 based on studies on optimization studies both systemically and neuro (Dexter JNA) and brain phys which suggests active vasocilation in brain starts about Hb 10. So if there is compromised reserve (eg already maximal vasodil and unable to dilate more for anemia) injury can arise. of course no one knows if this physiology applies to the eye.

dont know what acetazolamide would do for the increased iop. In the brain it increases cbf to increase icp before it decreases it from decreased csf production.

ak