Posterior Ischemic Optic Neuropathy (PION) - Cardiovascular Cause MCQ — NEET PG Practice Question | NEETPGAI
Posterior Ischemic Optic Neuropathy (PION) - Cardiovascular Cause
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eye Ophthalmology
A 58-year-old man undergoes a 9-hour prone spine fusion with an estimated blood loss of 2.5 L and intraoperative mean arterial pressure maintained at 55–60 mmHg. On awakening, he reports painless, severe bilateral vision loss. Visual acuity is hand motion in both eyes, and bilateral relative afferent pupillary defects are noted. Fundoscopy reveals the optic disc marked **A** to be pink, sharp, and without swelling. Which of the following best explains why the optic disc appears normal in the acute phase despite severe vision loss?
A. The short posterior ciliary arteries undergo vasodilation in response to hypotension, preserving disc perfusion while the retrobulbar nerve becomes ischemic
B. The optic nerve head is supplied by the central retinal artery, which is resistant to hypotensive injury during prone positioning
C. The ischemic lesion lies posterior to the lamina cribrosa, beyond the visible optic disc margin, so acute swelling cannot develop until wallerian degeneration occurs weeks later
D. Retinal ischemia causes vision loss before optic nerve head ischemia, so the disc remains normal until retinal infarction spreads posteriorly
Explanation
Why option 1 is correct
Posterior ischemic optic neuropathy (PION) is defined by infarction of the retrobulbar optic nerve—the segment posterior to the lamina cribrosa. Because the lesion lies behind the visible optic disc margin (marked A), acute disc swelling cannot occur. Swelling develops only weeks later when wallerian degeneration of infarcted axons produces optic atrophy and gliosis. This normal-appearing disc in the setting of severe, painless bilateral vision loss is the pathognomonic fingerprint of PION. The infarct results from watershed vulnerability of short posterior ciliary pial perforators; prone positioning raises intraorbital pressure while systemic hypotension (MAP 55–60 mmHg) drops perfusion pressure across these small vessels. (AAO BCSC Neuro-Ophthalmology; Lee Anesthesia Closed Claims)
Why each distractor is wrong
Option 2: The optic nerve head is supplied by short posterior ciliary arteries and branches of the ophthalmic artery—not the central retinal artery. These vessels are highly vulnerable to hypotensive injury, especially in the retrobulbar segment. This option misidentifies the vascular anatomy and incorrectly suggests resistance to hypotensive injury.
Option 3: PION is a posterior nerve lesion, not a retinal process. Retinal ischemia (e.g., central retinal artery occlusion) produces a cherry-red spot and retinal whitening—a dramatically abnormal fundus. PION causes vision loss with a normal fundus acutely because the infarct is behind the disc, not in the retina.
Option 4: Short posterior ciliary arteries do not undergo protective vasodilation during hypotension. Rather, they are watershed vessels that depend on adequate perfusion pressure. Hypotension combined with venous congestion from prone positioning creates a "steal" that ischemia the retrobulbar nerve while the disc remains perfused.
High-YieldNEET PG
PION = normal disc acutely + severe vision loss + prone surgery + hypotension; disc swelling appears only weeks later with atrophy. Differentiate from AION (pale swollen disc acutely) and CRAO (cherry-red spot).
AAO BCSC Neuro-Ophthalmology; Lee Anesthesia Closed Claims
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