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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)

Anterior ischemic optic neuropathy. VIII. Clinical features and pathogenesis of post-hemorrhagic amaurosis.

Visual disturbance after marked and/or recurrent blood loss has been known for at least 25 centuries, since Hippocrates; however, so far its clinical features have been controversial and its pathogenesis enigmatic. The author studied seven patients, four of whom were seen soon after the visual loss and followed prospectively. A detailed review of the extensive literature and analysis of the cases provide relevant information on the subject. The blood loss is usually from the gastrointestinal (GI) tract, less often from other sites. There is typically a time lag between the bleeding and the onset of visual loss--usually up to 10 days, less often even 2 to 3 weeks. The ocular findings are typically those of anterior ischemic optic neuropathy (AION) and are usually bilateral. Considerable evidence has accumulated that blood loss, with or without arterial hypotension, causes increase in release of renin and endogenous vasoconstrictor agents (e.g., angiotensin, epinephrine, and vasopressin) because of activation of the sympathoadrenergic system and vasomotor center. Our experimental studies on renovascular malignant hypertension indicate that endogenous vasoconstrictor agents produce choroidal ischemia and AION. In view of all the evidence, it is postulated that in the production of AION after blood loss, release of endogenous vasoconstrictor agents is probably a very important factor, with arterial hypotension an additional factor; increased platelet aggregation may also play a role.[1]


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