Concerning the pathology underlying these causes (except idiopathic), "some of the more frequent causes include atheromatous disease of the internal carotid or ophthalmic artery, vasospasm, optic neuropathies, giant cell arteritis, angle-closure glaucoma, increased intracranial pressure, orbital compressive disease, a steal phenomenon, and blood hyperviscosity or hypercoagulability." Embolic and hemodynamic origin
With respect to embolic and hemodynamic causes, this transient monocular visual loss ultimately occurs due to a temporary reduction in retinal artery, ophthalmic artery, or ciliary artery blood flow, leading to a decrease in retinal circulation which, in turn, causes retinal hypoxia. While, most commonly, emboli causing amaurosis fugax are described as coming from an atherosclerotic carotid artery, any emboli arising from vasculature preceding the retinal artery, ophthalmic artery, or ciliary arteries may cause this transient monocular blindness. Atherosclerotic carotid artery: Amaurosis fugax may present as a type of transient ischemic attack (TIA), during which an embolus unilaterally obstructs the lumen of the retinal artery or ophthalmic artery, causing a decrease in blood flow to the ipsilateral retina. The most common source of these athero-emboli is an atherosclerotic carotid artery. However, a severely atherosclerotic carotid artery may also cause amaurosis fugax due to its stenosis of blood flow, leading to ischemia when the retina is exposed to bright light. "Unilateral visual loss in bright light may indicate ipsilateral carotid artery occlusive disease and may reflect the inability of borderline circulation to sustain the increased retinal metabolic activity associated with exposure to bright light." Atherosclerotic ophthalmic artery: Will present similarly to an atherosclerotic internal carotid artery.
Chloroprocaine (pKa 8.7) is the drug of choice for epidural analgesia and a decompensating fetus, because it does not participate in ion trapping. Placental transfer of 2-chloroprocaine is not influenced by fetal acidosis.The in vitro half-life of chloroprocaine is 21 seconds for maternal and 43 seconds for fetal blood. In patients who are homozygous atypical for plasma cholinesterase, chloroprocaine typically exists for two minutes in circulation. Synthesis
The hydrochloride salt of 4-amino-2-chlorobenzoyl chloride is made by the reaction of 2-chloro-4-aminobenzoic acid with thionyl chloride. Synthesis of this drug is then accomplished by directly reacting the product of the last step with the hydrochloride salt of 2-diethylaminoethanol. References
External links
"Chloroprocaine". Drug Information Portal. U.S. National Library of Medicine.