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  • 2020–2021 BCSC Basic and Clinical Science Course™

    Go to Academy Store Learn more and Purchase.

    2 Fundamentals and Principles of Ophthalmology

    Part V: Ocular Pharmacology

    Chapter 16: Ocular Pharmacotherapeutics*

    Local Anesthetics

    Overview

    Local anesthetics are used extensively in ophthalmology. Topical preparations yield corneal and conjunctival anesthesia for comfortable performance of examination techniques, such as tonometry, gonioscopy, removal of superficial foreign bodies, corneal scraping for bacteriologic studies, and paracentesis, as well as for use of contact lenses associated with fundus examination and laser procedures. Topical and intracameral anesthesia has gained increasing acceptance in cataract, pterygium, and glaucoma surgery. Local retrobulbar, peribulbar, and eyelid blocks yield excellent anesthesia and akinesia for intraocular and orbital surgery (Tables 16-25, 16-26).

    The local anesthetic drugs used in ophthalmology are tertiary amines linked by either ester or amide bonds to an aromatic residue. Because the protonated form is far more soluble and these compounds undergo hydrolysis more slowly in acidic solutions, local anesthetic drugs are supplied in the form of their hydrochloride salts. When exposed to tissue fluids at pH 7.4, approximately 5%–20% of the anesthetic agent’s molecules will be in the unprotonated form, as determined by the pKa value (8.0–9.0) of the individual drug. The more lipid-soluble unprotonated form penetrates the lipid-rich myelin sheath and cell membrane of axons. Once inside, most of the molecules are again protonated. The protonated form gains access to and blocks the sodium channels on the inner wall of the cell membrane and increases the threshold for electrical excitability. As increasing numbers of sodium channels are blocked, nerve conduction is impeded and finally blocked.

    After administration of a local anesthetic, small or unmyelinated nerve fibers are blocked the most quickly because their higher discharge rates open sodium channel gates more frequently and because conduction can be prevented by the disruption of a shorter axon. In unmyelinated fibers, the action potential spreads continuously along the axon. In myelinated fibers, the action potential spreads by saltation. Thus, only a short length of an unmyelinated fiber needs to be functionally interrupted, whereas one or more nodes must be blocked in a myelinated fiber. In larger myelinated fibers, the nodes are farther apart.

    Table 16-25 Regional Anesthetics

    Table 16-26 Topical Anesthetic Drugs

    Clinically, local anesthetics first block the poorly myelinated and narrow parasympathetic fibers (as evidenced by pupil dilation) and sympathetic fibers (vasodilation), followed by the sensory fibers (pain and temperature), and finally the larger and more myelinated motor fibers (akinesia). The optic nerve, enclosed in a meningeal lining, is often not blocked by retrobulbar injections.

    For retrobulbar blocks, amide local anesthetics are preferred to ester drugs because the amides have a longer duration of action and less systemic toxicity. Amide local anesthetics are not metabolized locally but are inactivated in the liver primarily by dealkylation; thus, their duration of action is partly determined by diffusion from the site of injection.

    Ester anesthetics are susceptible to hydrolysis by serum cholinesterases in ocular vessels as well as by metabolism in the liver. When serum cholinesterase levels are low because of treatment with echothiophate eyedrops or a hereditary serum cholinesterase deficiency, toxicity may occur at lower doses of ester anesthetics.

    The toxic manifestations of local anesthetics are generally related to the dose. However, patients with severe hepatic insufficiency may have symptoms of toxicity even at lower doses of either amide or ester local anesthetics. These manifestations include restlessness and tremor that may proceed to convulsions and respiratory and myocardial depression. CNS stimulation can be counteracted by intravenous diazepam; respiratory depression calls for ventilatory support.

    Because local anesthetics block sympathetic vascular tone and dilate vessels, a 1:200,000 concentration of epinephrine is frequently added to shorter-acting drugs to retard vascular absorption. Such use of epinephrine raises circulating catecholamine levels and may cause systemic hypertension and cardiac arrhythmias.

    Topically applied anesthetics disrupt intercellular tight junctions, increasing corneal epithelial permeability to subsequently administered drugs (ie, dilating drops). They also interfere with corneal epithelial metabolism and repair and thus cannot be used for long-term pain relief. Because topical anesthetics can become drugs of abuse that can eventually lead to chronic pain syndromes and vision loss, they should not be dispensed to patients.

    Excerpted from BCSC 2020-2021 series: Section 2 - Fundamentals and Principles of Ophthalmology. For more information and to purchase the entire series, please visit https://www.aao.org/bcsc.

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