Local Anesthesia of the Cornea

Abstract

Purpose Local anesthetics act by blocking the conduction of impulses along the neuronal membrane. Many types of chemical structures do so to some degree, including ethanol and barbiturates. However, those agents that are clinically useful as local anesthetics are more potent in this regard and are less toxic. Rationale Mechanism of Action and Efficacy Local anesthetics block the formation or conduction of action potentials. They stabilize the neuronal membrane and prevent the generation of impulses; the standing potential remains intact. The action potential begins with extracellular sodium flowing into the neuron, followed by intracellular potassium flowing out of the neuron. At low concentrations, local anesthetics primarily affect sodium conductance. At higher concentrations, potassium conductance may also be affected. The clinically used local anesthetics act primarily by reversibly blocking the sodium ion channel at its internal neuronal membrane. Neuronal factors that affect local anesthetic activity are axon diameter, myelinization, and rate of firing. The greater the diameter of the axon, the more internal membrane surface area and number of sodium channels there are to block and, therefore, the lower the intensity and duration of anesthetic action (Staiman and Seeman 1977). The greater the amount of myelin, the less readily the anesthetic penetrates the axon. Frequency dependency describes the observed phenomenon that the more rapidly a neuron discharges, the more rapidly the anesthetic enters the axon. Anesthetic agents whose molecules alternate between positively charged and neutral form at physiologic pH are most likely to show frequency dependency. Benzocaine, which is uncharged at physiologic pH, does not show frequency dependency. The principal manufacturing factors that affect activity are the drug concentration, pH of the solution, and presence of a vasoconstrictor. Cocaine contains intrinsic vasoconstrictor properties. It blocks the reuptake of norepinephrine released by sympathetic nerve endings. All other local anesthetics block sympathetic neuron release of norepinephrine, resulting in vasodilation. The addition of a vasoconstrictor reduces drug absorption by the vasculature, thereby increasing the local effect of the anesthetic, reducing in theory its systemic toxicity, and reducing surgical bleeding. Norepinephrine is less stable than epinephrine, the vasoconstrictor that is usually added. Concentrations of epinephrine of approximately 1/200,000 (i.e., 0.0005 %) are maximally effective.