Pain Control in Recovering Alcoholics: Effects of Local Anesthesia
Journal article by Louis Fiset, Brian Leroux, Marilynn Rothen, Chris Prall, Charlene Zhu, Douglas S. Ramsay; Journal of Studies on Alcohol, Vol. 58, 1997
Journal Article Excerpt
Pain control in recovering alcoholics: effects of local anesthesia. by Louis Fiset , Brian Leroux , Marilynn Rothen , Chris Prall , Charlene Zhu , Douglas S. Ramsay The medical literature suggests that a history of alcohol or nonalcohol drug abuse may predispose patients to achieve less effect from pharmacological methods for general anesthetics/pain control (Couderc et al., 1984; Fassoulaki et al., 1993; Han, 1969; St. Haxholdt et al., 1984; Swerdlow et al., 1990; Tammisto and Tigerstedt, 1977a, b). In dentistry, lack of adequate pain control may lead to fear and long-term avoidance of care, and deterioration of oral health (Kaufman et al., 1984; Milgrom et al., 1988; Weinstein et al., 1985). Empirical evidence suggests that systemic sedative agents, such as midazolam (Fiset et al., 1992), and common amide local anesthetics, like lidocaine (Scheutz, 1982), are less effective for dental patients with a history of alcohol or drug abuse. Such patients represent a significant subset of dental patients who have pain/anxiety control problems and who may be predisposed to poorer outcomes (Milgrom et al., 1993). Pain is a subjective experience reflecting a dynamic interaction between sensory, affective, motivational and cognitive systems. Because alcoholics are known to differ from nonalcoholics on a number of pain relevant psychological parameters (Turk et al., 1983), it is possible that differences between alcoholics and nonalcoholics in any of these categories could account for differences in effective pain management. Epidemiological studies, together with several clinical investigations of hospitalized alcoholics, have demonstrated a high comorbidity between alcoholism and mental disorders such as anxiety and depression (Bowen et al., 1984; Chambless et al., 1987; Coxetal., 1990; Regieretal., 1990). Differences in pain control between alcoholics and nonalcoholics could therefore be related to these comorbid conditions. In addition, alcoholics may differ from nonalcoholic patients regarding their expectations for effective pain control. Expectations can influence a drug's effects (Cutter et. al., 1986; deBoer et al., 1993; Marlatt, 1978, 1979; Wigmore and Hinson, 1991). Alterations in an individual's expectations about the effectiveness of a pain-controlling drug have been shown to influence the pain and/or anxiety that subjects report (Dworkin et al., 1983,1984; Martin et al.,1994). An alternative explanation for why alcoholics may experience less effective pain control may reside with chronic alcohol exposure and its consequent physiological alterations. Such pathophysiological alterations could include pharmacodynamic or pharmacokinetic changes that render the individual tolerant to ethanol and possibly cross-tolerant to therapeutic pain-controlling drugs. Animal research has demonstrated that chronic ethanol exposure can cause the development of cross-tolerance to local anesthetics (Fassoulaki et al., 1990) and nitrous oxide (Henry et al., 1990; Koblin et al., 1980). Human studies, however, are lacking. Local anesthetics exert their effects at the sensory nerve membrane by decreasing the rate of depolarization during that phase of the action potential, thus preventing cellular depolarization and development of a propagated action potential. The conduction block results from a decrease in the permeability of the nerve membrane to sodium ions. The duration of anesthetic effect depends on the concentration of the anesthetic at the nerve site. The vasodilatory properties of most commercially available local anesthetics (mepivicaine is an exception) cause the effects to be short lived in the absence of a chemical astringent such as epinephrine or other vasoconstrictor which decreases tissue perfusion to the local area. Most local anesthetics in use today are biotransformed in the liver and excreted through the kidneys. In contrast to the local anesthetics, agents used during induction of general anesthesia act upon the central nervous system. One agent cited in anesthesia experiments comparing dosage requirements of alcoholic and nonalcoholic patients is the sedative hypnotic, thiopental (Couderc et al., 1984; Swerdlow et al., 1990), a barbiturate. Thiopental acts on the reticular activating system, depressing ascending neuronal conduction to the cerebral cortex. A second agent used in the study of alcoholic populations is the nonbarbiturate, propofol (Fassoulaki et al., 1993), which acts at a recognition site on the GABA receptor. These short-acting, rapid onset, agents are administered by IV injection to induce general anesthesia, and are usually followed by additional, longer acting, agents for maintenance of anesthesia, such as the synthetic opioid, fentanyl (St. Haxholdt et al., 1984; Tammisto and Tigersted, 1977b). Each is biotransformed in the liver and excreted through the kidneys.While physiological, pharmacological and psychological hypotheses exist to explain what appears to be "cross-tolerance" of ethanol with pain control agents, whether acting locally or centrally, the phenomenon has been poorly documented. The belief that pain control is more difficult to achieve among alcoholics is, at the ... |
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