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Cyclic Antidepressant Drugs SI Conversion: [AUQ: Dr 834 II: THERAPEUTIC DRUGS 127. Spiker DG, Pugh DD. Combining tricyclic and monoamine oxidase inhibi- 145. Chambost M, Liron L, Peillon D, et al. [Serotonin syndrome during fluoxetine tor antidepressants. Arch Gen Psychiatry 1976;33(7):828–830. poisoning in a patient taking moclobemide.] Can J Anaesth 2000;47(3):246– 128. Peebles-Brown AE. Hyperpyrexia following psychotropic drug overdose. 250. Anaesthesia 1985;40(11):1097–1099. 146. Myrenfors PG, Eriksson T, Sandsted CS, et al. Moclobemide overdose. J 129. Tuck JR, Punell G. Uptake of (3H)5-hydroxytryptamine and (3H)noradrenaline Intern Med 1993;233(2):113–115. by slices of rat brain incubated in plasma from patients treated with chlorimi- 147. Pounder DJ, Jones GR. Post-mortem drug redistribution––a toxicological pramine, imipramine or amitriptyline. J Pharm Pharmacol 1973;25(7):573–574. nightmare. Forensic Sci Int 1990;45(3):253–263. 130. Gillman PK. Successful treatment of serotonin syndrome with chlorproma- 148. Lichtenwalner MR, Tully RG, Cohn RD, et al. Two fatalities involving zine. Med J Aust 1996;165(6):345–346. phenelzine. J Anal Toxicol 1995;19(4):265–266. 131. Graham PM. Successful treatment of the toxic serotonin syndrome with 149. Yonemitsu K, Pounder DJ. Postmortem changes in blood tranylcypromine chlorpromazine. Med J Aust 1997;166(3):166–167. concentration: competing redistribution and degradation effects. Forensic 132. Tackley RM, Tregaskis B. Fatal disseminated intravascular coagulation fol- Sci Int 1993;59(2):177–184. lowing a monoamine oxidase inhibitor/tricyclic interaction. Anaesthesia 150. Baselt RC, Shaskan E, Gross EM. Tranylcypromine concentrations and 1987;42(7):760–763. monoamine oxidase activity in tissues from a fatal poisoning. J Anal Toxicol 133. Bieck PR, Antonin KH. Tyramine potentiation during treatment with MAO 1977;1:168–170. inhibitors: brofaromine and moclobemide vs irreversible inhibitors. J Neural 151. Boniface PJ. Two cases of fatal intoxication due to tranylcypromine over- Transm Suppl 1989;28:21–31. dose. J Anal Toxicol 1991;15(1):38–40. 134. Gieschke R, Schmid-Burgk W, Amrein R. Interaction of moclobemide, a new 152. Musshoff F, Varchmin-Schultheiss K, Madea B. Suicide with moclobemide reversible monoamine oxidase inhibitor with oral tyramine. J Neural Transm and perazine. Int J Legal Med 1998;111(4):196–198. 1988;26[Suppl]:97–104. 153. Kapur S, Zipursky RB, Jones C, et al. Cyproheptadine: a potent in vivo sero- 135. Patat A, Berlin I, Durrieu G, et al. Pressor effect of oral tyramine during tonin antagonist [Letter]. Am J Psychiatry 1997;154(6):884. treatment with befloxatone, a new reversible monoamine oxidase-A inhibi- 154. Gillman PK. The serotonin syndrome and its treatment. J Psychopharmacol tor, in healthy subjects. J Clin Pharmacol 1995;35(6):633–643. 1999;13(1):100–109. 136. Provost JC, Funck-Brentano C, Rovei V, et al. Pharmacokinetic and pharma- 155. 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Ann Pharmacother 2001;35(7–8):870–873. 1994;24(5):983–985. 159. Buckley NA, Dawson AH, Whyte IM. Specific serotonin reuptake inhibitors 140. Klysner R, Larsen JK, Sorensen P, et al. Toxic interaction of venlafaxine and (SSRIs). HyperTox: assessment and treatment of poisoning. Newcastle, Austra- isocarboxazide. Lancet 1995;346(8985):1298–1299. lia: MediTox Pty Ltd, 2002. 141. Phillips SD, Ringo P. Phenelzine and venlafaxine interaction. Am J Psychia- 160. Tatsumi M, Jansen K, Blakely RD, et al. Pharmacological profile of neurolep- try 1995;152(9):1400–1401. tics at human monoamine transporters. Eur J Pharmacol 1999;368(2–3):277– 142. Kolecki P. Venlafaxine induced serotonin syndrome occurring after absti- 283. nence from phenelzine for more than two weeks. J Toxicol Clin Toxicol 161. Braunlich H, Greger J, Traeger A. [The phenelzine poisoning and the possi- 1997;35(2):211–212. bilities of its treatment in animal experiments.] Z Arztl Fortbild (Jena) 143. Brubacher JR, Hoffman RS, Lurin MJ. Serotonin syndrome from venlafax- 1966;60(15):914–921. ine-tranylcypromine interaction. Vet Hum Toxicol 1996;38(5):358–361. 162. Reid DD, Kerr WC. Phenelzine poisoning responding to phenothiazine. 144. Hodgman MJ, Martin TG, Krenzelok EP. Serotonin syndrome due to ven- Med J Aust 1969;2(24):1214–1215. lafaxine and maintenance tranylcypromine therapy. Hum Exp Toxicol 163. Richelson E, Souder T. Binding of antipsychotic drugs to human brain 1997;16(1):14–17. receptors focus on newer generation compounds. Life Sci 2000;68(1):29–39. CHAPTER 134 See Figure 1. Compounds included: See Table 1. Molecular formula and weight: See Table 1. Cyclic Antidepressant Drugs SI conversion: [AUQ: Dr. Rivard 7/29.] CAS Registry No.: See Table 1. Andrew H. Dawson Therapeutic levels: See Table 8. Special concerns: Abrupt deterioration with seizures or ventricular dys- rhythmias Antidotes: Sodium bicarbonate, hyper- tonic sodium chloride OVERVIEW soning (2–4). Up to 90% of TCA suicide deaths occur outside of hospital (5,6). One-half of the in-hospital fatalities have trivial Cyclic antidepressants are pharmacologically dirty drugs: although toxicity on arrival to hospital but develop major toxicity within their primary therapeutic effect is to block presynaptic catechola- 1 hour (5). This reflects the rapid absorption of TCA and onset of mine and serotonin reuptake, most of their adverse effects and tox- cardiac and central nervous system toxicity. Whereas a number icity is mediated by their effects of blocking of cellular ion channels of electrocardiogram (ECG) abnormalities are predictive of seri- as well as α-adrenergic, histaminergic, and muscarinic receptors. ous toxicity, a normal ECG does not exclude serious toxicity. Common adverse effects are sedation and anticholinergic symp- Decontamination, management of airway, and adjustment of toms. The group is dominated by tricyclic antidepressants (TCA) in pH to a mild systemic alkalosis with sodium bicarbonate are the number, clinical experience, and extent of toxicity. mainstays of successful management. Despite changes in antidepressant prescribing patterns, TCA The primary indication for all of these drugs is depression. remain a common cause for admission (1) and death from poi- TCAs have also been used for panic disorder (imipramine), 134: CYCLIC ANTIDEPRESSANT DRUGS 835 Figure 1. Structures of the cyclic anti- depressant drugs. obsessive-compulsive disorders (clomipramine), cataplexy and tetracyclics vary (Table 1). Many TCAs have active metabo- associated with narcolepsy (clomipramine), and attention defi- lites that contribute to their therapeutic effect (Table 2). cit hyperactivity disorder (imipramine, nortriptyline). Medical The ingestion of 15 to 20 mg/kg or more of a TCA is poten- uses include adjunctive treatment in pain management (ami- tially fatal, although there are significant differences in toxicity triptyline, doxepin) and treatment of nocturnal enuresis or urge within the drug class (8–10). Tetracyclics and bicyclics appear to incontinence (amitriptyline, imipramine, nortriptyline) (7). be less toxic in overdose than TCA. Small children can potentially Viloxazine is a bicyclic antidepressant with predominant seroto- develop life-threatening toxicity with ingestion of 1 to 2 tablets. nin reuptake inhibition; no deaths are reported. Mianserin and In a pediatric series of TCA poisonings, all single ingestions of maprotiline are both tetracyclic compounds with similar indica- less than 5 mg remained asymptomatic. Minor toxicity can result tions and mechanism of action to TCAs. from ingestion of more than 5 mg/kg (11). Deaths have been reported rarely with chronic therapeutic doses (desipramine, 3.3 mg/kg per day; imipramine, 6 mg/kg per day) (12). In these TOXIC DOSE cases, other factors such as impaired metabolism due to either genetic variation, drug-induced enzyme inhibition, or preexisting The adult and pediatric therapeutic dose is provided in Table 1. The cardiac conduction defects have been implicated. normal therapeutic dose of most TCAs in both adults and chil- Risk for major toxicity varies within the class. Initially, a dren is 1 to 3 mg/kg given once a day. The doses for the bicyclic number of mortality studies examined the relative risk of death TABLE 1. Physical characteristics and dosage and elimination half-life of the cyclic antidepressants Oral dose Elimination half-lives Molecular formula, molecular weight range of drug and active Compounds included (g/mol), CAS Registry No. Formulation (mg/d) metabolitesa,b (h) Amineptine hydrochloride (Sur- C22H27NO2,HCl; 373.9; 30272-08-3 NR 100–200 1, 2.5 vector) Amitriptyline hydrochloride C20H23N,HCl; 313.9;
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