Tricyclic antidepressants overdose

Sodium bicarbonate administration for cardiac arrest is controversial because there are few clinical data supporting its use, and it may have some detrimental effects. Sodium bicarbonate can be used in special circumstances (i.e., underlying metabolic acidosis, hyperkalemia, salicylate overdose, or tricyclic antidepressant overdose). The dosage should be guided by laboratory analysis if possible. 

Frommer DA, Kulig KW, Marx JA, Rumack B. Tricyclic antidepressant overdose. A review. JAMA 1987 257(4) 521-6. 

Kerr GW, McGuffle AC, Wilkie S. Tricyclic antidepressant overdose areview. Emerg Med J 2001 18(4) 236-41. 

Goldberg RJ, Capone RJ, Hunt JD Cardiac complications following tricyclic antidepressant overdose issues for monitoring policy. JAMA 254 1772-1775, 1985... 

Swartz CM, Sherman A. The treatment of tricyclic antidepressant overdose with repeated charcoal. J Ctin Psychopharmacol 1984 4 336-340. 

Physostigmine Suggested for antimuscarinic anticholinergic agents not for tricyclic antidepressants Adult dose is 0.5-1 mg IV slowly. The effects are transient (30-60 minutes), and the lowest effective dose may be repeated when symptoms return. May cause bradycardia, increased bronchial secretions, seizures. Have atropine ready to reverse excess effects. Do not use for tricyclic antidepressant overdose. 

Tada H, Sticherling C, Oral H, Morady F. Brugada syndrome mimicked by tricyclic antidepressant overdose. J Cardiovasc Electrophysiol 2001 12 275. 

Tricyclic Antidepressants Tricyclic antidepressant overdose increases suicidal tendency and may be fatal.134... 

Spiker DG, Weiss AN, Chang SS, Ruwitch JF Jr, Biggs JT. Tricyclic antidepressant overdose clinical presentation and plasma levels. Clin Pharmacol Ther 1975 18(5 Part 1) 539 I6. 

Langou RA, Van Dyke C, Tahan SR, Cohen LS. Cardiovascular manifestations of tricyclic antidepressant overdose. Am Heart J 1980 100(4) 458-64. 

Hoffman JR, McElroy CR. Bicarbonate therapy for dysrhythmia hypotension in tricyclic antidepressant overdose. West J Med 1981 134(l) 60-4. 

McAlpine SB, Calabro JJ, Robinson MD, Burkle FM Jr. Late death in tricyclic antidepressant overdose revisited. Ann Emerg Med 1986 15(ll) 1349-52. 

Hulten BA, Adams R, Askenasi R, Dallos V, Dawling S, Volans G, Heath A. Predicting severity of tricyclic antidepressant overdose. J Toxicol Clin Toxicol 1992 30(2) 161-70. 

Toxicity. Serious medication-related adverse effects associated with actual or potential damage to tissues, organs, or the entire body system. Toxicity may be directly related to critically elevated blood levels of a drug and may be acute (as in tricyclic antidepressant overdose) or chronic (as in prolonged, moderately elevated lithium level). A drug may also produce "toxic effects" at therapeutic doses (such as phenothiazine s potential for inducing bone marrow damage, which in turn causes decreased production of white blood cells). 

Pentel P and Peterson CD (1980) Asystole complicating physostigmine treatment of tricyclic antidepressant overdose. Annals of Emergency Medicine 9 588-590. 

Fluoxetine has been found to cause selective central nervous system (CNS) neuronal uptake inhibition of serotonin. While fluoxetine may bind to adrenergic, muscarinic, and histaminic receptors, it has not been shown to have the profound effects on catecholamines that are common to tricyclic antidepressant overdose patients. 

Once touted as the medication of choice to treat lethal tricyclic antidepressant overdoses, physostigmine (antilirium ) has very limited uses today in overdose management. Physostigmine is a cholinesterase inhibitor and finds its primary application in the treatment of severe anticholinergic poisoning. When indicated, physostigmine is administered preferably in small incremental doses of 2 mg mixed in 10 cc of saline by slow intravenous infusion over 10 min. 

Early signs of tricyclic antidepressant toxicity are due to anticholinergic effects and include tachycardia, mydriasis, dry mouth, low-grade fever, diminished bowel sounds, CNS excitation, and delirium. More serious toxicity is manifested by coma, respiratory depression, seizures, and cardiovascular toxicity including conduction disturbances, hypotension, ventricular arrhythmias, and asystole. Seizures cause hyperthermia, rhabdomyolysis, and metabolic acidosis. Clinical deterioration can be rapid and catastrophic in patients with tricyclic antidepressant overdose. Death most often occurs due to dysrhythmia and circulatory collapse. The typical therapeutic dose of a tricyclic antidepressant is 2-4 mg kg day Doses of 15-20 mg kg are potentially lethal. Therapeutic drug levels for most tricyclic antidepressants range from 100 to... 

The flow of saliva is largely under the control of the parasympathetic nervous system. Collection of saliva may therefore be difficult from individuals who experience anticholinergic symptomatology (e.g., dry mouth associated with tricyclic antidepressant overdose). In addition, salivary flow may be impaired in some alcoholics. 

The CNS manifestations of tricyclic antidepressant overdose may vary from mild agitation or drowsiness to delirium, coma, respiratory depression, or seizures. These manifestations are thought to result in part from central anticholinergic and antfliistaminic actions of these drugs. 

In addition to general supportive measures (gastric lavage, activated charcoal, and IV fluids), therapy for tricyclic antidepressant overdose includes administration of NaHCOs for dysrhythmias (alkahnization causes tricyclic antidepressants to dissociate from the membrane sodium channels and Na" provides a favorable gradient for Na" channel activated... 

Therapy for phenothiazines is generally supportive and similar to that for tricyclic antidepressant overdose. Physostigmine can reverse the central and peripheral anticholinergic manifestations of phenothiazines however, because these manifestations are rarely life-threatening and because physostigmine may cause severe bradycardia or asystole it is not recommended for treatment of pheno-thiazine overdose. Because of the large volume of distribution and extensive protein binding, hemodialysis or hemoperfusion is not beneficial for phenothiazine overdose. 

Smith RK, O Mara K. Tricyclic antidepressant overdose. J Family Pract 1982 15 247-53. 

Patients may deteriorate rapidly and progress from no symptoms to life-threatening cardiotoxicity or seizures within 1 hour. Major symptoms of tricyclic antidepressant overdose typically are manifest within 6 hours of ingestion. The principal effects of tricyclic antidepressant poisoning involve the cardiovascular system and the central nervous system and can result in arrhythmias, hypotension, coma, and seizures (see below). 

In severe tricyclic antidepressant overdose, it would NOT be of value to (A) Administer lidocaine (to control cardiac arrhythmias)... 

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